1. Moscow state medical and dental University. A. I. Evdokimov (Moscow, Russian Federation)

Keywords:polymorbidity, comorbidity, multimorbidity, definition, analysis

Abstract:The semantic problem of designation of a set of diseases is a subject for wide discussion both in the world medical community and in Russia. The article analyzes and clarifies the definitions of “polymorbidity”, “comorbidity” and “multi-morbidity” proposed to refer to the plurality of diseases in one patient. This allows you to objectively look at such a complex and multifaceted problem, which is a multiple pathology.

• References total 18 ⇓ :: .
  1. Tokmachev Yu.K., Lazebnik L. B., Efremov L. I. And etc. the Reasons for diagnostic difficulties and errors in geriatrics. Rubbed.archive, 1984, – № 10, 145–148;
  2. Tokmachev Yu.K., Lazebnik L. B., Efremov L. I., etc. Ethics in geriatrics. Rubbed.archive, 1987, – № 11, 119–122
  3. Lazebnik L. B. Aging and polymorbidity // Consil. med. – 2005. – № 12. – P. 993–996.
  4. Feinstein AR. The pre-therapeutic classification of comorbidity in chronic disease. Journal of Chronic Diseases. 1970;23(7):455–468.
  5. Aryeva G. T., Sovetkina N. V. Ovsyannikova N. A. etc. and multimorbidity Comorbid condition in geriatrics (review) // Uspekhi gerantol. 2011. No. 4. S. 612–619
  6. Vertkin A. L., Skotnikov A. S. Comorbidity. lechashchij vrach. 6, 2013, 54–65
  7. Gudkov R. A., Konovalov O. E. the Comorbidity, multimorbidity, polypathy – three views of concurrent pathology. Bulletin of The peoples ‘ Friendship University of Russia. Series: medicine. 2015, 1,39–45
  8. van Oostrom S. H., Picave tHS, van Gelder B. M., Lemmens L. C., Hoeymans N., van Dijk C. E., Verheij R. A. Multimorbidity and comorbidity in the Dutch population – data from general practices. FGBMCPublicHealth. 2013 Aug30;12:715. doi: 10.1186/1471–2458–12–715.
  9. Komorbidnaya patologiya v klinicheskoj praktike. Klinicheskie rekomendacii. Obshcherossijskaya obshchestvennaya organizaciya Associaciya vrachej obshchej praktiki (semejnyh vrachej). Sekciya “Sochetannye patologii” 2017, otv. red. R. G. Oganov
  10. Tokmachev Yu. K., Lazebnik L. B., Efremov L. I. and others on the teaching of geriatrics in the clinic of internal diseases. Sov.medicine., 1988, vol. 9, 95–98
  11. Lazebnik L. B., Vyortkin A. L., Konev Yu.V., Li E. D., Skotnikov A. S. Starenie. Professional’nyj vrachebnyj podhod. EHksimo. Moskva.2014. 319 S.
  12. Lazebnik L. B., Konev V. Yu., Yefremov, I. L. Polypharmacy: geriatric aspect of the problem. Consilium medicum. 2007, vol. 9, № 12, 29–34
  13. Uemura M, Imataki O., Kawachi Y., Kawakami K., Hoshijima Y., Matsuoka A., Kadowaki. More detailed discussion of the nature of the NNT measure can be found in the EBM Note on summarising the effects of therapy in the journal Evidence-Based Medicine 1997;2:103–4.
  14. N. Charlson comorbidity index predicts poor outcome in CML patients treated with tyrosine kinase inhibitor. Int J Hematol. 2016 Nov;104(5):621–627. Epub 2016 Aug 4.
  15. Dunlay S. M., Chamberlain A. M. Multimorbidity in Older Patients with Cardiovascular Disease. Curr Cardiovasc Risk Rep. Author manuscript; available in PMC2017 Jan 1. Published in final edited form as: Curr Cardiovasc Risk Rep. 2016 Jan; 10: 3. Published online 2016 Jan 26. doi: 10.1007/s12170–016–0491–8 PMCID: PMC4889124
  16. Multimorbidity: Assessment, Prioritisation and Management of Care for People with Commonly Occurring Multimorbidity. NICE Guideline, No. 56. National Guideline Centre (UK).2017
  17. Jakovljević M., Ostojić L. Comorbidity and multimorbidity in medicine today: challenges and opportunities for bringing separated branches of medicine closer to each other. PsychiatrDanub. 2013 Jun;25 Suppl 1:18–28
  18. Morrison D, Agur K, Mercer S, Eiras A, González-Montalvo JI, Gruffydd-Jones K. Managing multimorbidity in primary care in patients with chronic respiratory conditions. NPJ Prim Care Respir Med. 2016 Sep 15;26:16043. doi: 10.1038/npjpcrm.2016.43.

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Lazebnik L. B., Konev Yu. V. HISTORICAL FEATURES AND SEMANTIC DIFFICULTIES OF USING THE TERMS DENOTING MULTIPLICITY OF DISEASES IN ONE PATIENT.Experimental and Clinical Gastroenterology Journal. 2018;154(06):04-09
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1. Gamaleya National Research Centre for Epidemiology and Microbiology, Ministry of Public Health (Moscow, Russian Federation)
2. Lomonosov Moscow State University (Moscow, Russian Federation)
3. Sechenov The First Moscow Medical University, Ministry of Public Health (Moscow, Russian Federation)
4. Federal Research and Clinical Center of Specialized Medical Care and Medical Technologies, Federal Medical and Biological Agency of Russia (Moscow, Russian Federation)

Keywords:Helicobacter pylori, photosensitizers, antimicrobial photo-dynamic therapy

Abstract:Helicobacter pylori, an etiopathogenetic factor of gastritis and gastric and duodenal ulcer disease, is highly sensitive in vitro to antimicrobial photodynamic therapy with zinc octakis(cholinyl)phthalocyanine (o-PCZ). The photosensitizing activity of o-PCZ with molecules bearing eight positively charged substituents, is due to electrostatic binding with negatively charged surface of the cell walls of bacteria. In the bound state, when excited by light, o-PCZ generates singlet oxygen, which has a bactericidal effect. Intensive absorption of o-PCZ in the far-red region of the spectrum allows to use in photodynamic therapy light of wavelengths with high penetrating capacity in the biological environment from led sources.

• References total 30 ⇓ :: .
  1. Eusebi L.H., Zagari R. M., Bazzoli F. Epidemiology of Helicobacter pylori infection // Helicobacter. - 2014. - v. 19. - Suppl. 1. - P. 1-5.
  2. Amieva M. R., El-Omar E. M. Host-bacterial interactions in Helicobacter pylori infection // Gastroenterology. - 2008. - v. 134. - P. 306-323.
  3. Wroblewski L.E., Peek R. M., Wilson K. T. Helicobacter pylori and gastric cancer: factors that modulate disease risk // Clin. Microbiol. Rev. - 2010. - v. 23. - P. 713-739.
  4. Kyburz A., Müller A. Helicobacter pylori and extragastric diseases // Curr. Top. Microbiol. Immunol. - 2017. - v. 400. - P. 325-347. doi: 10.1007/978-3-319-50520-6_14.
  5. Salama N.R., Hartung M. L., Müller A. Life in the human stomach: persistence strategies of the bacterial pathogen Helicobacter pylori // Nat. Rev. Microbiol. - 2013. - v. 11. - No 6. - P. 385-399.
  6. Yuan Y., Ford A. C., Khan K. J. et al. Optimal duration of regimens for Helicobacter pylori eradication // Cochrane Database Syst. Rev. - 2013. - v. 12. - CD008337. doi: 10.1002/14651858.CD008337.pub2
  7. Malfertheiner P., Megraud F., O’Morain C. et al. Management of Helicobacter pylori infection - the Maastricht V / Florence consensus report // Gut. - 2017. - v. 66. - № 1. - P. 6-30. doi:10.1136/gutjnl-2016-312288.
  8. De Francesco V., Bellesia A., Ridola L. et al. First-line therapies for Helicobacter pylori eradication: a critical reappraisal of updated guidelines // Ann. Gastroenterol. - 2017. - v. 30. - P. 373-379.
  9. Graham D.Y, Fischbach L. Helicobacter pylori treatment in the era of increasing antibiotic resistance // Gut. - 2010. - v. 59. - № 8. - P. 1143-1153.
  10. Mégraud F. Antimicrobial resistance and approaches to treatment. In: Sutton P., Mitchell H. M. (eds.). “Helicobacter pylori in the 21st century”. - 2010. - CAB International, Oxfordshire, UK. - 302 P. - P. 45-68.
  11. Pellicano R., Ribaldone D. G., Fagoonee S. et al. A 2016 panorama of Helicobacter pylori infection: key messages for clinicians // Panminerva Medica. - 2016. - v. 58. - № 4. - P. 304-317.
  12. Sperandio F.F., Huang Y. Y., Hamblin M. R. Antimicrobial photodynamic therapy to kill Gram-negative bacteria // Rec. Pat. Antiinfect. Drug Discov. - 2013. - v. 8. - № 2. - P. 108-120.
  13. Jemli M., Alouini Z., Sabbahi S., Gueddari M. Destruction of fecal bacteria in wastewater by three photosensitizers // J. Environ. Monit. - 2002. - v. 4. - № 4. - Р. 511-516.
  14. Marciel L., Teles L., Moreira B. et al. An effective and potentially safe blood disinfection protocol using tetrapyrrolic photosensitizers // Future Med. Chem. - 2017. - v. 9. - № 4. - P. 365-379.
  15. Jori G., Fabris C., Soncin M. et al. Photodynamic therapy in the treatment of microbial infections: basic principles and perspective applications // Lasers Surg. Med. - 2006. - v. 38. - № 5. - Р. 468-481.
  16. Wainwright M., Maisch T., Nonell S. et al. Photoantimicrobials - are we afraid of the light? // Lancet Infect. Dis. - 2017. - v. 17. - № 2. - Р. e49 - e55.
  17. Karlyshev A.V., Ketley J. M., Wren B. W. The Campylobacter jejuni glycome // FEMS Microbiol. Rev. - 2005. - v. 29. - № 2. - P. 377-390.
  18. Nikaido H. Molecular basis of bacterial outer membrane permeability revisited // Microbiol. Mol. Biol. Rev. - 2003. - v. 67. - № 4. - Р. 593-656.
  19. Maisch T. A new strategy to destroy antibiotic resistant microorganisms: antimicrobial photodynamic treatment // Mini Rev. Med. Chem. - 2009. - v. 9. - № 8. - Р. 974-983.
  20. Strakhovskaya M. G., Antonenko Y. N., Pashkovskaya A. A., Kotova E. A., Kireev V., Zhukhovitsky V. G., Kuznetsova N. A., Yuzhakova O. A., Negrimovsky V. M., and Rubin A. B. Electro-static binding of substituted metal phthalocyanines to enterobacte-rial cells: Its role in photodynamic inactivation. Biochemistry (Moscow). 2009;74(12):1305–1314.
  21. Strakhovskaya M. G., Antonenko Y. N., Pashkovskaya A. A., Kotova E. A., Kireev V., Zhukhovitsky V. G., Kuznetsova N. A., Yuzhakova O. A., Negrimovsky V. M., and Rubin A. B. Electro-static binding of substituted metal phthalocyanines to enterobacte-rial cells: Its role in photodynamic inactivation. Biochemistry (Moscow). 2009;74(12):1305-1314.
  22. Zhang W., Shi X., Huang J. et al. Bacitracin-conjugated superparamagnetic iron oxide nanoparticles: synthesis, characterization and antibacterial activity // Chemphyschem. - 2012. - v. 13. - № 14. - P. 3388-3396.
  23. Soon R.L., Nation R. L., Cockram S.et al. Different surface charge of colistin-susceptible and -resistant Acinetobacter baumannii cells measured with zeta potential as a function of growth phase and colistin treatment // J. Antimicrob. Chemother. - 2011. - v. 66. - № 1. - Р. 126-133.
  24. Nguyen V.T., Turner M. S., Dykes G. A. Influence of cell surface hydrophobicity on attachment of Campylobacter to abiotic surfaces // Food Microbiol. - 2011. - v. 28. - № 5. - P. 942-950.
  25. Parreira P., Magalhães A., Gonçalves I. C. et al. Effect of surface chemistry on bacterial adhesion, viability, and morphology // J. Biomed. Mater. Res. Part A. - 2011. - v. 99. - № 3. - P. 344-353.
  26. Ma H., Cummins D. D., Edelstein N. B. et al. Modeling diversity in structures of bacterial outer membrane lipids // J. Chem. Theory Comput. - 2017. - v. 13. - № 2. - P. 811-824.
  27. Stephenson H.N., John C. M., Naz N. et al. // J. Biol. Chem. - 2013. - v. 288. - № 27. - P. 19661-19672.
  28. Safavi M., Sabourian R., Foroumadi A. Treatment of Helicobacter pylori infection: Current and future insights // World J. Clin. Cases. - 2016. - v. 4. - № 1. - P. 5-19.
  29. Simon C., Mohrbacher C., Hüttenberger D. et al. In vitro studies of different irradiation conditions for photodynamic inactivation of Helicobacter pylori. J. Photochem. Photobiol. B. - 2014. - v. 141. - P. 113-118.
  30. Holst O., Moran A. P., Brenan P. J. Overview of the glycosylated components of the bacterial cell envelope // In: Moran A. P. “Microbial glycobiology” (ed.-in-chief), Elsevier, Amsterdam … Tokyo, 2009, 1016 pp. - P. 3-13.

Full text is published :
Zhukhovitsky V.G., Kholina E.G., Strakhovskaya M.G. HELICOBACTER PYLORI PHOTODYNAMIC INACTIVATION IN VITRO WITH ZINC OCTAKIS (CHOLINYL) PHTHALOCYANINE.Experimental and Clinical Gastroenterology Journal. 2018;154(06):10-15
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1. Smolensk state medical University (Smolensk, Russian Federation)

Keywords:chronic gastritis, Helicobacter pylori, hygiene, periodontitis

Abstract:Aim. In the article frequency of defeat of mucous membranes of organs of cavity of mouth and tissues of paradontium is examined at intensifying of chronic erosive gastritis associated with Helicobacter pylori and herpes viral infection. Result. As a result of the study in patients suffering from chronic erosive gastritis associated with Helicobacter pylori and herpesvirus infection, Helicobacter pylori was detected in 100% of cases in the gastric mucosa in the study of biopsies by PCR, urease test, microscopy of smears and in the oral cavity in the study by urease test and PCR method, while the degree of contamination was regarded as high and medium. All patients were divided into 2 groups depending on the severity of the disease. Significantly more often in the first group of studies compared with the second identified high and very high rate of the CPU (χ²=14,280 at p<0.01); the index of hygiene is very poor and unsatisfactory (χ²=11,752; χ²=11,509, at p<0.01, respectively); gingivitis severe (χ²=20,847 when p<0.01); severe inflammation of the gums (χ²=14,849, p<0.01); the third stage of periodontal disease (χ²=26,615 at p<0.05) in the assessment of dental status. No periodontitis was observed in the control group. Conclusions. The infection of Helicobacter pylori serves as the base-line factor of forming of inflammatory diseases of paradontium, initiating development of active erosive gastritis, nosotropic closely associated with gingivitis and periodontitis.

• References total 19 ⇓ :: .
  1. Tsimbalistov A. V., Robakidze NS. Pathophysiological aspects of the development of combined pathology of the oral cavity and gastrointestinal tract, Dentistry for all, 2005, 1, 28–34.
  2. Valenkevych, L. N., Yakhontova O. I. Diseases of the digestive system. Management of gastroenterology for doctors. – SPb. Publishing house DEAN, 2006, 656 p.
  3. Rapoport S. I. Gastrity. Posobie dlya vrachej. Moskva, 2010, 20 s.
  4. Zimmerman Ya. S. Etiology, pathogenesis and treatment of peptic ulcer disease, as-associated with Helicobacter pylori infection: state of the art and prospects, Clinical medicine, 2006, № 3, P. 1–7.
  5. Al-Hawajri A.A., Keret D., Simhon A. et al. Helicobacter pylori DNA in dental plaques, gastroscopy, and dental devices, Digestion disease science, 2004, Vol. 49, № 7/8, P. 1091–1094.
  6. Chumpitaz C.J., Gutierraz M. J., Cordova A. R. et al. isolation of helicobacter pylori in dental plaque in patients with gastritis at «Angamos» clinic, Review gastroenterology Peru, 2006, Vol. 26, № 4, P. 373–376.
  7. Honda K., Ohrusa T., Takashimuzu I. et al. High risk of Helicobacter pylori infection in young Japanese dentists, Journal of gastroenterology and hepatology, 2001, Vol. 16, № 8, P. 862–865.
  8. Chisazi M.t., Fattahi E., Farahani R. M. et al. Helicobacter pylori in the dental plaque: is it of diagnostics value for gastric infection? Medical oral pathology and oral cirbucalis, 2006, Vol. 11, № 4, P. 325–328.
  9. Czesnikiewicz-Guzik M., Bielanski W., Guzikt.J. et al. Helicobacter pylori in the oral cavity and its implications for gastric infection, periodontal health, immunology and dyspepsia, Journal of physiology and pharmacology, 2005, Vol. 56. (Suppl 6), P. 77–89.
  10. Nasrolahei M., Malekii., Emadian O. Helicobacter pylori colonization in dental plaque and gastric infection, Rom journal of gastroenterology, 2003, Vol. 12, № 4, P. 293–296.
  11. Ogunbodede E.O., Lawal O. O., Lamikanra A. et al. Helicobacter pylori in the dental plaque and gastric mucosa of dyspeptic Nigerian patients, tropical gastroenterology, 2002, Vol. 23, № 3, P. 127–133.
  12. Umeda M., Kobayashi Y., Takeuchi Y et al. High prevalence of Helicobacter pylori detected by PCR in the jral cavities of periodontitis patients, Journal of periodontology, 2003, Vol. 74, № 1, P. 129–134
  13. Bazikyan E. A., Mayev I. V., Nikolaeva E. N. Comparison of invasive and non-invasive methods of detection of Helicobacter pylori in the stomach and mouth position in patients with acid-dependent diseases. RJGHC. – 2008. – Vol.18. – No4. – P. 32–37
  14. Neisberg D. M., Stjuf I. Y. The Role of ectopic foci of Helicobacter pylori in chronic periodontitis generalizovannom. Periodontalogia. 2011;59(2):9–13.
  15. Tsimbalistov A. V., Robakidze N. With. The influence of dental hundred-Tusa patients with peptic ulcer disease to infection of the oral cavity and gastric mucosa of Helicobacter pylori. Klin. Dentistry, 2000, № 3, P. 16–18.
  16. Gebara E.C., Faria C. M., Pannuti C. et al. Persistence of Helicobacter pylori in the oral cavity after systemic eradication therapy, J. Clin. Periodontol, 2006, Vol. 33, N5, P. 329–333.
  17. Ozdemir A., Mas M. R., Sahin S. et al. Department of Periodontology, Gеlhane Military Medical Academy, QuintessenceInt, 2001, Vol. 32, N2, P. 131–134.
  18. Anand P.S., NandakumarК., Shenoy К. Т. Are dental plaque, poor oral hygiene, and periodontal disease associated with Helicobacter pylori infection? JPeriodontal, 2006, 77, 4, 692–698.
  19. Aruin L. I. Helicobacter pylori: how one pathogen causes various diseases. Experimental and clinical gastroenterology 2004;1:36–41.

Full text is published :
Afanasenkova T. E., Dubskaya E. E., Dеvlikanova L. I. CHANGES OF THE MUCOUS MEMBRANE OF THE ORAL CAVITY IN THE CHRONIC EROSIVE GASTRITIS ASSOCIATED WITH HELICOBACTER PYLORI AND HERPES INFECTION.Experimental and Clinical Gastroenterology Journal. 2018;154(06):16-21
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1. GBUZ Moscow clinical scientific center of the Department of Health of Moscow (Moscow, Russian Federation)

Keywords: upper digestive tract, motor function, gastroesophageal reflux disease, abdominal obesity

Abstract:Aim. Dyskinesia of the upper digestivel tract is accompanied by the development of gastroesophageal reflux disease (GERD) in abdominal obesity. GERD occurs in the United States at 29.8% of men and 32.5% women and 30% of adults in Western Europe. However, clinical and instrumental characteristics of GERD in obesity are not well understood. The aim - to explore the clinical and instrumental characteristics of GERD in obesity. Methods. The survey included 52 patients with clinical, radiographic and electromyographic studies. The control group consisted of 36 patients. Results. Electromyographic marked increase in retrograde motility of the stomach and esophagus, as well as reduced motor function of duodenum. X-ray showed signs characteristic of GERD. Esophageal pH monitoring revealed the presence of alkaline reflux. Conclusions. The features of GERD in abdominal obesity is the prevalence of dyspepsia and heartburn absence, motor-evacuation disorders showing a decrease in evacuation function of the stomach and the presence of predominantly alkaline reflux.

• References total 19 ⇓ :: .
  1. Dolgikh V. V., Klimkina Yu. N., Rychkova L. V., & Korovin S. A. Epidemiological features of psychosomatic disorders on the example of obesity. // Byul Sib Department of RAMS, 2014;4(98):19–23.
  2. WHO Regional Office for Europe. The challenge of obesity in the WHO European Region and the strategies for response [Digital Source] / Ed. by F. Branca. – 2007. – Access on-line: http://www.euro.who.int/document/E90711.pdf.
  3. Global status report on noncommunicable diseases 2014. WHO, 2014
  4. Berstein L. M. Obesity and cancer: an old problem in the new world. // Obesity and metabolism. 2006;1 (6): 42–47
  5. Zvenigorodskaya L. A. Gastroehzofageal’naya reflyuksnaya bolezn’ u bol’nyh s ozhireniem (klinika, diagnostika, lechenie). Metodicheskie rekomendacii / L. A. Zvenigorodskaya, E.YU. Bondarenko, A.A. CHurikova, T. V. Mishchenkova – M. – 2011. – S.13.
  6. Zvenigorodskaya L. A. Clinical and morphological features of gastroesophageal reflux disease in patients with abdominal obesity / L. A. Zvenigorodskaya, E. Y. Bondarenko, S. G. Khomeriki // Consil. med. Of gastroenterology. 2010;12 (8):5–9.
  7. Lazebnik L. B. Metabolicheskij sindrom i organy pishchevareniya / L. B. Lazebnik, L. A. Zvenigorodskaya // Moscow. Anaharsis Publ. 2009. 146–170.
  8. Lazebnik L. B. results of a multicenter study “Epidemiology of gastroesophageal reflux disease in Russia” (MEGRE) / L. B. Lazebnik, A. A. Masharova, D. S. Bordin et al. / / Ter.archive. 2011;1: 45–50.
  9. Yu. P. Uspensky, E. V. Balukova, N. B. Baryshnikova Gastroesophageal reflux disease in patients with obesity. // Polyclinic. Issue. Of gastroenterology. 2015;2: 14–16.
  10. El-Serag H., Graham D., Satia J. Obesity is independent risk factor for GERD symptoms and erosive esophagitis. // Am. J. Gastroenterol. 2005;10:1243–1250.
  11. Egorova E. G., Zvenigorodskaya L. A., Lazebnik L. B. Metabolic syndrome from the position of gastroenterologist // Ros.Med.Journ. 2005;13 (26):1706–1712.
  12. Anisimova E. V. disorders of the digestive system in obesity. // Saratov scientific-.med. journal. 2011:7(4): 851–856.
  13. Corley D. A., Kubo A. Body mass index and gastroesophageal reflux disease: a systematic review and meta-analysis // Am. J. Gastroenterol. 2006;101:2619–2628.
  14. Di Pietro S. High body mass index does not increase risk of Barrett’s esophagus. 16th United European Gastroenterology Week / Di Pietro S., Marsci E., Stillittano D. et al. // Gut 2008; Vol.-57 (Suppl II): A.108.
  15. Choi C. W. Is obesity associated with gastrophаryngeal reflux disease? / Choi C. W., Kim G. H., Song G. et al. 16th United European Gastroenterology Week. // Gut. 2008;57 (Suppl II): 314.
  16. Lychkova A. E. Coordination of myoelectric activity of the small and large intestine. Experimental and clinical gastroenterology. 2012;3: 59–61.
  17. Lychkova A. E., Puzikov A. M. Electrical activity of the digestive tract and its enteral correction Experimental and clinical Gastroenterol 2015;120(8):25–29.
  18. Ahmetov V. A. Reflyuksnaya bolezn’ i organy-misheni. – M.: MIA, 2007. – S. 12.
  19. Ivashkin V. T. evolution of ideas about the role of motor function disorders esophagus in the pathogenesis of gastroesophageal reflux disease / V. T. Ivashkin, A. S. Trukhmanov / / Russian journal of Gastroenterol, Hepatol and coloproctol. 2010;20 (2):13–19.
  20. Roschina, T. V. Supraesophageal manifestations of gastroesophageal reflux disease. //Clinical prospects of gastroenterology, gepatol. 2003;1: 27–30.
  21. Kachina A. A. Gastroehzofageal’naya reflyuksnaya bolezn’ i ozhirenie: hronobiologicheskie pokazateli serdechno-sosudistoj sistemy i faktory kardiovaskulyarnogo riska. Avtoref dis… kand med nauk. Perm’, 2013
  22. Mayev I. V. Dicheva D. T., Andreev D. N. Approaches to individualization of treatment of gastroesophageal reflux disease. Effective pharmacotherapy. Gastroenterology. 2012. No. 4, p. 18–22

Full text is published :
Zvenigorodskaya L. A., Lychkova A. E., Shinkin M. V., Puzikov A. M. DISTURBANCES OF MOTOR FUNCTION OF THE UPPER DIGESTIVE TRACT WITH THE DEVELOPMENT OF GASTROESOPHAGEAL REFLUX DISEASE IN ABDOMINAL OBESITY.Experimental and Clinical Gastroenterology Journal. 2018;154(06):22-28
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1. Pirogov Russian National Research Medical University. Russian Clinical Research Center for Gerontology (Moscow, Russian Federation)
2. Moscow institute of physics and technology (Moscow, Russian Federation)
3. “National Medical Research Center of Cardiology” of the Ministry of Healthcare of the Russian Federation (Moscow, Russian Federation)

Keywords: gut microbiota, obesity

Abstract:Purpose of the study. To study the association between the gut microbiota composition and body mass index and abdominal obesity in participants without clinical chronic diseases. Materials and methods. The study included 92 residents from Moscow and the Moscow region, men and women aged 25 to 76 years without clinical chronic non-communicable diseases are not receiving medication, but with the possible presence of cardiovascular risk factors, including obesity. All participants underwent a thorough preliminary examination, including physical examination, clinical and biochemical blood tests, electrocardiography, treadmill test, evaluation of the presence of the cardiovascular risk factors, as well as the sequencing of the variable regions of the V3-V4 16S rRNA gene of the gut microbiota and diet analysis. Results. The study revealed that opportunistic bacteria of the genera Serratia and Prevotella were largely represented in overweight patients and / or patients with abdominal obesity. Amylolytic bacteria of the genus Oscillosipa were less represented in individuals with abdominal obesity. Probiotic bacteria of the genus Bifidobacterium producing SCFA were significantly less represented in people who consumed a lot of cholesterol or ethanol. Conclusion. Gut microbiota imbalance with an increase in opportunistic bacteria level and a decrease in strictly anaerobic amylolytic bacteria is associated with obesity.

• References total 29 ⇓ :: .
  1. Cani P.D., Neyrinck A. M., Fava F., Knauf C., Burcelin R. G., Tuohy K. M., Gibson G. R., Delzenne N. M. Selective increases of bifidobacteria in gut microflora improve high-fat-diet-induced diabetes in mice through a mechanism associated with endotoxaemia // Diabetologia. 2007. Т. 50. № 11. - C. 2374-83.
  2. Cani P.D., Amar J., Iglesias M. A., Poggi M., Knauf C., Bastelica D., Neyrinck A. M., Fava F., Tuohy K. M., Chabo C., Waget A., Delmee E., Cousin B., Sulpice T., Chamontin B., Ferrieres J., Tanti J. F., Gibson G. R., Casteilla L., Delzenne N. M., Alessi M. C., Burcelin R. Metabolic endotoxemia initiates obesity and insulin resistance // Diabetes. 2007. Т. 56. № 7. - C. 1761-72.
  3. Ding S., Chi M. M., Scull B. P., Rigby R., Schwerbrock N. M., Magness S., Jobin C., Lund P. K. High-fat diet: bacteria interactions promote intestinal inflammation which precedes and correlates with obesity and insulin resistance in mouse // PLoS One. 2010. Т. 5. № 8. - C. e12191.
  4. Backhed F., Ding H., Wang T., Hooper L. V., Koh G. Y., Nagy A., Semenkovich C. F., Gordon J. I. The gut microbiota as an environmental factor that regulates fat storage // Proc Natl Acad Sci U S A. 2004. Т. 101. № 44. - C. 15718-23.
  5. Turnbaugh P.J., Ley R. E., Mahowald M. A., Magrini V., Mardis E. R., Gordon J. I. An obesity-associated gut microbiome with increased capacity for energy harvest // Nature. 2006. Т. 444. № 7122. - C. 1027-31.
  6. Ley R.E., Turnbaugh P. J., Klein S., Gordon J. I. Microbial ecology: human gut microbes associated with obesity // Nature. 2006. Т. 444. № 7122. - C. 1022-3.
  7. Turnbaugh P.J., Hamady M., Yatsunenko T., Cantarel B. L., Duncan A., Ley R. E., Sogin M. L., Jones W. J., Roe B. A., Affourtit J. P., Egholm M., Henrissat B., Heath A. C., Knight R., Gordon J. I. A core gut microbiome in obese and lean twins // Nature. 2009. Т. 457. № 7228. - C. 480-4.
  8. Schwiertz A., Taras D., Schafer K., Beijer S., Bos N. A., Donus C., Hardt P. D. Microbiota and SCFA in lean and overweight healthy subjects // Obesity (Silver Spring). 2010. Т. 18. № 1. - C. 190-5.
  9. Duncan S.H., Lobley G. E., Holtrop G., Ince J., Johnstone A. M., Louis P., Flint H. J. Human colonic microbiota associated with diet, obesity and weight loss // Int J Obes (Lond). 2008. Т. 32. № 11. - C. 1720-4.
  10. Xiong Y., Miyamoto N., Shibata K., Valasek M. A., Motoike T., Kedzierski R. M., Yanagisawa M. Short-chain fatty acids stimulate leptin production in adipocytes through the G protein-coupled receptor GPR41 // Proc Natl Acad Sci U S A. 2004. Т. 101. № 4. - C. 1045-50.
  11. Kimura I., Ozawa K., Inoue D., Imamura T., Kimura K., Maeda T., Terasawa K., Kashihara D., Hirano K., Tani T., Takahashi T., Miyauchi S., Shioi G., Inoue H., Tsujimoto G. The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43 // Nat Commun. 2013. Т. 4. - C. 1829.
  12. Dewulf E.M., Cani P. D., Claus S. P., Fuentes S., Puylaert P. G., Neyrinck A. M., Bindels L. B., de Vos W. M., Gibson G. R., Thissen J. P., Delzenne N. M. Insight into the prebiotic concept: lessons from an exploratory, double blind intervention study with inulin-type fructans in obese women // Gut. 2013. Т. 62. № 8. - C. 1112-21.
  13. Kadooka Y., Sato M., Imaizumi K., Ogawa A., Ikuyama K., Akai Y., Okano M., Kagoshima M., Tsuchida T. Regulation of abdominal adiposity by probiotics (Lactobacillus gasseri SBT2055) in adults with obese tendencies in a randomized controlled trial // Eur J Clin Nutr. 2010. Т. 64. № 6. - C. 636-43.
  14. Yumuk V., Tsigos C., Fried M., Schindler K., Busetto L., Micic D., Toplak H. Obesity Management Task Force of the European Association for the Study of O. European Guidelines for Obesity Management in Adults // Obes Facts. 2015. Т. 8. № 6. - C. 402-24.
  15. Caporaso J.G., Kuczynski J., Stombaugh J., Bittinger K., Bushman F. D., Costello E. K., Fierer N., Pena A. G., Goodrich J. K., Gordon J. I., Huttley G. A., Kelley S. T., Knights D., Koenig J. E., Ley R. E., Lozupone C. A., McDonald D., Muegge B. D., Pirrung M., Reeder J., Sevinsky J. R., Turnbaugh P. J., Walters W. A., Widmann J., Yatsunenko T., Zaneveld J., Knight R. QIIME allows analysis of high-throughput community sequencing data // Nat Methods. 2010. Т. 7. № 5. - C. 335-6.
  16. Zhang H., Lu N., Feng C., Thurston S. W., Xia Y., Zhu L., Tu X. M. On fitting generalized linear mixed-effects models for binary responses using different statistical packages // Stat Med. 2011. Т. 30. № 20. - C. 2562-72.
  17. Thomas V., Clark J., Dore J. Fecal microbiota analysis: an overview of sample collection methods and sequencing strategies // Future Microbiol. 2015. Т. 10. № 9. - C. 1485-504.
  18. Arumugam M., Raes J., Pelletier E., Le Paslier D., Yamada T., et al. Enterotypes of the human gut microbiome // Nature. 2011. Т. 473. № 7346. - C. 174-80.
  19. Kida Y., Inoue H., Shimizu T., Kuwano K. Serratia marcescens serralysin induces inflammatory responses through protease-activated receptor 2 // Infect Immun. 2007. Т. 75. № 1. - C. 164-74.
  20. Wright D.P., Rosendale D. I., Robertson A. M. Prevotella enzymes involved in mucin oligosaccharide degradation and evidence for a small operon of genes expressed during growth on mucin // FEMS Microbiol Lett. 2000. Т. 190. № 1. - C. 73-9.
  21. Tims S., Derom C., Jonkers D. M., Vlietinck R., Saris W. H., Kleerebezem M., de Vos W. M., Zoetendal E. G. Microbiota conservation and BMI signatures in adult monozygotic twins // ISME J. 2013. Т. 7. № 4. - C. 707-17.
  22. Konikoff T., Gophna U. Oscillospira: a Central, Enigmatic Component of the Human Gut Microbiota // Trends Microbiol. 2016. Т. 24. № 7. - C. 523-4.
  23. Simpson H.L., Campbell B. J. Review article: dietary fibre-microbiota interactions // Aliment Pharmacol Ther. 2015. Т. 42. № 2. - C. 158-79.
  24. Wang J.H., Bose S., Kim H. G., Han K. S., Kim H. Fermented Rhizoma Atractylodis Macrocephalae alleviates high fat diet-induced obesity in association with regulation of intestinal permeability and microbiota in rats // Sci Rep. 2015. Т. 5. - C. 8391.
  25. DiRienzo D. B. Effect of probiotics on biomarkers of cardiovascular disease: implications for heart-healthy diets // Nutr Rev. 2014. Т. 72. № 1. - C. 18-29.
  26. Guardamagna O., Amaretti A., Puddu P. E., Raimondi S., Abello F., Cagliero P., Rossi M. Bifidobacteria supplementation: effects on plasma lipid profiles in dyslipidemic children // Nutrition. 2014. Т. 30. № 7-8. - C. 831-6.
  27. Liu S., Ren F., Zhao L., Jiang L., Hao Y., Jin J., Zhang M., Guo H., Lei X., Sun E., Liu H. Starch and starch hydrolysates are favorable carbon sources for bifidobacteria in the human gut // BMC Microbiol. 2015. Т. 15. - C. 54.
  28. Zi-Ni T., Rosma A., Napisah H., Karim A. A., Liong M. T. Characteristics of Metroxylon sagu resistant starch type III as prebiotic substance // J Food Sci. 2015. Т. 80. № 4. - C. H875-82.
  29. Kirpich I.A., Solovieva N. V., Leikhter S. N., Shidakova N. A., Lebedeva O. V., Sidorov P. I., Bazhukova T. A., Soloviev A. G., Barve S. S., McClain C.J., Cave M. Probiotics restore bowel flora and improve liver enzymes in human alcohol-induced liver injury: a pilot study // Alcohol. 2008. Т. 42. № 8. - C. 675-82.

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Kashtanova D. A., Tkacheva O. N., Kotowska Yu.V., Popenko A. C. et al. THE COMPOSITION OF THE INTESTINAL MICROBIOTA FROM HEALTHY RESIDENTS OF MOSCOW AND MOSCOW REGION WITH OBESITY.Experimental and Clinical Gastroenterology Journal. 2018;154(06):29-35
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1. Federal State Budgetary Scientific Institution “Federal Research Centre “Krasnoyarsk Science Centre” of the Siberian Branch of Russian Academy of Science” (FRC KSC SB RAS), “Scientific Research Institute of medical problems of the North” (SRI MPN) (Krasnoyarsk, Russia)
2. NUZ Road Clinical Hospital (Krasnoyarsk, Russia)
3. Federal State-Funded Educational Institution of Higher Professional Education “Katanov Khakass State University” (Abakan, Russia)

Keywords:GERD, dyspepsia, heartburn, esophagitis, overlap

Abstract:Aim. To study the overlap syndrome of GERD and dyspepsia in a population study. Methods: A clinical and epidemiological study was performed, during which 1411 adult patients (506 indigenous and 905 alien inhabitants) were examined in an organized population with a coverage of 93%. Results. The prevalence of weekly heartburn was 12.2% in Caucasians and 8.3% in Khakassians (p = 0.03). Dyspepsia was detected in 20.2% of alien inhabitants and in 15.8% of indigenous people (p = 0.05). Dyspepsia was registered 7.1 times more often in Caucasians with weekly heartburn (p <0.001) and 6.3 times more often in the same group of Khakassians (p <0.001) compared to those without heartburn. Conclusions. It was concluded that there is overlap syndrome of GERD and dyspepsia in indigenous and alien inhabitants of Khakassia.

• References total 15 ⇓ :: .
  1. Park K.S., Jee S. R., Lee B. E. et al. Nationwide Multicenter Study for Overlaps of Common Functional Gastrointestinal Disorders in Korean Patients With Constipation // J. Neurogastroenterol. Motil. - 2017. - Vol. 23, № 4. - P. 569-577
  2. Richter J.E., Rubenstein J. H. Presentation and Epidemiology of Gastroesophageal Reflux Disease // Gastroenterology. - 2018. - Vol. 154, № 2. - P. 267-276.
  3. Eusebi L.H., Ratnakumaran R., Bazzoli F., Ford AC. Prevalence of Dyspepsia in Individuals With Gastroesophageal Reflux-Type Symptoms in the Community: A Systematic Review and Meta-analysis // Clin. Gastroenterol. Hepatol. - 2018. - Vol. 16, № 1. - P. 39-48.
  4. Takeuchi T., Takahashi Y., Kawaguchi S. et al. Therapy of gastroesophageal reflux disease and functional dyspepsia overlaps with symptoms after usual-dose proton pump inhibitor: Acotiamide plus usual-dose proton pump inhibitor versus double-dose proton pump inhibitor // J. Gastroenterol. Hepatol. - 2018. - Vol. 33, № 3. - P. 623-630.
  5. Vakil N., van Zanten S. V., Kahrilas P. et al. The Montreal definition and classification of gastroesophageal reflux disease: a global evidence-based consensus // Am J Gastroenterol. - 2006. - Vol.101, № 8. - P. 1900-1920.
  6. Tack J., Talley N. J., Camilleri M. et al. Functional gastroduodenal disorders // Gastroenterology. - 2006. - Vol. 130, № 5. - P. 1466-1479.
  7. Talley N.J., Vakil N. B., Moayyedi P. American gastroenterological association technical review on the evaluation of dyspepsia // Gastroenterology. - 2005. - Vol. 129, № 5. - P. 1756-1780.
  8. Ghoshal U.C., Singh R., Chang F. Y. et al. Epidemiology of uninvestigated and functional dyspepsia in Asia: facts and fiction // J. Neurogastroenterol. Motil. - 2011. - Vol. 17, № 3. - P. 235-244.
  9. Aziz I., Palsson O. S., Törnblom H. et al. Epidemiology, clinical characteristics, and associations for symptom-based Rome IV functional dyspepsia in adults in the USA, Canada, and the UK: a cross-sectional population-based study // Lancet Gastroenterol. Hepatol. - 2018. - Vol. 3, № 4. - P. 252-262.
  10. Shtygasheva O. V., Tsukanov V. V. Association of Cag a and Vac a of helicobacter pylori and pulmonary diseases in the organized population of Abakan. RJGHC. – 2004. – Vol.14. – No2. – P. 84–87.
  11. Ageyeva Ye.S., Shtygasheva O. V., Ryazantseva N. V., Tsukanov V. V. Molecular genetic factors influencing outcomes of Helicobacter pylori infection at Khakasia republic inhabitants. RJGHC. – 2010. – Vol.20. – No4. – P. 16–21.
  12. Tsukanov V. V., Khomenko O. V., Rzhavicheva O. S., Butorin N. N., Shtygasheva O. V., Maady A. S., Bichurina T. B., Amelchugova O. S. Prevalence of Helicobacter pylori and GERD at Mongoloids and Caucasians of Eastern Siberia. RJGHC. – 2009. – Vol.19. – No3. – P. 38–41.
  13. Rasmussen S., Jensen T. H., Henriksen S. L. et al. Overlap of symptoms of gastroesophageal reflux disease, dyspepsia and irritable bowel syndrome in the general population // Scand. J. Gastroenterol. – 2015. – Vol. 50, № 2. – P. 162–169.
  14. Min B.H., Huh K. C., Jung H. K. et al. Prevalence of uninvestigated dyspepsia and gastroesophageal reflux disease in Korea: a population-based study using the Rome III criteria // Dig. Dis. Sci. – 2014. – Vol. 59, № 11. – P. 2721–2729.
  15. Hsu C.S., Wen S. H., Hung J. S. et al. Overlap of Dyspepsia in Patients with Gastroesophageal Reflux Disease: Impact of Clinical, Metabolic, and Psychosocial Characteristics // Dig. Dis. Sci. – 2017. – Vol. 62, № 4. – P. 994–1001.

Full text is published :
Tsukanov V. V., Vasyutin A. V., Tonkikh J. L., Rzhavicheva O.S. et al. OVERLAP SYNDROME OF GERD AND DYSPEPSIA.Experimental and Clinical Gastroenterology Journal. 2018;154(06):36-39
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1. State educational government-financed institution of higher professional education “Far East state medical university”, Ministry of Healthcare of the Russian Federation (Khabarovsk, Russia)
2. Non-government healthcare institution “Khabarovsk-1 Road clinical hospital, Open Society «Russian Railways»” (Khabarovsk, Russia)

Keywords:irritable bowel syndrome, fecal calprotectin, small intestinal bacterial overgrowth, ileum mucosal inflammation

Abstract:Aim. We aimed to determine possible interrelation between fecal calprotectin (FC) level, that small intestinal bacterial overgrowth (SIBO) and ileum mucosal inflammation in patients with irritable bowel syndrome (IBS). Methods. Based on Rome III criteria, 495 IBS patients (376 female, mean age 36,6±0,4 years) were included. All patients underwent FC levels, ileocolonoscopy with biopsies of the terminal ileum and H2 lactulose breath test to evaluate the presence of SIBO. Results. Among the 495 IBS patients 57% had reproducibly elevated calprotectin, including 17% with levels higher than 100 µg/g. SIBO was more frequent among IBS patients with elevated FC levels (>100 μg/g) than in those with normal FC levels (0-50μg/g) (77,1% vs 64,8%, р=0,011). We found a correlation between abnormal levels of FC and the presence of SIBO (Spearman r=0,153, p=0,001). Faecal calprotectin greater than 100 µg/g was predictive of ileum mucosal inflammation in IBS patients (OR6,19, 95%CI 3,99-9,61, р<0,0001). The abnormal calprotectin level was correlated with the grade ileum mucosal inflammation (Spearman r=0,399, p<0,0001). Conclusion. In IBS patients with SIBO the low-grade ileum mucosal inflammation was more frequent than in patients with IBS without SIBO (OR2.69, 95% CI 1.79-4.04, p <0.0001). Elevated FC levels (>100μg/g) were associated with low-grade ileum mucosal inflammation in IBS patients (OR6,19, 95%CI 3,99-9,61, р<0,0001).

• References total 16 ⇓ :: .
  1. Schmulson M., Bielsa M. V., Carmona-Sánchez R. et al. Microbiota, gastrointestinal infections, low-grade inflammation, and antibiotic therapy in irritable bowel syndrome: an evidence-based review // Rev. Gastroenterol. Mex. - 2014. - Vol. 79, N3. - P. 96-134.
  2. Sydora M.J., Sydora B. C., Fedorak R. N. Validation of a point-of-care desk top device to quantitate fecal calprotectin and distinguish inflammatory bowel disease from irritable bowel syndrome // J. Crohns Colitis. - 2012. - Vol. 6, N2. - P. 207-214.
  3. Montalto M., Santoro L., Dalvai S. et al. Fecal calprotectin concentrations in patients with small intestinal bacterial overgrowth / // Dig Dis. - 2008. - Vol. 26, N2. - P. 183-186.
  4. Melchior C., Aziz M., Aubry T. et al. Does calprotectin level identify a subgroup among patients suffering from irritable bowel syndrome? Results of a prospective study // United European Gastroenterology Journal. - 2017. - Vol. 5, N2. - Р: 261-269.
  5. David L., Babin A., Picos A. et al. Small Intestinal Bacterial Overgrowth is Associated with Intestinal Inflammation in the Irritable Bowel Syndrome // Clujul Medical. - 2014. - Vol. 87, N3. - P. 163-165.
  6. Longstreth G.F., Thompson W. G., Chey W. D. et al. Functional bowel disorders // Gastroenterology. - 2006. - Vol. 130, N5. - P. 1480-1491.
  7. Francis C.Y., Morris J., Whorwell P. J. The irritable bowel severity scoring system: a simple method of monitoring irritable bowel syndrome and its progress. // Aliment Pharmacol Ther. - 1997. - Vol. 11, № 2. - P. 395-402.
  8. Poluektova Ye.A., Lyashenko O. S., Shifrin O. S., Sheptulin A. A., Ivashkin V. T. Modern methods of studying of human gastro-intestinal microflora // Ros. zhurn. gastroenterol. gepatol. koloproktol. – 2014. – Vol.24, N2. – Р. 85–91.
  9. Schwartz M., Regueiro M. Prevention and treatment of postoperative Crohn’s disease recurrence: an update for a new decade // Curr. Gastroenterol. Rep. - 2011. - Vol.13, N1. - Р. 95-100.
  10. Keohane J., O’Mahony C., O’Mahony L. et al. Irritable bowel syndrome-type symptoms in patients with inflammatory bowel disease: a real association or reflection of occult inflammation? // Am. J. Gastroenterol. - 2010. - Vol.105, N8. - Р. 1789-1794.
  11. Osipenko M. F., Skalinskaya M. I. The role of calprotectin in the diagnosis of diseases of the intestine // Consilium medicum. Gastroenterol. – 2013. – N2. – Р. 38–40.
  12. Öhman L., Törnblom H., Le Neve B. et al. The pathophysiology and severity of symptoms in IBS patients are not associated with mucosal immune activity as determined by fecal calprotectin // Gastroenterology. - 2013. - Vol. 144, N5: Supplement 1 - P. S-725.
  13. González-Castro A.M., Martínez C., Salvo-Romero E. et al. Mucosal pathobiology and molecular signature of epithelial barrier dysfunction in the small intestine in Irritable Bowel Syndrome // J Gastroenterol Hepatol. - 2017. - Vol. 32, N1. - P. 53-63.
  14. Däbritz J., Musci J., Foell D. Diagnostic utility of faecal biomarkers in patients with irritable bowel syndrome // World J. Gastroenterol. - 2014. - Vol. 20, N2. - P. 363-375.
  15. Nicolas S., Blasco-Baque V., Fournel A. et al. Transfer of dysbiotic gut microbiota has beneficial effects on host liver metabolism // Molecular Systems Biology. - 2017. - Vol. 13, N3. - P. 921.
  16. Barbara G., Zecchi L., Barbaro R. et al. Mucosal permeability and immune activation as potential therapeutic targets of probiotics in irritable bowel syndrome // J Clin Gastroenterol. - 2012. - Vol. 46, S. - P. 52-55.

Full text is published :
Alexeenko S. A., Krapivnaia O. V. INTERRELATION BETWEEN FECAL CALPROTECTIN LEVEL, SMALL INTESTINAL BACTERIAL OVERGROWTH AND HISTOLOGICAL MUCOSAL INFLAMMATION IN THE TERMINAL ILEUM IN IBS PATIENTS. Experimental and Clinical Gastroenterology Journal. 2018;154(06):40-44
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1. “Peoples Friendship University of Russia” (Moscow, Russian Federation)

Abstract:Aim: The aim of this study was to assess the incidence, clinical and instrumental associations and prognostic value of cardiohepatic syndrome (CHS) phenotypes CHS in decompensated heart failure (DHF). Methods: CHS was diagnosed in 322 patients with DHF (190 male, 70±11 years (M±SD), arterial hypertension 87%, myocardial infarction 57%, atrial fibrillation 65%, type 2 diabetes mellitus 42%, left ventricular ejection fraction (EF) 38±13%, EF<40% 50%, NYHA IV 56%) when at least one liver function test (LFT) level exceeded upper normal limit on admission. Only alanine transaminase (ALT) and/or aspartate transaminase (AST) increase was considered as hepatocellular CHS, isolated increase of gamma-glutamyl transpeptidase (GGT), alkaline phosphatase (AP), direct bilirubin (DB) and total bilirubin (TB) due DB increase - as cholestatic CHS, the simultaneous increase of markers of cytolysis and cholestasis - as mixed CHS. Mann-Whitney U, Kruskal-Wallis and Pearson’s chi-square tests were used. P <0.05 was considered significant for paired comparison, <0,017 - for comparison of 3 groups. Results: CHS occurs in 85,1% patients, predominantly mixed (66,8%) and moderate (LFT increase ≤ 3UNL). Patients with mixed vs cholestatic CHS had higher levels of LFT, incidence of cholestatic markers increase, NT-proBNP level, hypoperfusion (high heart rate, lower systolic blood pressure (BP) and pulse BP on admission), higher rate of incidence of EF<35% and vasopressor therapy. No significant differences in signs of congestion were observed between groups. Mixed CHS was associated with higher all-cause death in 6 months (30 vs 23%, p<0.05). Conclusions: Mixed CHS predominates in patients with DHF and is associated with more pronounced LFT increase, higher NT-proBNP levels, hypoperfusion (lower systolic and pulse BP, EF <35%, use of vasopressors and inotropes, worse prognosis.

• References total 27 ⇓ :: .
  1. Harjola V.P., Mullens W., Banaszewski M., et al. Organ dysfunction, injury and failure in acute heart failure: from pathophysiology to diagnosis and management. A review on behalf of the Acute Heart Failure Committee of the Heart Failure Association (HFA) of the European Society of Cardiology (ESC). Eur J Heart Fail., 2017, vol. 19, no. 7, pp. 821-836.
  2. Laribi S., Mebazaa A. Cardiohepatic Syndrome: Liver Injury in Decompensated Heart Failure. Curr Heart Fail Rep., 2014, vol. 11, no. 3, pp. 236-40.
  3. Samsky M.D., Patel C. B. et al. Cardiohepatic Interactions in Heart Failure An Overview and Clinical Implications. J Am Coll Cardiol, 2013, vol. 61, pp. 2397-405.
  4. Poelzl G., Auer J. Cardiohepatic syndrome. Curr Heart Fail Rep., 2015, vol. 12, no. 1, pp. 68–78.
  5. Podymova S. D. Liver lesions in patients with acute and chronic heart diseases. Clinical prospects of gastroenterology, Hepatology, 2014, № 4, c. 9–15.
  6. Кобалава Ж.Д., Виллевальде С. В., Соловьева А. Е. Сердечно-печеночный синдром при сердечной недостаточности: распространенность, патогенез, прогностическое значение. Кардиология, 2016, № 12, c. 63–71.
  7. Cardio-hepatic Syndrome in Heart Failure: Prevalence, Pathogenesis and Prognostic Significance. Kardiologiia. 2016; 54 (12):63-71
  8. DOI: http://dx.doi.org/10.18565/cardio.2016.12.63-7
  9. Storozhakov G. I., Oskanova R. S., Ilchenko L. Yu., et al. Hypoxic hepatitis. Archives of internal medicine, 2014, vol. 6, No. 20, p. 42–47.
  10. Ponikowski P., Voors A. A., Anker S. D., et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. Eur J Heart Fail., 2016, vol. 18, no. 8, pp. 891–975.
  11. Mareev V. Yu., Fomin I. V., Ageev F. T., et al. Clinical guidelines. Chronic heart failure (CHF). Journal of Heart Failure, 2017, T. 18, No. 1, C. 3–40.
  12. Ambrosy A.P., Vaduganathan M., Huffman M. D., et al. Clinical course and predictive value of liver function tests in patients hospitalized for worsening heart failure with reduced ejection fraction: an analysis of the EVEREST trial. Eur J Heart Fail., 2012, vol. 14, no. 3, pp. 302–311.
  13. Samsky M.D., Dunning A., DeVore A.D., et al. Liver function tests in patients with acute heart failure and associated outcomes: insights from ASCEND-HF. Eur J Heart Fail., 2016, vol. 18, no. 4, 424–432.
  14. Nikolaou M., Parissis J., Yilmaz M. B., et al. Liver function abnormalities, clinical profile, and outcome in acute decompensated heart failure. Eur Heart J, 2013, vol. 34, no. 10, pp. 742-9.
  15. van Deursen V. M., Edwards C., Cotter G., et al. Liver function, in-hospital, and post-discharge clinical outcome in patients with acute heart failure-results from the relaxin for the treatment of patients with acute heart failure study. J Card Fail., 2014, vol. 20, no. 6, pp. 407-413.
  16. Vyskocilova K., Spinarova L., Spinar J., et al. Prevalence and clinical significance of liver function abnormalities in patients with acute heart failure. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub,. 2015, vol. 159, no. 3, pp. 429-36.
  17. Brisco M.A., McCauley B.D., Chen J., et al. Biochemical evidence of mild hepatic dysfunction identifies decompensated heart failure patients with reversible renal dysfunction. J Card Fail., 2013, vol. 19, no. 11, pp. 739-745.
  18. Parissis J.T., Farmakis D., Andreoli C., et al. Cardio-reno-hepatic interactions in acute heart failure: the role of γ-glutamyl transferase. Int J Cardiol., 2014, vol. 173, no. 3, pp. 556-557.
  19. Akhmatov J. R., T. A. Abdullaev, B. U. Mardanov, et al. Systemic disorders in patients with cardiomyopathy: biochemical profile depending on the clinical form of the disease. Eurasian cardiology journal, 2014, № 3, p. 24–29
  20. Yudin A. L., Afukov O. A., Klyanchin A. A., A. A. Uchevatkin A Visualization congestive hepatopathy. Medical imaging, 2016, № 5, p. 59–66.
  21. Kinzerskaya M. L. the Relationship of myocardial remodeling with structural-functional characteristics of the liver in chronic heart failure. Ultrasonic and functional diagnostics, 2006, № 6, p. 58–64.
  22. Biegus J., Hillege H. L., Postmus D., et al. Abnormal liver function tests in acute heart failure: relationship with clinical characteristics and outcome in the PROTECT study. Eur J Heart Fail., 2016, vol. 18, no. 7, pp. 830-839
  23. Binanay C.I., Califf R. M., Hasselblad V., et al. Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness: the ESCAPE trial. JAMA, 2005, vol. 294, no. 13, pp. 1625-1633
  24. Scholfield M., Schabath M. B., Guglin M. Longitudinal Trends, Hemodynamic Profiles, and Prognostic Value of Abnormal Liver Function Tests in Patients with Acute Decompensated Heart Failure: an Analysis of the ESCAPE Trial. J Card Fail., 2014, vol. 20, no. 7, pp. 476-84
  25. Shinagawa H., Inomata T., Koitabashi T., et al. Prognostic significance of increased serum bilirubin levels coincident with cardiac decompensation in chronic heart failure. Circ J., 2008, vol.72, pp.364-369
  26. Ford R.M., Book W., Spivey J. R. Liver disease related to the heart. Transplantation Reviews, 2015, vol. 29, pp. 33-37
  27. von Haehling S., Schefold J. C., Jankowska E. A., et al. Ursodeoxycholic acid in patients with chronic heart failure: a double-blind, randomized, placebo-controlled, crossover trial. J Am Coll Cardiol., 2012, vol. 59, no. 6, pp. 585-592

Full text is published :
Soloveva A. E., Bayarsaikhan M., Villevalde S. V., Kobalava Z. D. LIVER INJURY MARKERS IN DECOMPENSATED HEART FAILURE: PHENOTYPES, CLINICAL AND PROGNOSTIC VALUE. Experimental and Clinical Gastroenterology Journal. 2018;154(06):45-51
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1. “Peoples Friendship University of Russia” (Moscow, Russian Federation)

Keywords:alcohol, liver liver, cardiac dysfunction, cardiac remodeling

Abstract:Objective: To evaluate structural and functional cardiac changes in patients with alcoholic cirrhosis in relation to the severity of liver disease. Methods: Study included 80 patients with alcoholic liver cirrhosis (LC) without history of cardiovascular and respiratory disease. ECG, echocardiography were performed. Plasma values of NT-proBNP were evaluated in 60 patients. Results: Left ventricular ejection fraction was normal in all patients (mean value 65,3 ± 5,8%). Left ventricular hypertrophy (LVH) (LVMI 149,8 ± 20 g/m 2) and LV diastolic dysfunction were observed in 33 (40,7%) and 58 (71,6%) patients, respectively. Median NT-proBNP value was 621,5 pg/ml (min 33 pg/ml; max 3849 pg/ml), NT-proBNP elevation (> 125 pg/ml) was observed in 47 (58%) patients. NT-proBNP level positively correlated with the number of points on the Child-Pugh score (R =0,27, p < 0,05). There was no relationship between the severity of cirrhosis and structural and functional cardiac changes. Conclusion: Patients with alcoholic LC frequently demostrate structural and functional cardiac changes such as left ventricular hypertrophy, diastolic dysfunction. NT-proBNP elevation was observed in more than half of the patients and directly correlated with the severity of cirrhosis.

• References total 26 ⇓ :: .
  1. Klatsky A.L, Friedman G.D, Siegelaub A.B, et al: Alcohol consumption and blood pressure. N Engl J Med 1977; 296:1194-1200
  2. Kowalski H, Abelmann W.H. The cardiac output at rest in Laennec’s cirrhosis. J Clin Invest 1953;32:1025-1033.
  3. Moller S, Henriksen J.H. Cardiovascular complications of cirrhosis. Gut 2008;57:268-278.
  4. Sola E, Gines P. Renal and circulatory dysfunction in cirrhosis: current management and future perspectives. J Hepatol. 2010;53:1135-1145.
  5. Martell M, Coll M, Ezkurdia N, Raurell I, Genesca J. Physiopathology of splanchnic vasodilation in portal hypertension. World J Hepatol 2010;2:208-220.
  6. Limas C.J, Guiha N.H, Lekagul O, Cohn J.N. Impaired left ventricular function in alcoholic cirrhosis with ascites. Ineffectiveness of ouabain. Circulation 1974;49:754-760.
  7. Caramelo C, Fernandez-Munoz D, Santos J.C, Blanchart A, Rodriguez-Puyol D, Lopez-Novoa J.M, Hernando L: Effect of volume expansion expansion on hemodynamics, capillary permeability and renal function in conscious, cirrhotic rats. J Hepatol 1986;6:129-134.
  8. Ingles A.C, Hernandez I, Garcia-Estan J, Quesada T, Carbonell L.F. Limited cardiac preload reserve in conscious cirrhotic rats. Am J Physiol 1991;260: H1912-917.
  9. Lee S.S, Marty J, Mantz J, Samain E, Braillon A, Lebrec D: Desensitization of myocardial β-adrenergic receptors in cirrhotic rats. J Hepatol 1990;12:481-485.
  10. Donovan, C.L., et al. Two dimensional and dobutamine stress echocardiography in the prospective assessment of patients with end stage liver disease prior to orthotopic liver transplantation. Transplantation. 1996;61:1180-1188.
  11. Myers, R.P. and Lee, S.S. (2000) Cirrhotic cardiomyopathy and liver transplantation. Liver Transpl. 2000;6; S44-S52.
  12. Therapondos G, Flapan A.D, Plevris J.N, Hayes P.C: Cardiac morbidity and mortality related to orthotopic liver transplantation. Liver Transpl 2004;10:1441-1453.
  13. Castell J, Margarit C, Esteban R, Guardia J, Genesca J: Cardiac alterations in cirrhosis: reversibility after liver transplantation. J Hepatol. 2005;42:68-74.
  14. Fischer D.R, Mathews R.A, Neches W.H, Zuberbuhler J.R: Echocardiographic findings before and after liver transplantation. Am J Cardiol 1985;55:1373-1378.
  15. Glauser F.L: Systemic hemodynamic and cardiac function changes in patients undergoing orthotopic liver transplantation. Chest 1990;98:1210-1215.
  16. Singal A.K, Kamath P.S. Model for End-stage Liver Disease. J Hepatol. 2013;3(1):50-60.
  17. Alkogol’naya bolezn’. Porazhenie vnutrennih organov. Pod redakciej akad. RAMN Moiseeva V. S., 2014, 480 s.
  18. Goncharov A. S., Kliniko-gemodinamicheskie osobennosti i immunovospalitel’nye izmeneniya u bol’nyh hronicheskoj serdechnoj nedostatochnost’yu, zloupotreblyayushchih alkogolem. Diss. Na soiskanie uchenoj stepeni kandidata medicinskih nauk. Moskva, 2013, 115 s.
  19. Keller H, Bezjak V, Stegaru B, Buss J, Holm E, Heene D.L. Ventricular function in cirrhosis and portosystemic shunt: a two-dimensional echocardiographic study. J Hepatol. 1988;8:658-662.
  20. Ahmed S.S, Howard M, Hove W.t, Leevy C.M, Regan T.J. Cardiac function in alcoholics with cirrhosis: absence of overt cardiomyopathy - myth or fact? J Am Coll Card 1984;3:696-702.
  21. Sampaio F, Pimenta J, Bettencourt N, et al. Systolic and diastolic dysfunction in cirrhosis: a tissue-Doppler and speckle tracking echocardiography study. Liver Int. 2013;33:1158-65.
  22. Nazar A, Guevara M, Sitges M, et al. LEFT ventricular function assessed by echocardiography in cirrhosis: relationship to systemic hemodynamics and renal dysfunction. J Hepatol. 2012;58:51-7.
  23. Wong F, Villamil A, Merli M, Romero G, Angeli P, Caraceni P, Steib C.J, Baik S.K, Spinzi G, Colombato L.A, Salerno F. Prevalence of diastolic dysfunction in cirrhosis and its clinical significance. J Hepatol. 2011;54(Suppl 1): A475-476.
  24. Kazankov K, Holland-Fischer P, Andersen N.H, Torp P, Sloth E, Aagaard N.K, Vilstrup H. Resting myocardial dysfunction in cirrhosis quantified by tissue Doppler imaging. Liver Int 2011;31:534-540.
  25. Lunseth J.H, Olmstead E.G, Abboud F. A study of heart disease in one hundred eight hospitalized patients dying with portal cirrhosis. Arch Intern Med 1958;102:405-413.
  26. Henriksen J.H, Gøtze J.P, Fuglsang S, Christensen E, Bendtsen F, Møller S. Increased circulating pro-brain natriuretic peptide (proBNP) and brain natriuretic peptide (BNP) in patients with cirrhosis: relation to cardiovascular dysfunction and severity of disease. Gut. 2003;52(10):1511-7.

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Ivanov A. S., Romanova V. A., Kolesnikova I. A., Arisheva O. S. et al. CARDIAC DYSFUNCTION IN ALCOHOLIC LIVER CIRRHOSIS. Experimental and Clinical Gastroenterology Journal. 2018;154(06):52-57
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1. I. M. Sechenov First Moscow State Medical University (Moscow, Russian Federation)
2. Smolensk state medical University Ministry Of Health (Moscow, Russian Federation)

Keywords:arterial hypertension, obesity, women of reproductive age, liver remodeling

Abstract:The aim was to improve and optimize the management tactics of women of reproductive age with somatic diseases on the basis of a comprehensive assessment of the main structural and functional characteristics of the hepatobiliary system at various stages of physiological gestation in the presence or absence of somatic pathology, as well as in the process of complex dynamic observation and examination for three years after delivery. Materials and methods: there were examined 535 outpatient and inpatient patients aged 16 to 45 years (mean age 27.9 ± 4.7 years, m 28, Mo 25) was conducted, including 383 patients with somatic pathology during pregnancy: group 1 (n=183) with gestational hypertension (GAG), group 2 (n=66) with chronic arterial hypertension (HAG), group 3 (n=134) of obese pregnant women. The control group consisted of 152 pregnant women without somatic pathology. Results: Analysis of structural and functional parameters of the hepato-biliary system showed that pregnant women with obesity have a moderate increase in one share of the liver (42.11% of cases), moderate hyperechogenicity of parenchyma (36.84%), difficulty in visualization of the diaphragm contour (26.31%). In gestational and chronic hypertension without obesity, these changes are expressed slightly. Conclusion: Linear and estimated the ultrasonic parameters of the liver (distal attenuation of the echo signal, hepatomegaly, hyperechogenicity, increased ehoplotnosti of the liver parenchyma and disruption of its calibre in conjunction with the expansion of the vena portae) correlated with hemodynamic, nutritional parameters and periods of gestation and are biomarkers of hypertension and obesity in women of reproductive age.

• References total 12 ⇓ :: .
  1. Russian guidelines for the diagnosis and treatment of cardiovascular diseases in pregnancy 2013//Russian cardiology journal.-2013. – № 4.-140 p.
  2. Stryuk R. I., Bukhonkina Yu. M., Sokova E. A., et al. Pharmacotherapy and analysis of pregnancy and perinatal outcomes in women with arterial hypertension. Cardiology.-2009. – № 12. – P. 29–32.
  3. Konyshko N. Ah. Morozova I. E. Clinical and ultrasonographic features in women with gestational hypertension. Cardiology.-2016. – № 10. – P. 41–45.
  4. Конышко Н.А., Морозова Т. Е. Факторы патогенеза гестационной гипертензии. Российский кардиологический журнал. –2015. –№ 4. – С. 118–121.
  5. Конышко Н.А., Морозова Т. Е. Клинические и ультрасонографические особенности у женщин с гестационной артериальной гипертензией. Кардиология. –2016. –№ 10. – С. 41–45.
  6. Burkov S. G. strategy of diagnosis and drug treatment of digestive diseases in pregnant women. Experimental and clinical gastroenterology, 2009, no 7. – pp. 72–78.
  7. Karpeev S. A., Karpeeva J. S., Balukova E. V. Chronic diseases of the hepatobiliary system in the Genesis of habitual noncarrying of pregnancy. Experimental and clinical gastroenterology. 2017;143(7):65–70.
  8. Ivanyuk E. S., Khlynova O. V., Lozhkina N. B. The structure of digestive diseases in people with hypertension and symptoms of dyspepsia. Experimental and clinical gastroenterology. 2016;127(3):60–60a.
  9. Eremina E. Yu., Gerasimenko I. V., Chernova O. V. Medicinal hepatitis in pregnant women. Experimental and clinical gastroenterology. 2017;141(5):29–32.
  10. Yajnik C. S. Transmission of obesity-adiposity and related disorders from the mother to the baby. Ann Nutr Metab. – 2014. –№ 4. – С. 8–17.
  11. Konyshko N. A. Morozova T. E. Constitutional features of women with somatic pathology during pregnancy. Preventive and clinical medicine. – 2014. – № 4. – P. 72–78.
  12. Marinkin I. O., Sokolova T. M., Kiseleva T. V., Kuleshov V. M., Makarov K. Yu., Yakimova A. V. Cholestasis in pregnant women. Experimental and clinical gastroenterology. 2016;133(9):81–85.

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Morozova T. E., Konyshko N. A. STRUCTURAL AND FUNCTIONAL FEATURES OF THE HEPATOBILIARY SYSTEM IN WOMEN WITH ARTERIAL HYPERTENSION AND OBESITY IN THE GESTATION PERIOD AND AFTER DELIVERY. Experimental and Clinical Gastroenterology Journal. 2018;154(06):58-63
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1. Ufa Research Institute of Occupational Health and Human Ecology (Ufa, Russian Federation)

Keywords:petrochemical plants, occupational toxic hepatitis, gene polymorphism

Abstract:The aim of this study was to investigate the association of polymorphism of the glutathione-S-transferase genes with the risk of occupational liver diseases in workers of petrochemical plants. Materials and Methods. 544 DNA samples of petrochemical workers and 322 healthy persons DNA sample were used for genotyping by polymerase chain reaction and restriction fragment length polymorphism. Results. It was found that the genotype Val/Val of polymorphic locus rs1695 of GSTP1 gene is less common in patients with toxic hepatitis (χ²=4,405, р=0,036) than in healthy workers. Analysis of the association of polymorphic loci GSTM1 and GSTT1 with the development of occupational liver lesions revealed no statistically significant results. Conclusion. The data obtained suggest that the homozygous genotype Val/Val of polymorphic locus rs1695 of the GSTP1 gene is protective of the development of occupational toxic hepatitis.

• References total 17 ⇓ :: .
  1. Sorkina N. S, Izmerova N. I., Ivanova L. A. i soavt. Professional’nye zabolevaniya s preimushchestvennym porazheniem gepatobiliarnoj sistemy // Izmerov N. F. Professional’naya patologiya: nacional’noe rukovodstvo – M.: GEHOTAR-Media, 2011. – 784 s.
  2. Spicyn V. A. EHkologicheskaya genetika cheloveka. – M.: Nauka, 2008. – 503 s.
  3. Gusmanova G. T., H. D. Kalimullina, Bakirov A. B., Khusainova R. I., the Search for genetic factors predisposing to the development of liver cirrhosis in the outcome of viral hepatitis b In patients from the Republic of Bashkortostan // Kazan medical journal. – 2012. – T. 93, No. 2. – P. 197–203.
  4. Lukmanova, L. I., Davletshin R. A., Yuldashev V. L. et al. Search of clinical and genetic associations in alcoholic liver disease / / Practical medicine. – 2012. – № 3 (58). – P. 72–74.
  5. Hayes J., Strange R. C. Glutathione S-transferase polymorphisms and their biological consequences // Pharmacology. – 2000. – Vol. 61, № 3. – P. 154–166.
  6. White D. L., Li D., Nurgalieva Z., El-Serag H. B. Genetic variants of glutathione S-transferase as possible risk factors for hepatocellular carcinoma: A HuGE systematic review and meta-analysis // Am. J. Epidemiol. – 2007. – Vol. 167, № 4. – P. 377–389.
  7. Stickel F., Osterreicher C. The role of genetic polymorphisms in alcoholic live disease // Alcohol Alcohol. – 2006. – Vol. 41, № 3. – P. 209–224.
  8. Pai G. V., Kuzmina L. P., Movchan O. V. et al. Genetic markers of bronchopulmonary diseases of professional Genesis on the example of polymorphic genes glutathione-S-trasferase M1 and cytochrome p-4501A1 // Medical genetics. – 2003. – Vol. 2, № 5. – P. 223–226
  9. Thier R., Lewalter J., Kempkes M. et аl. Haemoglobin adducts of acrylonitrile and ethylene oxide in acrylonitrile workers, dependent on polymorphisms of the glutathione transferases GSTT1 and GSTM1 // Arch. Toxicol. – 1999. – Vol. 73, № 4–5. – P. 197–202.
  10. Goncharova I. A., Rachkovsky M. I., Beloborodova E. V. et al. Pathogenetics of liver cirrhosis: polymorphism of glutathione-S-transferase genes / / Molecular biology. – 2010. – Vol. 44., No. 3. – P. 431–438.
  11. Hashemi M., Eskandari-Nasab E., Fazaeli A. et аl. Association of genetic polymorphisms of glutathione-S-transferase genes (GSTT1, GSTM1, and GSTP1) and susceptibility to nonalcoholic fatty liver disease in Zahedan, Southeast Iran // DNA Cell Biol. – 2012. – Vol. 31, № 5. – P. 672–677.
  12. Vasieva O. The many faces of glutathione transferase pi // Curr Mol Med. – 2011. – Vol. 11, № 2. – P. 129–139.
  13. Strange R. C., Spiteri M. A., Ramachandran S., Fryer A. A. Glutathione-S-transferase family of enzymes // Mutat Res. – 2001. – Vol. 482, № 1–2. – P. 21–26.
  14. Vodicka P., Stetina R., Koskinen M. et аl. New aspects in the biomonitoring of occupational exposure to styrene // Int. Arch. Occup. Environ. Health. – 2002. – Vol.75. – P. 75–85.
  15. Haufroid V., Jakubowski M., Janasik B. et аl. Interest of genotyping and phenotyping of drug-metabolizing enzymes for the interpretation of biological monitoring of exposure to styrene // – 2002. – Vol. 12, № 9. – P. 691–702.
  16. Ma Q., Lin G., Qin Y. et аl. GSTP1 A1578G (Ile105Val) polymorphism in benzidine-exposed workers: an association with cytological grading of exfoliated urothelial cells // Pharmacogenetics. – 2003. – Vol. 13, № 7. – P. 409–15.
  17. Mapp C. E., Fryer A. A., De Marzo N. et аl. Glutathione S-transferase GSTP1 is a susceptibility gene for occupational asthma induced by isocyanates // J. Allergy Clin. Immunol. – 2002. – Vol. 109, № 5. – P. 867–72.

Full text is published :
Valeeva Je. T., Bakirov A. B., Galimova R. R., Mukhammadiyeva G. F. THE ROLLE OF GENETIC PREDISPOSITION FOR OCCUPATIONAL LIVER DISEASES IN WORKERS OF PETROCHEMICAL PLANTS. Experimental and Clinical Gastroenterology Journal. 2018;154(06):64-68
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1. First MOSCOW state medical University. I. M. Sechenov of the Ministry of health of the Russian Federation (Sechenov University) (Moscow, Russian Federation)
2. Clinic “First doctor” (Moscow, Russian Federation)

Keywords:comorbidity, risk factors, rural areas

Abstract:Purpose. To analyze the features of formation of comorbidity and age-related patterns of distribution of risk factors (RF) in patients with diseases of the gastrointestinal tact (GIT) living in rural areas. Materials and methods. In 2015-2017.d. a retrospective analysis of the database of 2500 patients at two sites of General practitioners of Konakov district of Tver region was conducted. Of these, 350 (14% of all the studied out-patient charts) out-patient charts of patients aged 44-53 years (164 men and 186 women) were selected, which contained more complete information about the annual medical examination of the population. In addition, a survey of this population group was conducted for a more detailed retrospective analysis of the incidence and presence of PD during life depth up to 25-35 years. Results. Gastrointestinal diseases were detected in 42 patients (12% of the total group of patients studied); dorsopathy - in 84 patients (24%); arterial hypertension (AH) in 178 patients (50,86%); chronic kidney disease in 12 (3,4%), diabetes in 10 (2,9%) people; other diseases accounted for no more than 3% and 35 (10%) patients had no registered diseases. Basic FRENCH men for life was Smoking. Despite the high percentage of Smoking women aged 18-23 years (47.52%), almost all patients left a bad habit of 34 years. In an additional survey, 97% of women who had smoked earlier explained Smoking cessation to 34 g of children in their family and only 3% of respondents attributed Smoking cessation to deterioration of their health. It is important to note that although the prevalence of overweight in men increased slightly more than in women (40.3% and 36.6%, respectively) with age to 53 years, differences in the increase in the incidence of associated GC increased disproportionately (48.05% and 22.77%, respectively) Conclusion. Thus, the formation of comorbidity in rural areas occurs mainly at the age of 44-53 years. Among the features of comorbidity in these patients, it should be noted the frequent combination of gastrointestinal diseases with hypertension and dorsopathy, and relatively rare-with chronic obstructive pulmonary disease and cerebrovascular diseases. The “diagnostic failure” observed at the age of 24-43 dictates the need to pay special attention to this age category for the purpose of timely examination and early detection of the initial stages of diseases.

• References total 8 ⇓ :: .
  1. Lazebnik L. B., Stefanyuk O. V Looking into the future of digestive health. Eksperimental’naya i Klinicheskaya Gastroenterologiya 2015;117(5):51–57.
  2. van den Akker, M. Comorbidity or multimorbidity: what’s in a name? A review of the literature / M. van den Akker, F. Buntinx, S. Roos, J. A. Knottnerus // Eur. J. Gen. Pract. – 1996. – Vol. 2, No. 2. – P. 65–70.
  3. Lazebnik, L. B. Rehabilitation of patients with gastric ulcer and duodenal ulcer / L. B. Lazebnik, G. V. Sukhareva / Ter.ARH. – 2003. – № 2. – P. 70–72.
  4. Lazebnik L. B., Vasilyev Yu. V and others Helicobacter pylori: prevalence, diagnosis, treatment // Experimental and clinical gastroenterology. 2010. No. 2. P. 3–7.
  5. Lazebnik L. B., Bordin D. S. i dr. Hronicheskij gastrit. Metodicheskie rekomendacii. M.: CNIIG, 2011. 34 s.
  6. Stepanisheva L. A., Sarsenbaeva A. S., Fattakhova N. V. The influence of comorbid diseases and risk factors on the development of the combined peptic ulcer of stomach and duodenum. Experimental and clinical gastroenterology.2013 № 8.p. 34–40.
  7. Shalnova S. A., Deev A.D, Karpov Y. A. The arterial hypertension and ischemic heart disease in actual practice cardiologist // Cardiovascular Therapy and Prevention 2006. Vol. 5, № 2. Р. 73–80. (In Russ.)
  8. Denisov N. L., Grinevich V. B., Chernetsova Ye.V., Kravchuk Yu.A., Ivashkin K. V. The role of non-alcoholic fatty liver disease in the formation of atherosclerotic vascular lesions in patients with abdominal obesity. Ross z gastroenterol gepatol koloproktol 2017; 27(1):62–71 (In Russ.) DOI: 10.22416/1382–4376–2017–27–1–62–71

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Denisov I.N., Zaugol’nikova T.V., Popova T. S., Morozova T.E. A RETROSPECTIVE ANALYSIS OF COMORBIDITY IN RURAL PATIENTS WITH DISEASES OF THE GASTROINTESTINAL TRACT. Experimental and Clinical Gastroenterology Journal. 2018;154(06):69-73
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1. Anokhin Research Institute of Physiology (Moscow, Russian Federation)
2. Shemyakin & Ovchinnikov Institute of Bioorganic Chemisitry (Moscow, Russian Federation)

Keywords: E-cadherin, desmoglein 2, cathepsin G, intestinal epithelium, epithelial barrier, immunofluorescence

Abstract:Aim of the study. Determination of the potential opportunity of immune protease cathepsin G (Cat G) to participate in the regulation of homeostasis and protective reactions in the intestinal epithelium by interacting with cell adhesion proteins (cadherins). Materials and methods. Biopsies of the human duodenal mucosa were examined by confocal immunofluorescence microscopy using specific antibodies to desmogleins 1-3 (DSGs 1-3), E-cadherin and Cat G of human. Results. The presence of DSG 2 in the contact area of the basolateral membrane of epitheliocytes of intestinal villi and intestinal glands (crypts) with the basal membrane was demonstrated. DSGs 1 and 3 were not detected in the test samples. E-cadherin is located in the zone of the basolateral membrane of enterocytes, goblet cells and Paneth cells. E-cadherin-specific fluorescence is also found between the secretory granules of Paneth cells, which indicates the synthesis of this protein by Paneth cells and/or E-cadherin role in intracellular signaling. In inflammation (duodenitis II-III degree) Cat G-containing granules are localized near the basal membrane of villi and intestinal glands. Conclusions. The catalytic properties of Cat G and its close proximity to the cell adhesion proteins (DSG 2 and E-cadherin) indicate the possibility of interaction of these proteins and their role in the regulation of tissue metabolism, modification and maintenance of the barrier properties of the epithelium during the development of protective and / or pathological processes.

• References total 16 ⇓ :: .
  1. Groschwitz K. R., Hogan S. P. Intestinal barrier function: molecular regulation and disease pathogenesis. J. Allergy Clin. Immunol., 2009, vol.124, no.1, pp. 3-20.
  2. Maretzky T., Reiss K., Ludwig A., et al. ADAM10 mediates E-cadherin shedding and regulates epithelial cell-cell adhesion, migration, and beta-catenin translocation. Proc. Natl. Acad. Sci. U S A, 2005, vol.102, no.26, pp. 9182-9187.
  3. Halbleib J. M., Nelson W. J. Cadherins in development: cell adhesion, sorting, and tissue morphogenesis. Genes and development, 2006, no. 20, pp. 3199-3214.
  4. Sumagin R., Parkos C. A. Epithelial adhesion molecules and the regulation of intestinal homeostasis during neutrophil transepithelial migration. Tissue Barriers, 2015, vol. 3, no.1-2, p. e969100.
  5. Escaffit F., Perreault N,. Jean D. et al. Repressed E-cadherin expression in the lower crypt of human small intestine: a cell marker of functional relevance. Exp Cell Res, 2005, vol.302, no.2, pp. 206-220.
  6. Schneider M. R., Dahlhoff M., Horst D. et al. A key role for E-cadherin in intestinal homeostasis and Paneth cell maturation. PLoS One, 2010, vol.5, no.12, p. e14325.
  7. Korkmaz B., Moreau T., Gauthier F. Neutrophil elastase, proteinase 3 and cathepsin G: physicochemical properties, activity and physiopathological functions. Biochimie, 2008, vol. 90, no. 2, pp. 227-242.
  8. Packer M., Patterson-Kane J.C., Smith K. C., Durham A. E. Quantification of immune cell populations in the lamina propria of equine jejunal biopsy specimens. J. Comp. Pathol., 2005, vol.132, no.1, pp. 90-95.
  9. Hasan M., Hay F., Sircus W., Ferguson A., Nature of the inflammatory cell infiltrate in duodenitis., J. Clin. Pathol., 1983, vol. 36, no. 3, pp.280-288.
  10. Zamolodchikova T. S., Shoibonov B. B., Svirshchevskaya E. V., Shcherbakov I. T., Khrennikov B. N. Cathepsin G in the immune defense of the human duodenum: New sources for biosynthesis. Human Physiology. 2017;43(3):102–110.
  11. Yui S., Osawa Y., Ichisugi T., Morimoto-Kamata R. Neutrophil Cathepsin G, but Not Elastase, Induces Aggregation of MCF-7 Mammary Carcinoma Cells by a Protease Activity-Dependent Cell-Oriented Mechanism. Mediators Inflamm., 2014, vol. 2014, p.971409, doi: 10.1155/2014/971409.
  12. Jerke U., Hernandez D. P., Beaudette P. et al. Neutrophil serine proteases exert proteolytic activity on endothelial cells. Kidney Int., 2015, vol. 88, no.4, pp.764-775.
  13. Gumber S., Nusrat A., Villinger F. Immunohistological characterization of intercellular junction proteins in rhesus macaque intestine. Exp Toxicol Pathol., 2014, vol. 66, no. 9-10, pp. 437-444.
  14. Son E. D., Kim H., Choi H. et al. Cathepsin G increases MMP expression in normal human fibroblasts through fibronectin fragmentation, and induces the conversion of proMMP-1 to active MMP-1. J. Dermatol. Sci., 2009, vol. 53, no. 2, pp.150-152.
  15. Zamolodchikova T. S., Tolpygo S. M., Svirshchevskaya Ye. V. The role of cathepsin G in the modulation of immune reactions involving local renin-angiotensin systems. Medical Immunology (Russia) – Meditsinskaya Immunologiya. 2017;19(S):41
  16. Liu T. J., Shi Y. Y., Wang E. B. et al. AT1R blocker losartan attenuates intestinal epithelial cell apoptosis in a mouse model of Crohn’s disease. Mol. Med. Rep., 2016, vol.13, no. 2, pp.1156-1162

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Zamolodchikova T.S., Tolpygo S.M., Svirshchevskaya E.V. СADHERINS AND СATHEPSIN G IN THE REGULATION OF HOMEOSTASIS AND PROTECTIVE REACTIONS IN THE INTESTINAL EPITHELIUM. Experimental and Clinical Gastroenterology Journal. 2018;154(06):74-77
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1. Moscow clinical scientific and practical center. A. S. Loginov (Moscow, Russian Federation)

Keywords: GERD, constipation, motor activity of intestine

Abstract:The aim is to study the electromotor activity of the gastrointestinal tract in patients with GERD with concomitant functional constipation Material and methods. A study was made of the electromotor activity of the gastrointestinal tract in 70 patients with GERD with concomitant functional constipation and 64 patients with GERD with normal stool. Electromotor activity (EMA) was recorded with the help of skin electrodes in the area of the projection of the stomach and sigmoid colon on the anterior abdominal wall. The amplitude-frequency characteristics of slow-wave and spike activity on the electromyogram curve were measured. Results. EMA of the stomach in patients with endoscopically confirmed GERD and the presence of constipation was characterized by increased slow-wave and spike activity. Thus, the frequency of slow waves of the EMA of the stomach exceeds the norm by 78%. The amplitude of slow waves exceeds the norm by half. EMA of the sigmoid colon in patients with endoscopically confirmed GERD and the presence of constipation was characterized by a decrease in slow-wave activity: the frequency of slow waves of the sigmoid colon EMA was 70% of the norm; The amplitude of the slow wave activity is only 0.13 ± 0.06 mV. Conclusion. In patients with GERD and concomitant functional constipation, the incidence of gastroesophageal reflux is high, the gastrointestinal tract EMA was characterized by a more pronounced motor activity of the smooth muscles of the stomach and reduced motor activity of the sigmoid colon, which creates the conditions for an increase in intestinal pressure.

• References total 5 ⇓ :: .
  1. Vasiliev Y. Gastroesophageal reflux disease in the stage of reflux esophagitis: diagnosis and therapy/V. Vasilyev//Farmateka. – 2004. – № 13. – P. 1–5
  2. Lychkova A. E. Serotonin regulation of motor function of the small intestine. Experimental and clinical gastroenterology 2011; 3:130–135.
  3. Sanders K. M. A case for interstitial cells of Cajal as pacemakers and mediators of neurotransmission in the gastrointestinal tract // Gastroenterology. – 1996. – Vol. 111. – Р. 492–515.
  4. Shemerovskij K. A. Hronofiziologicheskie osobennosti gastroduodenal’noj mioehlektricheskoj aktivnosti i ehvakuatornoj funkcii kishechnika. Avtoref dis dokt med nauk. Spb., 2004
  5. Lychkova A. E., Puzikov A. M. Electrical activity of the digestive tract and its enteral correction Experimental and clinical gastroenterology 2015;120(8):25–29.

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Lychkova A. E., Puzikov A. M. GASTROESOPHAGEAL REFLUX DISEASE IN COMBINATION WITH CONSTIPATION: FEATURES OF THE MOTOR FUNCTION OF THE STOMACH AND SIGMOID COLON. Experimental and Clinical Gastroenterology Journal. 2018;154(06):78-80
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1. Federal public budgetary educational institution of higher education “Altay State Medical University” of the Ministry of Healthcare of Russia (Barnaul, Russia)

Keywords: peptide complex, peptic ulcer disease, experimental gastropathy, oxidative stress, cyclooxygenase, antioxidant activity

Abstract:The aim was to investigate the influence of the peptide complex from pork kidney tissues on indicators of free radical oxidation and the expression of COX-1,2 in experimental Indometacine-induced gastropathy. Materials and methods: There were examined 67 male Wistar rats. Experimental peptic ulcer disease was reached by the injection into the stomach of 60mg/kg Indometacine. The experimental group had got 75mg/kg for 7 days up to the Indometacine injection. The concentration of enzymes COX-1, 2 in blood plasma and gastric homogenate were determined by the method of enzyme immunoassay. The activity of free radical oxidization processes was evaluated by the coloring intensity of the products of the corresponding biochemical reactions. Results: In the experimental group the concentration of COX-2 in the gastric mucosa was reduced by 26.5% comparing to the intact group. Thiobarbituric acid-reactive substances concentration was redused in 2,3 times comparing to the control group. Increased under the effect of indomethacin, the concentrations of superoxide dismutase and glutathione peroxidase were equal the concentrations of healthy rats. Conclusion: The injection of a peptide complex from pork kidney tissues for 7 days is accompanied by reducing of the inflammatory process in the gastric mucosa, as evidenced by a decrease in the concentration of COX-2 in the stomach homogenate, as well as reducing of oxidative damage to gastric cells and strengthening their enzyme antioxidant protection.

• References total 9 ⇓ :: .
  1. Lorenc C. E. Zharikov A. Yu., Bobrov I. P. et al. Gastroprotective effect of peptide complex / / Siberian scientific medical journal. – 2017. – Vol. 37, № 6. – P. 5–9.
  2. Novikov V. E., Kryukova N. Oh. Krikova A. V. NSAIDS-induced gastropathies and their prevention // Reviews of clinical pharmacology and drug therapy. – 2008. – Vol. 6, № 1. – P. 26–30.
  3. Kursov S. V., Nikonov V. V. Cyclooxygenase: physiological effects, inhibitor action and prospects for further use of paracetamol (analytical review) // medicine of emergency conditions. –2016. – Vol. 76, № 5. – P. 27–35.
  4. Radbil O. S. Free radicals and diseases of the digestive system // Clinical medicine – 1989. – № 3. – P. 17–21.
  5. Shcherbatykh A. V., Kulinsky V. I., Bolsheshapov A. A., Sokolova S. V. lipid Peroxidation and antioxidant system in gastric ulcer, duodenal ulcer and postgastrectomy syndromes // Siberian scientific medical journal.. – 2005. – № 3. – P. 9–13.
  6. Lelyavina T. I., Ineshina E. G., ZHigaev, G. F., et al. lipid Peroxidation and nonhealing gastroduodenal ulcer// Siberian scientific medical journal – 2002. – Vol. 34, № 5. – P. 46–48.
  7. Zharikova G. V., Zharikov A. Yu., Kiselev V. I. et al. The influence of peptide complex from the tissues of pig kidneys on the indicators of free radical oxidation in experimental urolithiasis // Siberian scientific medical journal 2017. – Vol. 37, № 2. – P. 17–21
  8. Stepanov Yu. M., Breslavets Yu. S. Dynamics of the content of COX-2 in the mucosa of the stomach and duodenum on the background of medicamentous correction of NSAID-gastropathy. Gastroenterology, 2013, volume 47 No. 1, C36–42
  9. Usmanova sh. e, Yakubov A. V. the state of oxidative stress in the gastric mucosa and ways of its correction in indomethacin-induced gastropathy. Modern medicine, topical issues, 2014, № 28, p. 88–97

Full text is published :
Lorents S. E., Zharikov A. Yu., Mazko O. N., Makarova O. G. et al. INFLUENCE OF THE PEPTIDE COMPLEX FROM PORK KIDNEYS TISSUES ON INDICATORS OF FREE RADICAL OXIDATION AND THE EXPRESSION OF COX-1,2 IN EXPERIMENTAL GASTROPATHY. Experimental and Clinical Gastroenterology Journal. 2018;154(06):81-85
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1. N. V. Sklifosovsky Research Institute for Emergency Medicine of the Moscow Healthcare (Moscow, Russian Federation)

Keywords: acetaminophen, intestinal microflora, experiment, rats

Abstract:Objective: To study the qualitative and quantitative composition of microflora in the jejunum and the cecum in acetaminophen administration. Materials and methods: The experiments were carried out on 30 rats male Wistar rats weighing 400-450 g. The influence of intragastric administration of acetaminophen (500 mg/kg) on the microflora in the jejunum and cecum has been studied. Results: It is shown that administration of acetaminophen within 21 days no changes composition of the jejunal microbiota, but leads to decrease species composition and to significant inhibition of lactobacillus and bifidobacterium in the cecum..

• References total 9 ⇓ :: .
  1. Fedos’ina E. A., Zharkova M. S., Mayevskaya M. V. Bacterial intestinal microflora and liver diseases // Russian journal of gastroenterology, Hepatology and Coloproctology – 2009. – Vol. 19. – № 6. – P. 73–81.
  2. Larson A.M., Polson J., Fontana R. J., Davern T. J. et al. Acetaminophen-induced acute liver failure: results of a United States multicenter, prospective study // Hepatology. – 2005. – Vol. 42, № 6. – Р. 1364–1372.
  3. Bessems J.G., Vermeulen N. P. Paracetamol (acetaminophen)-induced toxicity: molecular and biochemical mechanisms, analogues and protective approaches // Crit. Rev. Toxicol. – 2001. – Vol.31, № 1. -Р. 55–138.
  4. Iqubal A., Iqubal M. K., Haque S. E. Experimental hepatotoxicity Inducing agents: A Review // International Journal of Pharmacological Research. – 2016.-Vol. 6,№ 11.-Р.325–335.
  5. Nikolaeva I. V., SHejbak V.M., Lelevich S. V., Kravchuk R. I. Struktura mikrobiocenoza kishechnika krys, poluchavshih acetaminofen // Vestnik Vitebskogo gosudarstvennogo medicinskogo universiteta. – 2014. – T. 13, № 1. – S. 56–62.
  6. Dresa I. K., Tchesevic V. T., Zabrodskaya S. V., Y. Z. Maksimchik, etc. Hepatotoxic effects of acetaminophen. Tread properties of tryptophan derivatives / / Biomedical chemistry. – 2010. – Vol. 56. – № 6. – P. 710–718
  7. Parmar S.R., Vashrambhai P. H., Kalia K. Hepatoprotective activity of some plants extract against paracetamol induced hepatotoxicity in rats // J Herbal Med Toxicol. –2010. – Vol. 4, № 2.-Р.101–106.
  8. Sivkov A. V., Sinyukhin V. N., Arzumanov S. V., Stetsyuk E. A., Korobova, T. A. Uremic toxins in blood of patients with end-stage renal failure with intestinal dysbiosis // Experimental and clinical urology. – 2014. – № 2. – P. 94–97.
  9. Wu G.D., Chen J., Hoffmann C., Bittinger K. et al. Linking long-term dietary patterns with gut microbial enterotypes // Science. –2011. -Vol.334.-№ 6052. – P. 105–108.
  10. Possamai L.A., McPhail M.J., Khamri W., Wu B. et al. The role of intestinal microbiota in murine models of acetaminophen induced hepatotoxicity // Liver Int. –2015. – Vol. 35, № 3.-Р.764–773.
  11. Clayton T.A., Baker D., Lindon J. C., Everett J. R., Nicholson J. K. Pharmacometabonomic identification of a significant host-microbiome metabolic interaction affecting human drug metabolism // Proc Natl Acad Sci USA. – 2009. – Vol. 106, № 34.-Р. 14728–14733.
  12. Nowak A, Libudzisz Z. Ability of intestinal lactic bacteria to bind or/and metabolise phenol and p-cresol // Ann Microbiol. –2007. -Vol. 57, № 3. – P 329–335.

Full text is published :
Tropskaya N. S., Vilkova I. G., Kislykova E. A., Kislicina O. S. et al. THE CHANGE OF INTESTINAL MICROFLORA IN NONSTEROIDAL ANTI-INFLAMMATORY DRUG ACETAMINOPHEN ADMINISTRATION. Experimental and Clinical Gastroenterology Journal. 2018;154(06):86-89
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1. Moscow clinical scientific and practical center. A. S. Loginov (Moscow, Russian Federation)
2. Moscow Research and Practical Centre for Narcology of the Department of Public Health (Moscow, Russian Federation)
3. Federal State Budgetary Educational Establishment of Higher Education Russian State University of Physical Education, Sport, Youth and Tourism (SCOLIPE) (Moscow, Russian Federation)
4. Federal State-Funded Educational Institution of Higher Education "Financial University under the Government of the Russian Federation" (Moscow, Russian Federation)

Keywords: Alcohol, rat, alcohol-associated internal injuries

Abstract:Purpose. Experimentally determine the volume and time stages of damage formation associated with the use of low-alcohol (SAN) and energy drinks (EN) in rats. Material and methods. 45 white Wistar rats were used, the experimental animals were divided into three series consisting of three groups. The first a series of age - 1.5 month; the second a series of - 12 months. The third series-24 months. In each series of 3 groups: 1-I control (intact), animals had the free access to clean water and customary food. 2nd experimental group rats with free access to water and food was added to the drinking bowl with AL “Red Bull” or SAN “Black Russian”. Autopsy after 14 and 45 days, or if necessary, when the animals died from drinking. After the autopsy, the abdominal and thoracic cavities were examined. To assess the revealed injuries, the damage index (di) was calculated, which was calculated by the number of organs with injuries and divided by the number of animals in the group. Conclusion. Experimental animal studies have established a single pathogenetic mechanism and cause-and-effect relationship between blood flow disorders associated with alcohol and multiple (polymorbidity) internal injuries. Low-alcohol drinks (cocktails) are not harmless drinks, they cause multiple toxic damage to the internal organs in the “young” rats appear damage characteristic of the “old” animals. In this case, aging is not age, but disease. Low-alcohol and energy drinks are conducive to the use of stronger drinks (“Rare” - Red bull + vodka). Decrease in the instinct of self-preservation-refusal of food and drink in combination with polymorbidity of lesions of internal organs leads to death of animals. Easy access for young people and the widespread availability of low-alcohol and energy drinks (cocktails) are a subject of discussion and attention for educators and doctors.

• References total 9 ⇓ :: .
  1. Лазебник Л. Б. Полиморбидность у пожилых // Сердце. 2007. № 7. С. 25–27 [Lazebnik L. B. Polimorbidnost’ u pozhilyh // Serdce. 2007. № 7. S. 25–27 (in Russian)].
  2. Pakhomova IG, Zinovieva E. N. Gastroesophageal reflux disease in a polymorbid patient: features of therapy / / BC. – № 10 of May 30, 2017. Pp. 760–764.
  3. Gubergric N.B, Krjuk N. A. Osobennosti lechenija bol’nyh hronicheskim pankreatitom v sochetanii s gastrojezofageal’noj refljuksnoj bolezn’ju // Gastrojenterologija Sankt-Peterburga. 2007. № 1–2. S. 114 (in Russian).
  4. Torosyan EA, Torosyan A. C., Semerjyan V. V. “Black hole” of medicine – polymorbidity Bulletin of new medical technologies. 2008. T. 15. No. 1. P. 202–204.
  5. Lazebnik LB, Konev Yu.V., Efremov L. I. Polymorbidity in geriatric practice: quantitative and qualitative assessment. Clinical gerontology. 2012. T. 18. № 1–2. Pp. 36–42.
  6. Pavlova TV, Maslov PV, Markovskaya VA, Pavlova LA, Proschayev KI, Goncharov I. Yu., Kolesnikov DA Pathomorphological mechanisms of kidney involvement in the polymorbide continuum of a human with thermal trauma (experimental study) Modern problems of science and education. 2012. № 4. S. 59.
  7. Serebrova SY, Prokofiev AB, Zhuravleva MV, Sichinava IV, Smolyarchuk EA, Galstyan LR, Kurguzova D. O., Pankratova N. A. Comorbidity and polymorbidity in adults and children in the light of the problem of NVP-gastropathy. Experimental and clinical gastroenterology. 2016. No. 6 (130).
  8. Mysak A. R. Polymorbidity of internal pathology in females with mammary tumors. Issues of regulatory legal regulation in veterinary medicine. 2013. № 3. P. 79–81.
  9. Briskin B. S. Polymorbidity of the elderly and surgical problems. Clinical gerontology. 2007. T. 13. № 5. S. 3–7.

Full text is published :
Fedotova Т.F., Mikhalev I.V., Efremov L.I., Kleschev V.N. et al. ALCOHOL ASSOCIATED INTERNAL INJURY IN RATS. Experimental and Clinical Gastroenterology Journal. 2018;154(06):90-93
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1. Moscow regional scientific and clinical research Institute named after M. F. Vladimirsky (Moscow, Russian Federation)

Keywords: acromegaly, gastrointestinal tract, neoplasms, colon polyps, colon diverticula

Abstract:Acromegaly is a severe neuroendocrine disease caused by increased production of somatotropic hormone by adenohypophysis tumor. The somatotropic hormone is indirectly, via insulin-like growth factor-1, acts on all organs and systems of the body, causing a large number of complications, including those of the gastrointestinal tract. Numerous cases of diagnosing both benign and malignant neoplasms have been described in the literature in this group of patients. About 15% of patients with acromegaly die from cancer, especially colon cancer, which frequency varies from 2 to 14 times the increase in comparison with the general population. However, there is an extremely low amount of studies of the upper part of the digestive tract in patients with acromegaly. The article reflects the results of various domestic and foreign studies on the upper and lower divisions of the gastrointestinal tract of patients with acromegaly, malignant and benign neoplasms of the stomach and colon, diverticular disease in patients with acromegaly, as well as possible prerequisites for their development, based on the pathogenesis of the underlying disease.

• References total 36 ⇓ :: .
  1. Beauregard C., Truong U., Hardy J. et al. Long- term outcome and mortality after transsphenoidal adenomectomy for acromegaly // J. Clin. Endocrinol.-2003. - Vol.58. - P. 86-91
  2. Gibney J., Healy M., Sonksen P. The growth hormone/insulin-like growth factor-1 axis in exercise and sport // J. Endocr. Rev. - 2007. - Vol. - 28. - P. 603-624.
  3. Melmed S., Casanueva F., Cavagnini F. et al. Consensus statement: medical management of acromegaly // Eur. J. Endocrinol. - 2005. - Vol.153. - P. 737-740.
  4. Arosio M, Reimondo G, Malchiodi E, et. al. Italian Study Group of Acromegaly. Predictors of morbidity and mortality in acromegaly: an Italian survey. Eur J Endocrinol. 2012;167(2):189-98. doi: 10.1530/EJE-12-0084
  5. Sherlock M, Ayuk J, Tomlinson J.W, et.al. Mortality in patients with pituitary disease. Endocr Rev. 2010;31(3):301-42.doi: 10.1210/er.2009-0033.
  6. Wright A.D, Hill D.M, Lowy C, Fraser T.R. Mortality in acromegaly. Q J Med. 1970;39(153):1-16.
  7. Loeper S, Ezzat S. Acromegaly: re-thinking the cancer risk. Rev Endocr Metab Disord. 2008;9(1):41-58. doi: 10.1007/s11154-007-9063-z.
  8. Nabarro J.D. Acromegaly. Clin Endocrinol (Oxf).1987;26(4):481-512. doi: 10.1111/j.1365-2265.1987.tb00805.x.
  9. Bengtsson B.A, Edén S, Ernest I, et.al. Epidemiology and long-term survival in acromegaly. A study of 166 cases di agnosed between 1955 and 1984. Acta Med Scand. 1988;223(4):327-35. doi: 10.1111/j.0954-6820.1988.tb15881.x.
  10. Etxabe J, Gaztambide P, Latorre P, Vazquez J.A. Acromegaly: an epidemilogical study. J Endocrinol Invest. 1993;16(3):181-7. doi: 10.1007/BF03344942.
  11. Bates A.S, Van’t Hoff W, Jones J.M, Clayton R.N. An audit of outcome of treatment in acromegaly. Q J Med. 1993;86(5):293-9. doi: http://dx.doi.org/293-299.
  12. Rajasoorya C, Holdaway I.M, Wrightson P, et.al. Determinants of clinical outcome and survivial in acromegaly. Clin Endocrinol (Oxf). 1994;41(1):95-102. doi:10.1111/j.1365-2265.1994.tb03789.x
  13. Melmed S.M. J Clin Endocrinol Metabol 2001; 86: 2929-2934; Mestrón A., Webb S. M. In: Endocrine Society. San Francisco 2002; abstract AACE Acromegaly Guidelines Task Force, AACE Medical Guidelines for Clinical Practice for the diagnosis and treatment of acromegaly.// Endocr. Pract. 2011; 10(3): 213-25
  14. Dedov I. I., Molitvoslovova N. N., Rozhinskaya L. YA., Mel’nichenko G. A. Federal’nye klinicheskie rekomendacii po klinike, diagnostike, differencial’noj diagnostike i metodam lecheniya akromegalii.// Problemy ehndokrinologii. 2013. T. 59, N6. S. 4–18
  15. Baldvinsdottir T., Jonasson J. G., Thorsson A. V. Epidemiology of pituitary tumorous in Iceland 1955-2007: a Nationwide study. 10th European Congress of Endocrinology, 3-7 May, Berlin, Germany. Endocrine Abstracts 2008; 16: 315.
  16. Bates A.S., Vant Hoff W., Jones J. M. Does treatment of acromegaly affect life expectancy? Metabolism 1995; 44: Suppl 1: 1-5
  17. Baris D, Gridley G, Ron E, et al. Jr. Acromegaly and cancer risk: a cohort study in Sweden and Denmark. Cancer Causes Control. 2002;13(5):395-400. doi:10.1023/A:1015713732717
  18. Brunner J.E, Johnson C.C, Zafar S, et.al. Colon cancer and polyps in acromegaly: increased risk associated with family history of colon cancer. Clin Endocrinol (Oxf). 1990;32(1):65-71. doi: 10.1111/j.1365-2265.1990.tb03751.x.
  19. Mustacchi P, Shimkin M.B. Occurrence of cancer in acromegaly and in hypopituitarism.Cancer. 1957;10(1):100-4. doi: 10.1002/1097-0 1 4 2 (1 9 5 7 0 1 / 0 2) 1 0: 1 № 1 0 0:: A I D - C N -CR2820100113>3.0.CO;2-V
  20. Klein I, Parveen G, Gavaler J.S, Vanthiel D.H. Colonic polyps in patients with acromegaly. Ann Intern Med. 1982;97(1):27-30. doi:10.7326/0003-4819-97-1-27
  21. Ron E, Gridley G, Hrubec Z, et al. Jr. Acromegaly and gastrointestinal cancer. Cancer. 1991;68(8):1673-7.doi: 10.1002/1097-0142(19911015)68:8<1673: AID-CNCR2820680802>3.0.CO;2-0
  22. Kurimoto M, Fukuda I, Hizuka N, Takano K. The prevalence of benign and malignant tumors in patients with acromegaly at a single institute. Endocr J. 2008;55(1):67-71. doi: http://doi.org/10.1507/endocrj.K07E-010
  23. Rokkas T, Pistiolas D, Sechopoulos P, et al. Risk of colorectal neoplasm 42 in patients with acromegaly: a meta-analysis. World J Gastroenterol. 2008; 14: 3484-3489.
  24. Attanasio R, Mainolfi A, Grimaldi F, et al. Somatostatin analogs and 43 gallstones: a retrospective survey on a large series of acromegalic patients. J Endocrinol Invest. 2008; 31: 704-710.
  25. Cheng S., Gomez K., Serri O., et al. The role of diabetes in acromegaly associated neoplasia. PLoS One. 2015 May 21;10(5): e0127276. doi: 10.1371/journal.pone.0127276.eCollection 2015
  26. Bolfi F., Miot H. A., Resende M., et al. Frequency of various types of neoplasia in a group of acromegalic patients. Arq Bras Endocrinol Metabol. 2013 Nov;57(8):612-6.
  27. Kato K., Takeshita Y., Misu H., et al. Duodenal adenocarcinoma with neuroendocrine features in a patient with acromegaly and thyroid papillary adenocarcinoma: a unique combination of endocrine neoplasia. Endocr J. 2012;59(9):791-6. Epub 2012 May 31.
  28. Dworakowska D., Gueorguiev M., Kelly P., et al. Repeated colonoscopic screening of patients with acromegaly: 15-year experience identifies those at risk of new colonic neoplasia and allows for effective screening guidelines. Eur J Endocrinol 2010; 163: 1: 21-28.
  29. Oleynik OV, Molitvoslovova NN. Potential predictors and frequency of detection of thyroid and gastrointestinal tumors in patients with acromegaly. Problems of endocrinology. 2015;61 (2):4–7. doi:10.14341/probl20156124–7
  30. Wassenaar M.J, Cazemier M, Biermasz N.R, et al. Acromegaly is associated with an increased prevalence of colonic diverticula: a case-control study.// J Clin Endocrinol Metab, 2010, 95 (5): 2073-2079
  31. Baserga R, Prisco M, Hongo A. IGFs and cell growth. In: Roberts C.T, Rosenfeld R.G, eds. The IGF system. Molecular biology, physiology, and clinical applications. Totowa, NJ: Humana Press;1999, 329-353
  32. LeRoith D, Werner H, Beitner-Johnson D, Roberts Jr C.T. Molecular and cellular aspects of the insulin-like growth factor I receptor. Endocr Rev.1995.143-163
  33. LeRoith D. Regulation of proliferation and apoptosis by the insulin-like growth factor I receptor. Growth Horm IGF Res.2000, 1:12-13
  34. Ng S.T, Zhou J, Adesanya O.O, Wang J, et al. Growth hormone treatment induces mammary gland hyperplasia in aging primates.Nat Med. 1997, 3:1141-1144
  35. Colao A, Ferone D, Marzullo P, et. al. Systemic complications of acromegaly: epidemiology, pathogenesis, and management.// Endocr Rev 2004 25: 102-152
  36. Dutta P, Bhansali A, Vaiphei K, et al // Colonic neoplasia in acromegaly: increased proliferation or decreased apoptosis? Pituitary. 2012 Jun;15 (2):166-73

Full text is published :
Titaeva A. A., Belousova E. A., Tereshchenko S. G. BENIGN AND MALIGNANT NEOPLASMS OF THE GASTROINTESTINAL TRACT IN PATIENTS WITH ACROMEGALY. Experimental and Clinical Gastroenterology Journal. 2018;154(06):94-97
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1. Public budgetary educational institution of higher education «Ogarev Mordovia State University» of Ministry of Education of Russia (Saransk, Russian Federation)

Keywords: mechanical jaundice, Remaxol, reparative regeneration, oxidative stress, hypoxia, endogenous intoxication

Abstract:Goal. To study the effects of complex therapy with Remaksol on the reparative process of a laparotomic wound in the early postoperative period in patients with mechanical jaundice. Material and methods of investigation. We performed clinical and laboratory studies in 40 patients with mechanical jaundice of a non-tumoral nature, 22 patients received Remaxol in their early postoperative period (daily intravenous infusion of 400.0 ml for 5 days). The control group consisted of 18 patients with chronic calculous cholecystitis. Patients underwent cholecystectomy, choledochotomy with choledocholithoextraction or the formation of choledochoduodenoanastomosis. Results. Under mechanical jaundice the reparative potential of tissues is significantly reduced. One of the most important mechanisms of inhibition of tissue regeneration is the deterioration of their bioenergetics. Membrane destabilizing phenomena of regenerating structures are also of great importance due to excessive activity of peroxide oxidation of membrane lipids and activation of phospholipases. Negative factors, aggravating regeneration, in patients were hypoxia, endotoxemia and hypoalbuminemia. Application in the early postoperative period in the complex therapy of Remaxol leads to a significant correction of factors detrimental to the reparative process, which is responsible for the improvement of tissue healing in conditions of cholestasis. Correction of endogenous intoxication and hypoalbuminemia is associated with the hepatoprotective effect of the drug. Conclusion. The Remaxol use increases the reparative potential of laparotomic wounds in patients with mechanical jaundice.

• References total 7 ⇓ :: .
  1. Vinnik YuS, Pakhomova RA, Kochetova LV, Voronova EA, Kozlov VV, Kirichenko AK. Predictors of hepatic insufficiency in obstructive jaundice. Khirurgiya. Zhurnal imeni N. I. Pirogova. 2018;(3):37–41. https://doi.org/10.17116/hirurgia2018337–41
  2. Pakhomova R. A., Kochetova L. V. Clinical implications Ns of the mechanical icterus and liver failure Depending on severity of the mechanical icterus of the good – Quality genesis. Modern problems of science and education. 2017. no.6, р. 47
  3. Bolevich SB, Stupin VA, Gakhramanov TV, Khokonov MA, Silina EV, Men’shova NI, Bogdanova LS. Free radical processes at patients with pathologies of biliary ducts and methods of their correction. Khirurgiya. Zhurnal imeni N. I. Pirogova. 2010;(7):65–70.
  4. Silina E. V., Stupin V. A., Gakhramanov T. V., Khokonov M. A., Bolevich S. B., Men’shova N.I., Sinelnikova T. G. Oxidative stress in patients with mechanical jaundice of different origin and severity. Clinical Medicine. 2011;89(3):57–63
  5. Khilko S. S., Butyrskii A. G. About biochemical parameters in experimental obstructive jaundice and the ways of their correction. Tavricheskiy Mediko-Biologicheskiy Vestnik. 2017;20(2):134–139.
  6. Vinogradova T. I., Sukhanov D. S., Zabolotnykh N. V., Kovalenko A. L., Vasil’eva S. N., Romantsov M. G. Comparative study of remaxol and ademethionine effects on reparative regeneration processes in liver under surgical invasion conditions. Experimental and Clinical Pharmacology. 2011;74(2):34–38. https://doi.org/10.30906/0869–2092–2011–74–2–34–38
  7. Sukhanov D. S., Vinogradova T. I., Zabolotnyh N. V., Vitovskaya M. L., Momot D. S., Elkin A. V. The pharmacological activity of succinatecontaining hepatoprotectors in experimental liver damage. Scientific medical bulletin of Yugra. 2014;1–2(5–6):189–192

Full text is published :
Vlasov A. P., Zaitsev P. P., Vlasova T. I., Grigoriev A. G. et al. OPTIMIZATION OF A LAPAROTOMIC WOUND REPARATIVE REGENERATION UNDER MECHANICAL JAUNDICE. Experimental and Clinical Gastroenterology Journal. 2018;154(06):98-104
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1. M. Sechenov first Moscow state medical University (Moscow, Russian Federation)

Keywords: H. Pylori, iron deficiency, anemia

Abstract:The article analyzes the results of recent studies on the relationship of iron deficiency, iron deficiency anemia and H. Pylori infection. The results of recent epidemiological studies of the combination of these diseases and the proposed theory of the pathogenesis of iron deficiency in infection with HP, including the role of chronic inflammation supported by HP in the formation of anemia of chronic diseases.

• References total 75 ⇓ :: .
  1. Feeding and nutrition of infants and young children. Guidelines for the WHO European Region, with emphasis on the former Soviet countries. WHO Regional Publications, European Series, 87. WHO 2000, updated reprint 2003.
  2. Epidemiology of iron deficiency anaemia in four European countries: a population-based study in primary care // Eur J Haematol. 2016; 97(6):583–593
  3. Xia, W., Zhang, X., Wang, J., Sun, C. & Wu, L. Survey of anaemia and Helicobacter pylori infection in adolescent girls in Suihua, China and enhancement of iron intervention effects by H. pylori eradication. Br J Nutr 108, 357–362 (2012).
  4. Hu, Y. et al. Study on the anemia status of Chinese urban residents in 2010–2012. Chin J Prev Med 50, 213–216 (2016).
  5. Muhsen, K. & Cohen, D. Helicobacter pylori Infection and Anemia. Am J Trop Med Hyg 89, 398–398 (2013). Muhsen, K. & Cohen, D. Helicobacter pylori Infection and Anemia. Am J Trop Med Hyg 89, 398–398 (2013).
  6. Mei-Yan Xu, Bing Cao, Bao-Shi Yuan, Jian Yin1, Lan Liu & Qing-Bin Lu / Association of anaemia with Helicobacter pylori infection: a retrospective study // Scientific REPORTS |7: 13434 wwww.nature.com/scientific reports
  7. Choe YH, Kim SK, Hong YC. The relationship between Helicobacter pylori infection and iron deficiency: seroprevalence study in 937 pubescent children. Arch Dis Child 2003; 88:178; PMID:12538339; http://dx.doi.org/ 10.1136/adc.88.2.178-a
  8. Yang YJ, Sheu BS, Lee SC, Yang HB, Wu JJ. Children of Helicobacter pylori-infected dyspeptic mothers are predisposed to H. pylori acquisition with subsequent iron deficiency and growth retardation. Helicobacter 2005; 10:249–55; PMID:15904483; http://dx.doi.org/10.1111/j.1523–5378.2005.00317.x
  9. Baggett HC, Parkinson AJ, Muth PT, Gold BD, Gessner BD. Endemic iron deficiency associated with Helicobacter pylori infection among schoolaged children in Alaska. Pediatrics 2006; 117: e396–404; PMID:16452320; http://dx.doi.org/10.1542/ peds.2005– 1129
  10. Cardenas VM, Mulla ZD, Ortiz M, Graham DY. Iron deficiency and Helicobacter pylori infection in the United States. Am J Epidemiol 2006; 163:127–34; PMID:16306309; http://dx.doi.org/10.1093/aje/ kwj018
  11. Muhsen K, Barak M, Henig C, Alpert G, Ornoy A, Cohen D. Is the association between Helicobacter pylori infection and anemia age dependent? Helicobacter 2010; 15:467–72; PMID:21083753; http://dx.doi. org/10.1111/j.1523– 5378.2010.00793.x
  12. Afifi RAR, Ali DK, Shaheen IAM. A localized casecontrol study of extra-gastric manifestations of Helicobacter pylori infection in children. Indian J Pediatr 2011; 78:418–22; PMID:21165719; http:// dx.doi.org/1 0.1007/ s12098–010– 0308–6
  13. Queiroz DMM, Harris PR, Sanderson IR, Windle HJ, Walker MM, Rocha AMC, Rocha GA, Carvalho SD, Bittencourt PF, de Castro LP, et al. Iron status and Helicobacter pylori infection in symptomatic children: an international multi-centered study. PLoS One 2013; 8: e68833; PMID:23861946; http://dx.doi. org/10.1371/journal.pone.0068833
  14. Soglu OD, Gцkзe S, Saglam AT, Sцkьcь S, Saner G. Association of Helicobacter pylori infection with gastroduodenal disease, epidemiologic factors and iron-deficiency anemia in Turkish children undergoing endoscopy, and impact on growth. Pediatr Int 2007; 49:858–63; PMID:18045286; http://dx.doi. org/10.1111/j.1442–200X.2007.02444.x
  15. Berg G, Bode G, Blettner M, Boeing H, Brenner H. Helicobacter pylori infection and serum ferritin: A population-based study among 1806 adults in Germany. Am J Gastroenterol. 2001 Apr; 96(4):1014–1018.
  16. Milman N, Rosenstock S, Andersen L, Jorgensen T, Bonnevie O. Serum ferritin, hemoglobin, and Helicobacter pylori infection: a seroepidemiologic survey comprising 2794 Danish adults. Gastroenterology. 1998 Aug; 115(2):268–274.
  17. Yuan W, Li Y, Yang K, Ma B, Guan Q, Wang D, et al. Iron deficiency anemia in Helicobacter pylori infection: meta-analysis of randomized controlled trials. Scand J Gastroenterol. 2010 Jun; 45(6):665–676.
  18. Qu XH, Huang XL, Xiong P, Zhu CY, Huang YL, Lu LG, et al. Does Helicobacter pylori infection play a role in iron deficiency anemia? A meta-analysis. World J Gastroenterol. 2010 Feb 21; 16(7):886–896.
  19. Huang X, Qu X, Yan W, Huang Y, Cai M, Hu B, et al. Iron deficiency anaemia can be improved after eradication of Helicobacter pylori. Postgrad Med J. 2010 May; 86(1015):272–278.
  20. Zhang ZF, Yang N, Zhao G, Zhu L, Zhu Y, Wang LX. Effect of Helicobacter pylori eradication on iron deficiency. Chinese medical journal. 2010 Jul; 123(14):1924–1930.
  21. Y. H. Choe, J. E. Lee, and S. K. Kim, “Effect of Helicobacter pylori eradication on sideropenic refractory anaemia in adolescent girls with Helicobacter pylori infection,” Acta Paediatrica, International Journal of Paediatrics, vol. 89, no. 2, pp. 154–157, 2000.
  22. T. Sugiyama, M. Tsuchida, K. Yokota, M. Shimodan, and M. Asaka, “Improvement of long-standing iron-deficiency anemia in adults after eradication of Helicobacter pylori infection,” Internal Medicine, vol. 41, no. 6, pp. 491–494, 2002.
  23. D. Mahalanabis, M. A. Islam, S. Shaikh et al., “Haematological response to iron supplementation is reduced in children with asymptomatic Helicobacter pylori infection,” British Journal of Nutrition, vol. 94, no. 6, pp. 969–975, 2005.
  24. C. Ciacci, F. Sabbatini, R. Cavallaro et al., “Helicobacter pylori impairs iron absorption in infected individuals,” Digestive and Liver Disease, vol. 36, no. 7, pp. 455– 460, 2004.
  25. Duclaux-Loras R, Lachaux A. [Helicobacter pylori infection, a classic but often unrecognized cause of iron deficiency anemia in teenagers]. Arch Pediatr 2013;20(4):395–7.
  26. Yip, R. et al. Pervasive occult gastrointestinal bleeding in an Alaska native population with prevalent iron deficiency – Role of Helicobacter pylori gastritis. JAMA 277, 1135–1139 (1997).
  27. Blecker U, Renders F, Lanciers S, Vandenplas Y. Syncopes leading to the diagnosis of a Helicobacter pylori positive chronic active haemorrhagic gastritis. Eur J Pediatr 1991; 150:560–1; http://dx.doi.org/10.1007/BF02072207
  28. Rockey, D. C. & Cello, J. P. Evaluation of the Gastrointestinal-Tract in Patients with Iron-Deficiency Anemia. N Engl J Med 329, 1691–1695 (1993).
  29. Mubarak, N., Gasim, G. I., Khalafalla, K. E., Ali, N. I. & Adam, I. Helicobacter pylori, anemia, iron deficiency and thrombocytopenia among pregnant women at Khartoum, Sudan. Trans R Soc Trop Med Hyg 108, 380–384 (2014).
  30. Otto, B. R., Verweijvanvught, A. M. J. J. & Maclaren, D. M. Transferrins and Heme-Compounds as Iron Sources for Pathogenic Bacteria. Critical Reviews in Microbiology 18, 217–233 (1992).
  31. Andrews SC, Robinson AK, Rodriguez- Quinones F. Bacterial iron homeostasis. FEMS Microbiol Rev. 2003; 27: 215±237.
  32. Choe YH, Hwang TS, Kim HJ, Shin SH, Song SU, Choi MS. A possible relation of the Helicobacter pylori pfr gene to iron deficiency anemia? Helicobacter. 2001; 6: 55±59.
  33. Jeon BH, Oh YJ, Lee NG, Choe YH. Polymorphism of the Helicobacter pylori feoB gene in Korea: a possible relation with iron-deficiency anemia? Helicobacter. 2004; 9: 330±334. https://doi.org/10.1111/j. 1083–4389.2004.00239.x
  34. Muhsen K, Barak M, Shifnaidel L, Nir A, Bassal R, Cohen D. Helicobacter pylori infection is associated with low serum ferritin levels in Israeli Arab children: a seroepidemiologic study. J Pediatr Gastroenterol Nutr 2009; 49: 262– 264.
  35. Annibale B, Capurso G, Lahner E, Passi S, Ricci R, Maggio F, Delle Fave G. Concomitant alterations in intragastric pH and ascorbic acid concentration in patients with Helicobacter pylori gastritis and associated iron deficiency anaemia. Gut 2003; 52: 496–501.
  36. Choi JW. Serum-soluble transferrin receptor concentrations in Helicobacter pylori-associated iron- deficiency anemia. Ann Hematol 2006; 85: 735–737.
  37. Bini EJ. Helicobacter pylori and iron deficiency anemia: guilty as charged? Am J Med 2001; 111: 495–497. Kaptan K, Beyan C, Ugur U, et al. Helicobacter pylori – it is a novel causative agent in vitamin B12 deficiency? Arch Intern Med 2000;160:1349–53.
  38. Kuipers EJ, Perez-Perez GI, Meuwissen SG, Blaser MJ. Helicobacter pylori and atrophic gastritis: importance of the cagA status. J Natl Cancer Inst. 1995 Dec 6; 87(23):1777–1780. Wen S, Moss SF. Helicobacter pylori virulence factors in gastric carcinogenesis. Cancer Lett. 2009 Sep 8; 282(1):1–8.
  39. Anderson LA, Murphy SJ, Johnston BT, Watson RG, Ferguson HR, Bamford KB, et al. Relationship between Helicobacter pylori infection and gastric atrophy and the stages of the oesophageal inflammation, metaplasia, adenocarcinoma sequence: results from the FINBAR case-control study. Gut. 2008 Jun; 57(6):734– 739.
  40. Cardenas VM, Prieto-Jimenez CA, Mulla ZD, Rivera JO, Dominguez DC, Graham DY, et al. Helicobacter pylori eradication and change in markers of iron stores among non-iron- deficient children in El Paso, Texas: an etiologic intervention study. J Pediatr Gastroenterol Nutr. 2011 Mar; 52(3):326–332.
  41. Muhsen K, Barak M, Shifnaidel L, Nir A, Bassal R, Cohen D. Helicobacter pylori infection is associated with low serum ferritin levels in Israeli Arab children: a seroepidemiologic study. J Pediatr Gastroenterol Nutr. 2009 Aug; 49 (2):262–264.
  42. Prentice A M Clinical Implications of New Insights into Hepcidin-Mediated Regulation of Iron Absorption and Metabolism Ann Nutr Metab. 2017;71 Suppl 3:40–48. doi:10.1159/000480743. Epub 2017 Dec 22.
  43. Girelli D, Ugolini S, Busti F, Marchi G, Castagna A. Modern iron replacement therapy: clinical and pathophysiological insights Int J Hematol. 2018 Jan;107(1):16–30. doi: 10.1007/s12185–017–2373–3. Epub 2017 Dec 1.
  44. Park C.H., Valore E. V., Waring A. J. et al. Hepcidin: a urinary antibacterial peptide synthesized in the liver. J. Biol. Chem.2001; 276: 7806–7810.
  45. Hunter H.N., Fulton D. B., Vogel H. J. The solution structure of human hepcidin, a antibicrobial activity that is involved in iron uptake and hereditary hemochromatosis. J. Biol. Chem. 2002; 277: 37597–37603.
  46. Kanda J, Mizumoto C, Kawabata H, Tsuchida H, Tomosugi N, Matsuo K, Uchiyama T. Serum hepcidin level and erythropoietic activity after hematopoietic stem cell transplantation. Haematologica. 2008; 93: 1550‐1554. Darshan D, Anderson GJ. Interacting signals in the control of hepcidin expression. Biometals. 2009; 22: 77 ‐87.
  47. Guo P, Cui R, Chang YZ, Wu WS, Qian ZM, Yoshida K, Qiao YT, Takeda S, Duan XL. Hepcidin, an antimicrobial peptide is downregulated in ceruloplasmin‐deficient mice. Peptides. 2009; 30: 262‐266.
  48. Hoppe M, Lönnerdal B, Hossain B, Olsson S, Nilsson F, Lundberg P A, Rödjer S, Hulthén L. Hepcidin, interleukin‐6 and hematological iron markers in males before and after heart surgery. J Nutr Biochem. 2009; 20: 11‐16.
  49. Bansal SS, Halket JM, Bomford A, Simpson RJ, Vasavda N, Thein SL, Hider RC. Quantitation of hepcidin in human urine by liquid chromatography‐mass spectrometry. Anal Biochem. 2009; 384: 245‐253.
  50. Fleming RE. Iron and inflammation: cross‐ talk between pathways regulating hepcidin. J Mol Med. 2008; 86: 491‐ 494.
  51. Oliveras‐Verge’s A, Espel‐Masferrer E. Elevated basal hepcidin levels in the liver may inhibit the development of malaria infection: Another piece towards solving the malaria puzzle? Med Hypotheses. 2008; 70: 630‐634.
  52. Christiansen H, Saile B, Hermann RM, Rave‐ Fränk M, Hille A, Schmidberger H, Hess CF, Ramadori G. Cancer Res Clin Oncol. 2007; 133: 297‐304.
  53. Malyszko J, Malyszko JS, Pawlak K, Mysliwiec M: Hepcidin, an acute‐phase protein and a marker of inflammation in kidney transplant recipients with and without coronary artery disease. Transplant Proc. 2006; 38: 2895‐2898.
  54. Politou M, Papanikolaou G: Hepcidin: A key iron regulator involved in the pathogenesis of anaemia of chronic disease. Haema. 2004; 7: 165‐174.
  55. Swinkels DW, Drenth JPH. Hepcidin in the management of patients with mild non‐hemochromatotic iron overload: Fact or fiction? J Hepatol. 2008; 49: 680‐685.
  56. Ruivard M, Lainé F, Ganz T, Olbina G, Westerman M, Nemeth E, Rambeau M, Mazur A, Gerbaud L, Tournilhac V, Abergel A, Philippe P, Deugnier Y, Coudray C. Iron absorption in dysmetabolic iron overload syndrome is decreased and correlates with increased plasma hepcidin. J Hepatol. 2009; 50: 1219‐1225.
  57. CamaschellaC, SilvestriL. New and old playersinthe hepcidin pathway. Haematologica.2008;93:1441‐1444. Swinkels DW, Wetzels JFM. Hepcidin: a new tool in the management of anaemia in patients with chronic kidney disease? Nephrol Dial Transplant. 2008; 23: 2450‐2453.
  58. Fujita N, Sugimoto R, Motonishi S, Tomosugi N, Tanaka H, Takeo M, Iwasa M, Kobayashi Y, Hayashi H, Kaito M, Takei Y. Patients with chronic hepatitis C achieving a sustained virological response to peginterferon and ribavirin therapy recover from impaired hepcidin secretion. J Hepatol. 2008; 49: 702‐710.
  59. Oğuz A, Uzunlulu M, Hekim N. Hepcidin is not a marker of chronic inflammation in atherosclerosis. Anadolu Kardiyol Derg. 2006; 6: 239‐242.
  60. Arruda SF, de Almeida Siqueira EM, de Valência FF. Vitamin A deficiency increases hepcidin expression and oxidative stress in rat. Nutrition. 2009; 25: 472‐478.
  61. Kemna EH, Tjalsma H, Willems HL, Swinkels DW. Hepcidin: from discovery to differential diagnosis. Haematologica. 2008; 93: 90‐97.
  62. Chiang TH, Chiu SY, Chen SL, Yen AM, Fann JC, Liu CY, Chou CK, Chiu HM, Shun CT, Wu MS, Lin JT, Lee YC, Chen TH, Lin MW Serum Pepsinogen as a Predictor for Gastric Cancer Death: A 16 -Year Community-based Cohort Study. J Clin Gastroenterol. 2018 Jan 23. doi: 10.1097/MCG.0000000000000992.
  63. Burns M, Amaya A, Bodi C, Ge Z, Bakthavatchalu V, Ennis K, Wang TC, Georgieff M, Fox JG. Helicobacter pylori infection and low dietary iron alter behavior, induce iron deficiency anemia, and modulate hippocampal gene expression in female C57BL/6 mice. 2017 Mar 29;12(3): e0173108. doi: 10.1371/journal.pone.0173108. eCollection 2017.
  64. Siddique O, Ovalle A, Siddique AS, Moss SF. Helicobacter Pylori Infection: an Update for the Internist in the Age of Increasing Global Antibiotic Resistance. Am J Med. 2018 Jan 15. pii: S0002–9343(18)30013–5. doi: 10.1016/j.amjmed.2017.12.024.
  65. Schwarz P1, Kübler JA, Strnad P, Müller K, Barth TF, Gerloff A, Feick P, Peyssonnaux C, Vaulont S, Adler G, Kulaksiz H Hepcidin is localised in gastric parietal cells, regulates acid secretion and is induced by Helicobacter pylori infection. Gut. 2012 Feb;61(2):193–201. doi: 10.1136/gut.2011.241208. Epub 2011 Jul 13.
  66. Lee SY, Song EY, Yun YM, Yoon SY, Cho YH, Kim SY, et al. Serum prohepcidin levels in Helicobacter pylori infected patients with iron deficiency anemia. Korean J Intern Med 2010;25: 195e200.
  67. Azab SF, Esh AM. Serum hepcidin levels in Helicobacter pyloriinfected children with iron-deficiency anemia: a case-control study. Ann Hematol 2013;92:1477e83.
  68. Sato Y, Yoneyama O, Azumaya M, Takeuchi M, Sasaki SY, Yokoyama J, et al. The relationship between iron deficiency inpatients with Helicobacter pylori-infected nodular gastritis and the serum prohepcidin level. Helicobacter 2015;20:11e8.
  69. Ozkasap S, Yarali N, Isik P, Bay A, Kara A, Tunc B. The role of prohepcidin in anemia due to Helicobacter pylori infection. Pediatr Hematol Oncol 2013;30:425e31.
  70. Queiroz DMM, Rocha AMC, Melo FF, Rocha GA, Teixeira KN, Carvalho SD, Bittencourt PF, Castro LP, Crabtree JE. Increased gastric IL-1β concentration and iron deficiency parameters in H. pylori infected chil- dren. PLoS One 2013; 8: e57420; http://dx.doi.org/10.1371/journal.pone.0057420
  71. Inamura J, Ikuta K, Jimbo J, Shindo M, Sato K, Torimoto Y, Kohgo Y. Upregulation of hepcidin by interleukin- 1β in human hepatoma cell lines. Hepatol Res 2005; 33:198–205; http:// dx.doi.org/10.1016/j.hepres.2005.08.005
  72. Lee P, Peng H, Gelbart T, Wang L, Beutler E. Regulation of hepcidin transcription by interleu- kin-1 and interleukin-6. Proc Natl Acad Sci U S A 2005; 102:1906–10;; http://dx.doi. org/10.1073/pnas.0409808102
  73. Szu-Ta Chen, Yen-Hsuan Ni, Chuan-Chun Li, Shing-Hwa Liu / Hepcidin correlates with interleukin-1b and interleukin-6 but not iron deficiency in children with Helicobacter pylori infection The Korean Journal of Internal Medicine Vol. 25, No. 2, June 2010; р. 195–200
  74. Emiralioglu N, Yenicesu I, Sari S, Egritas O, Poyraz A, Pasaoglu OT, et al. An insight into the relationships between prohepcidin, iron deficiency anemia, and interleukin-6 values in pediatric Helicobacter pylori gastritis. Eur J Pediatr 2015;174:903e10.
  75. Choe YH, Oh YJ, Lee NG, Imoto I, Adachi Y, Toyoda N, Gabazza EC. Lactoferrin sequestration and its contribution to iron-deficiency anemia in Helicobacter pylori-infected gastric mucosa. J Gastroenterol Hepatol 2003; 18:980–5; http://dx.doi. org/10.1046/j.1440–1746.2003.03098.x

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Shulyat’eva N.V., Drozdov V. N., Serebrova S. Yu., Starodubcev A. K., Shih E. V. THE VALUE OF THE H. PYLORI INFECTION IN THE DEVELOPMENT OF IRON DEFICIENCY. Experimental and Clinical Gastroenterology Journal. 2018;154(06):105-110
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1. Institute of advanced training of the Federal medical and biological Agency of Russia» (Moscow, Russian Federation)
2. MSMSU them. A. I. Evdokimov (Moscow, Russian Federation)
3. Lyubertsy Kozhno-Venerologicheskiy Dispanser (Lyubertsy, Russian Federation)

Keywords: rosacea, Helicobacter pylori, proton pump inhibitors

Abstract:The available numerous literature data indicate that Helicobacter pylori infection (HP) plays an important role in the etiology and pathogenesis of diseases that are not related to the digestive system (atherosclerosis, diabetes, thrombocytopenic purpura, Sjogren’s disease), including skin diseases (chronic urticaria, atopic dermatitis, itching, psoriasis, red flat lichen, focal alopecia, rosacea, etc.). The role of Helicobacter pylori infection during these diseases is described in detail and the need for eradication therapy is proved. The importance of studying gastrointestinal lesions in patients with this pathology for the purpose of complex pathogenetic therapy is confirmed.

• References total 33 ⇓ :: .
  1. Rainer BM, Fischer AH, Luz Felipe da Silva D, Kang S, Chien AL. Rosacea is associated with chronic systemic diseases in a skin severity-dependent manner: results of a case-control study. J Am Acad Dermatol. 2015;73:604–608.
  2. Hua TC, Chung PI, Chen YJ, et al. Cardiovascular comorbidities in patients with rosacea: a nationwide case-control study from Taiwan. J Am Acad Dermatol. 2015;73:249–254.
  3. Egeberg A, Hansen PR, Gislason GH, Thyssen JP. Clustering of autoimmune diseases in patients with rosacea. J Am Acad Dermatol. 2016;74:667–672.
  4. Egeberg A, Hansen PR, Gislason GH, Thyssen JP. Association of rosacea with risk for glioma in a Danish nationwide cohort study. JAMA Dermatol. 2016;152:541–545.
  5. Potekayev N. N. Rosacea (etiology, clinic, therapy) Moscow, Binom Publ., 2000. 20 p.
  6. Egeberg, A. Rosacea and gastrointestinal disorders: a population-based cohort study /A. Egeberg, L. B. Weinstock, E. P. Thyssen, G. H. Gislason, J. P. Thyssen // Br. J. Dermatol. – 2017. – Vol. 176. – № 1. – P. 100–106.
  7. Perlamutrov YU.N. Comparative evaluation of the effectiveness of various methods of treatment of rosacea / YU.N. Perlamutrov, V.SH. Sajdalieva, K. B. Ol’hovskaya. journal of dermatology and venereology. 2011. no.3. pp. 73–79.
  8. Vemuri, R. C. Major pathophysiological correlations of rosacea: a complete clinical appraisal / R. C. Vemuri, R. Gundamaraju, S. D. Sekaran, R. Manikam // Int. J. Med. Sci. – 2015. – Vol. 12. – № 5. – P. 387–396.
  9. Lynn DD, Umari T, Dunnick CA, Dellavalle RP. The epidemiology of acne vulgaris in late adolescence. Adolescent Health, Medicine and Therapeutics. 2016;7:13–25.
  10. Tan J., Berg M. Rosacea: current state of epidemiology. J Am Acad Dermatol. 2013: 69: S27—S35.
  11. Tan J, Schöfer H, Araviiskaia E, et al. Prevalence of rosacea in the general population of Germany and Russia – The RISE study. Journal of the European Academy of Dermatology and Venereology. 2016;30(3):428–434.
  12. Fitzpatrick, T. B. (1975). “Soleil et peau” [Sun and skin]. Journal de Médecine Esthétique (in French) (2): 33–34 Chang AL, Raber I, Xu J, Li R, Spitale R, Chen J, Kiefer AK, Tian C, Eriksson NK, Hinds DA, Tung JY. Assessment of the genetic basis of rosacea by genome-wide association study. J Invest Dermatol. 2015 Jun;135(6): 1548–1555. https://doi.org/ 10.1038/jid.2015.53
  13. Chang AL, Raber I, Xu J, Li R, Spitale R, Chen J, Kiefer AK, Tian C, Eriksson NK, Hinds DA, Tung JY. Assessment of the genetic basis of rosacea by genome-wide association study. J Invest Dermatol. 2015 Jun;135(6): 1548–1555. https://doi.org/ 10.1038/jid.2015.53
  14. Aldrich N, Gerstenblith M, Fu P, Tuttle MS, Varma P, Gotow E, Cooper KD, Mann M, Popkin DL. Genetic vs environmental factors that correlate with rosacea: a cohort-based survey of twins. JAMA Dermatol. 2015 Nov; 151(11):1213–1219. https://doi.org/10.1001/jamadermatol.2015.2230
  15. Wilkin J, Dahl M, Detmar M, Drake L, Feinstein A, Odom R, Powell F. Standard classification of rosacea: report of the national rosacea society expert committee on the classification and staging of rosacea. J Am Acad Dermatol. 2002 Apr;46(4):584–587.
  16. Yamasaki K, Di Nardo A, Bardan A, Murakami M, Ohtake T, Coda A, Dorschner RA, Bonnart C, Descargues P, Hovnanian A, Morhenn VB, Gallo RL. Increased serine protease activity and cathelicidin promotes skin inflammation in rosacea. Nat Med. 2007;13(8):975–80.
  17. Two AM, Del Rosso JQ. Kallikrein 5-mediated inflammation in rosacea: clinically relevant correlations with acute and chronic manifestations in rosacea and how individual treatments may provide therapeutic benefit. J Clin Aesthet Dermatol. 2014;7(1):20–5.
  18. Coda AB, Hata T, Miller J, Audish D, Kotol P, Two A, Shafiq F, Yamasaki K, Harper JC, Del Rosso JQ, Gallo RL. Cathelicidin, kallikrein 5, and serine protease activity is inhibited during treatment of rosacea with azelaic acid 15% gel. J Am Acad Dermatol. 2013;69(4):570–7.
  19. Muto Y, Wang Z, Vanderberghe M, Two A, Gallo RL, Di Nardo A. Mast cells are key mediators of cathelicidin-initiated skin inflammation in rosacea. J Invest Dermatol. 2014;134(11):2728–36.
  20. Koczulla R, von Degenfeld G, Kupatt C, Krötz F, Zahler S, Gloe T, Issbrücker K, Unterberger P, Zaiou M, Lebherz C, Karl A, Raake P, Pfosser A, Boekstegers P, Welsch U, Hiemstra PS, Vogelmeier C, Gallo RL, Clauss M, Bals R. An angiogenic role for the human peptide antibiotic LL-37 /hCAP-18. J Clin Invest. 2003;111(11):1665–72.
  21. Egeberg A, Hansen PR, Gislason GH, Thyssen JP. Clustering of autoimmune diseases in patients with rosacea. J Am Acad Dermatol. 2016 Apr;74(4):667–72.e1. doi: 10.1016/j.jaad.2015.11.004.
  22. Spoendlin J, Karatas G, Furlano RI, Jick SS, Meier CR. Rosacea in Patients with Ulcerative Colitis and Crohn’s Disease: A Population-based Case-control Study. Inflamm Bowel Dis. 2016 Mar;22(3):680–7. doi:10.1097/MIB.0000000000000644.
  23. Egeberg A, Weinstock LB, Thyssen EP, Gislason GH, Thyssen JP. Rosacea and gastrointestinal disorders: a population-based cohort study. Br J Dermatol. 2017 Jan;176(1):100–106. doi: 10.1111/bjd.14930
  24. CHernyak A.YA., Rusak YU.EH., Berger V. V. EHndoskopicheskaya kartina porazhenij zheludka u bol’nyh rozacea, associirovannyh s Helicobacter pylori. Tezisy nauchnyh rabot YII Vserossijskogo s”ezda, ch. I «Dermatologiya», Moskva, 2001. – S.202
  25. Slesarenko N. A., Leonova M. A., Bakulev A. L., Davydova A. V., Slesarenko N. S., Katkova I. O. The role of Helicobacter pylori as a trigger factor in the development of rosacea and the effect of its eradication on the course of dermatosis. Bulletin of dermatology and venereology. 2012. no. 2. pp. 33–39.
  26. Samsonov A. A. proton pump Inhibitors-drugs of choice in the treatment of acid-dependent diseases. Pharmateca. 2007. No. 6. p. 10–15
  27. Minushkin O. N., Maslovskij L. V., Evsikov A. E., SHaposhnikova O. F., Makarova M. S. The effectiveness of injection and oral applications of proton pump inhibitor in the treatment of pancreatitis. Doktor.Ru Gastroenterology. 2015;103(2):19–24
  28. Sachs G. et al. Synthesis or rupture: duration of acid inhibition by proton pump inhibitors // Drugs Today. 2003. Vol. 39. Suppl. A.P. S11–14
  29. Uspenskij YU. P. 1, Pahomova I. G. The choice of proton pump inhibitors in polymorbid patients. Experimental and clinical gastroenterology, 2013, no. 2, pp. 65–71
  30. Mahov V. M., Turko T. V., Volodina T. V., Kulesh I. A. Proton pump inhibitors-the main link in the treatment of acid-dependent pathology// Russian medical journal. Gastroenterology. – 2013. – № 13. P. 698–701
  31. Masharova A. A., Bordin D. S., Kozhurina T.S, YAnova O.B., Kim V. A., Zelenikin S. A. Preimushchestva pantoprazola v terapii gastroehzofageal’noj reflyuksnoj bolezni. Lechashchij vrach, № 7, 2010. S.78
  32. Masharova A. A., YAnova O.B., Valitova EH.R., Kim V. A., Zelenikin S. A. The effectiveness of the drug Panum (pantoprazole) in the treatment of patients with GERD. Experimental and clinical gastroenterology. 2011. No. 4. P. 81–85
  33. Golofeevskij V.YU. Otkrytoe prospektivnoe issledovanie po principu «sluchaj-kontrol’». Zaklyuchenie o terapevticheskoj ehkvivalentnosti preparata «PANUM®». «Gastroehnterologiya Sankt-Peterburga», 2016, № 1–2, s. M8

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Matushevskaya E. V., Komissarenko I. A., Matushevskaya Yu.I. THE ROLE OF HELICOBACTER PYLORI IN THE PATHOGENESIS OF ROSACEA. TREATMENT WITH PROTON PUMP INHIBITORS. Experimental and Clinical Gastroenterology Journal. 2018;154(06):111-115
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1. Public budgetary educational institution of higher education “Ogarev Mordovia State University” of Ministry of Education of Russia (Saransk, Russian Federation)

Keywords: nausea, vomiting, diagnostics, treatment

Abstract:The article is devoted to the problem of the emetic syndrome. Details are presented etiology, basic variants and diagnostic criteria for the disease. The article focuses on the aspects of treatment of patients with an emetic syndrome.

• References total 17 ⇓ :: .
  1. Zagorenko Yu. A. Emeticheskiy sindrom: vse li my o nem znayem? Novosti meditsiny i farmatsii. Gastroenterologiya. 2008, no. 20, pp. 29–40.
  2. Drossman D.A., Hasler W. L. Rome IV – Functional GI disorders: disorders of gut-brain interaction // Gastroenterology. – 2016. – Vol.150, № 6. – Р.1257–1261.
  3. Toshnota i rvota v praktike gastroenterologa i ne tol'ko. Zdorov'ya Ukraini. 2012; 23(1): 56–57.
  4. Pasricha P., Colvin R., Yates K. et al. Characteristics of patients with chronic unexplained nausea and vomiting and normal gastric emptying // Clin. Gastroenterol. Hepatol. – 2011. – Vol. 19, no. 7. – Р. 567–576.
  5. Tkach C. M. Funktsional’naya dispepsiya v svete Rimskikh kriteriyev IV // Gastroenterologiya. 2016, vol. 62, no.4, pp. 65–71.
  6. Andreyev D. N., Zaborovskiy A. V., Trukhmanov A. S., Mayev I. V., Ivashkin V. T. Evolyutsiya predstavleniy o funktsional’nykh zabolevaniyakh zheludochno-kishechnogo trakta v svete Rimskikh kriteriyev IV peresmotra (2016 g.). Ros. zhurn. gastroenterol. gepatol. koloproktol. 2017, Vol. 27, no. 1. pp.4–11.
  7. Bessonova O. V., Sergiyenko Ye. I. Kharakteristika i patofiziologicheskiye mekhanizmy klinicheskikh proyavleniy funktsional’nykh rasstroystv gastroduodenal’noy zony. Gazeta «Novosti meditsiny i farmatsii». Gastroenterologiya. 2012, vol. 414. http://www.mif-ua.com/archive/article/30913.
  8. Sindrom toshnoty i rvoty // Meditsina neotlozhnykh sostoyaniy. 2012. vol. 44, no 5. http://www.mif-ua.com/archive/article/34111
  9. Burov N. Ye. Toshnota i rvota v klinicheskoy praktike (etiologiya, patogenez, profilaktika i lecheniye). Russkiy meditsinskiy zhurnal. 2002. no. 8–9. pp. 390–395.
  10. Louik C., Hernandez-Diaz S., Werler M. M., Mitchell A. A. Nausea and vomiting in pregnancy: maternal characteristics and risk factors // Paediatr. Perinat. Epidemiol. 2006, vol. 20, no.4, pp. 270–278.
  11. Zhao Y., Ke M., Wang Z. et al. Pathophysiological and psychosocial study in patients with functional vomiting // Neurogastroenterol. Motil. – 2010. – Vol.3, № 16. – pp. 274–280.
  12. Talley N.J., Ford A. C. Functional dyspepsia // N. Engl. J. Med. – 2015. – Vol.373, № 19. – Р.1853–1863.
  13. Ushkalova Ye.A., Romanova O. L., Illarionova T. S. Effektivnost’ i bezopasnost’ lekarstvennykh sredstv, primenyayemykh dlya lecheniya toshnoty i rvoty u beremennykh zhenshchin // Farmateka. 2011, no. 6. pp. 24–28.
  14. Fahridin S. Presentations of nausea and vomiting // Aust. Fam. Physician. – 2007. –Vol.36, № 9. – Р. 673–784.
  15. Jennifer R. Niebyl. Nausea and vomiting in pregnancy // N. Engl. J. Med. – 2010. – Vol. 363. – Р. 1544–1550.
  16. Taylor T. Treatment of nausea and vomiting in pregnancy // Aust. Prescr. – 2014. – Vol.37, № 2. – Р.42–45.
  17. King T.L., Murphy P. A. Evidence-based approaches to managing nausea and vomiting in early pregnancy // J. Midwifery Womens Health. – 2009. – Vol.54, № 6. –Р. 430–444.

Full text is published :
Strokova О. А., Ereminа E. Yu. EMETIC SYNDROME: PRINCIPLES OF DIAGNOSIS AND TREATMENT. Experimental and Clinical Gastroenterology Journal. 2018;154(06):116-121
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1. Scientific Research Institute of Molecular Biology and Medicine (Bishkek, Kyrgyzstan)
2. Kyrgyz State Medical Academy named after I. K. Akhunbayev (Bishkek, Kyrgyzstan)
3. Kyrgyz Russian Slavic University named after the First President of Russia B. N. Yeltsin (Bishkek, Kyrgyzstan)
4. FSAEI HE First Moscow State Medical University named after I. M. Sechenov (Moscow, Russian Federation)
5. Family Medicine Center № 7 (Bishkek, Kyrgyzstan)

Keywords: gut microbiota, dysbiosis, epigenome, regulation

Abstract:The development and introduction of high-performance molecular genetic methods into practice allowed us, in recent years, to increase our knowledge of the epigenome and microbiome, which shed light on the mechanisms of development of various pathologies, such as cancer, immune-mediated, metabolic and cardiovascular diseases. It was found that the dysbiosis of gut microbiota (GM), which often accompanies these diseases, can affect the epigenetic mechanisms of the regulation of the activity of individual genes either directly through a change in the composition of GM, or indirectly, through changes in metabolites, which are various biologically active substances (short-chain fatty acids, biotin, folic acid and other biologically active molecules). Indeed, correlations between epigenetic mechanisms regulating the activity of host genes, on one hand, and changes in the composition of its gut microbiota or metabolites produced by intestinal microorganisms, on the other, have been established in certain diseases. It served as the basis for assuming that GM can become a diagnostic marker for certain diseases, and that treating the intestinal dysbiosis by transplanting healthy microflora is an effective therapeutic strategy. In this article, we discuss the relationship between dysbiosis of the gut microbiota and the host’s epigenome, as well as the possibility of using the microbiome and epigenome as diagnostic and therapeutic targets.

• References total 73 ⇓ :: .
  1. Cortessis V. K., Thomas D. C., Levine A. J. et al. Environmental epigenetics: prospects for studying epigenetic modification of exposure-response relationships. Hum Genet. 2012; 131(10):1565-89. DOI:10.1007/s00439-012-1189-8.
  2. Bannister A. J., Kouzarides T. Regulation of chromatin by histone modifications. Cell Research 2011; 21(3):381-395. DOI:10.1038/cr.2011.22.
  3. Kohli R. M., Zhang Y. TET enzimes, TDG and the dynamics of DNA demethylation. Nature 2013; 502(7472):472-479. DOI:10.1038/nature12750.
  4. Пендина А. А., Гринкевич В. В., Кузнецова Т. В., Баранов В. С. Метилирование ДНК - универсальный механизм регуляции активности генов. Экологическая генетика 2004; II (1):27-37.
  5. Bartel D. P. MicroRNAs: target recognition and regulatory functions. Cell.2009;23:215-233. DOI:10.1016/j.cell.2009.01.002.
  6. Wu H. J., Ivanov I. I., Darce J. et al. Gut-residing segmented filamentous bacteria drive autoimmune arthritis via T helper 17 cells. Immunity 2010; 32: 815-827. DOI:10.1016/j.immuni.2010.06.001.
  7. McLoughlin R.M., Mills K. H. Influence of gastrointestinal commensal bacteria on the immune responses that mediate allergy and asthma. J Allergy Clin Immunol 2011; 127: 1097-107. quiz 1108-9. DOI:10.1016/j.jaci.2011.02.012.
  8. Torano E. G., Garcia M. G., Fernandez-Morera J.L. et al. The Impact of External Factors on the Epigenome: In Utero and over Lifetime. Biomed Res Int 2016: s2568635. DOI:10.1155/2016/2568635.
  9. Kumar H., Lund R., Laiho A. et al. Gut microbiota as an epigenetic regulator: pilot study based on whole-genome methylation analysis. MBio 2014; 5: e02113-14. DOI:10.1128/mBio.02113-14.
  10. Krautkramer K. A., Kreznar J. H., Romano K. A. et al. Diet-Microbiota Interactions Mediate Global Epigenetic Programming in Multiple Host Tissues. Mol Cell 2016; 64: 982-92. DOI:10.1016/j.molcel.2016.10.025.
  11. Lara E., Calvanese V., Fernandez A. F., Fraga M. F. Techniques to Study DNA Methylation and Histone Modification. Springer: London 2011; pp:21-39.
  12. Arumugam M., Raes J., Pelletier E. et al. Enterotypes of the human gut microbiome. Nature 2011;473:174–180. DOI:10.1038/nature09944.
  13. Eloe-Fadrosh E.A., Rasko D. A. The human microbiome: from symbiosis to pathogenesis. Ann Rev Med 2013;64:145-163. DOI:10.1146/annurev-med-010312-133513.
  14. Murray MPJ. Encyclopedia of natural medicine, 1988.
  15. Hawrelak J. A., Myers S. P. The causes of intestinal dysbiosis: a review. Altern Med Rev 2004; 9:180-197. PMID:15253677.
  16. Carding S., Verbeke K., Vipond D. T. et al. Dysbiosis of the gut microbiota in disease. Microb Ecol Health Dis 2015; 26: 26191. DOI:10.3402/mehd.v26.26191.
  17. Strauss J., Kaplan G. G., Beck P. L. et al. Invasive potential of gut mucosa-derived Fusobacterium nucleatum positively correlates with IBD status of the host. Inflamm Bowel Dis 2011;17:1971-1978. DOI:10.1002/ibd.21606.
  18. Brown K., DeCoffe D., Molcan E., Gibson D. L. Diet-induced dysbiosis of the intestinal microbiota and the effects on immunity and disease. Nutrients 2012;4:1095-1119. DOI:10.3390/nu4081095.
  19. Tanaka S., Kobayashi T., Songjinda P. et al. Influence of antibiotic exposure in the early postnatal period on the development of intestinal microbiota. FEMS Immunol Med Microbiol 2009;56:80-87. DOI: https://doi.org/10.1111/j.1574-695X.2009.00553.x.
  20. O’Mahony S.M., Marchesi J. R., Scully P. et al. Early life stress alters behavior, immunity, and microbiota in rats: implications for irritable bowel syndrome and psychiatric illnesses. Biol Psychiatry 2009;65:263-7. DOI:10.1016/j.biopsych.2008.06.026.
  21. Carrillo-Salinas F.J., Mestre L., Mecha M. et al. Gut dysbiosis and neuroimmune responses to brain infection with Theiler’s murine encephalomyelitis virus. Sci Rep 2017;7:44377. DOI:10.1038/srep44377
  22. Zechner E. L. Inflammatory disease caused by intestinal pathobionts. Curr Opin Microbiol 2017;35:64-69. DOI:10.1016/j.mib.2017.01.011.
  23. Lerner A., Aminov R., Matthias T. Transglutaminases in Dysbiosis As Potential Environmental Drivers of Autoimmunity. Front Microbio 2017; 8: 66. DOI:10.3389/fmicb.2017.00066.
  24. Fukuda S., Toh H., Hase K. et al. Bifidobacteria can protect from enteropathogenic infection through production of acetate. Nature 2011;469:543-547. doi: 10.1038/nature09646.
  25. Vindigni S. M., Zisman T. L., Suskind D.L, Damman C. J. The intestinal microbiome, barrier function, and immune system in inflammatory bowel disease: a tripartite pathophysiological circuit with implications for new therapeutic directions. Therap Adv Gastroenterol 2016;9:606-25. DOI:10.1177/1756283X16644242.
  26. Jiang C., Li G., Huang P. et al. The Gut Microbiota and Alzheimer’s Disease. J Alzheimers Dis 2017;58(1):1-15. DOI:10.3233/JAD-161141.
  27. Tang W. H., Kitai T., Hazen S. L. Gut Microbiota in Cardiovascular Health and Disease. Circ Res 2017; 120: 1183-1196. DOI:10.1161/CIRCRESAHA.117.309715.
  28. Durgan D. J. Obstructive Sleep Apnea-Induced Hypertension: Role of the Gut Microbiota. Curr Hypertens Rep 2017;19: 35. DOI:10.1007/s11906-017-0732-3.
  29. Nicolas S., Blasco-Baque V., Fournel A. et al. Transfer of dysbiotic gut microbiota has beneficial effects on host liver metabolism. Mol Syst Biol 2017;13:921.DOI:10.15252/msb.20167356.
  30. Sen T., Cawthon C. R., Ihde B. T. et al. Diet-driven microbiota dysbiosis is associated with vagal remodeling and obesity. Physiol Behav 2017;173:305-317. DOI:10.1016/j.physbeh.2017.02.027.
  31. Olszak T., An D., Zeissig S. et al. Microbial exposure during early life has persistent effects on natural killer T cell function. Science 2012;336:489-493. DOI:10.1126/science.1219328.
  32. Cohen N. R., Garg S., Brenner M. B. Antigen Presentation by CD1 Lipids, T Cells, and NKT Cells in Microbial Immunity. Adv Immunol 2009; 102: 1-94. DOI:10.1016/S0065-2776(09)01201-2.
  33. Matloubian M., David A., Engel S. et al. A transmembrane CXC chemokine is a ligand for HIV-coreceptor Bonzo. Nat Immunol 2000;1:298-304. DOI:10.1038/79738.
  34. David L. A., Maurice C. F., Carmody R. N. et al. Diet rapidly and reproducibly alters the human gut microbiome. Nature 2014;505:559-563. DOI:10.1038/nature12820.
  35. Jeffery I. B., O’Toole P. W. Diet-microbiota interactions and their implications for healthy living. Nutrients 2013;5:234-252. DOI:10.3390/nu5010234.
  36. LeBlanc J.G., Milani C., de Giori G. S. et al. Bacteria as vitamin suppliers to their host: a gut microbiota perspective. Curr Opin Biotechnol 2013;24:160-168. DOI:10.1016/j.copbio.2012.08.005.Shenderov B. A. Gut indigenous microbiota and epigenetics. Microb Ecol Health Dis.2012;23:17461.DOI:10.3402/mehd.v23i0.17195.
  37. Penberthy W. T., Kirkland J. B. Present Knowledge in Nutrition: Wiley-Blackwell 2012; pp:293-306. DOI:10.1002/9781119946045.
  38. Siudeja K., Srinivasan B., Xu L. et al. Impaired Coenzyme A metabolism affects histone and tubulin acetylation in Drosophila and human cell models of pantothenate kinase associated neurodegeneration. EMBO Mol Med 2011;3:755-766. DOI:10.1002/emmm.201100180.
  39. Cluntun A. A., Huang H., Dai L. et al. The rate of glycolysis quantitatively mediates specific histone acetylation sites. Cancer Metab 2015;3:10. DOI:10.3402/mehd.v24i0.20399.
  40. Shenderov B. A. Metabiotics: novel idea or natural development of probiotic conception. Microb Ecol Health Dis 2013;24:20399.DOI: 10.3402/mehd.v24i0.20399.
  41. Zempleni J. Uptake, localization, and noncarboxylase roles of biotin. Annu Rev Nutr 2005;25:175-196. DOI:10.1146/annurev.nutr.25.121304.131724.
  42. Crider K. S., Yang T. P., Berry R. J., Bailey L. B. Folate and DNA Methylation: A Review of Molecular Mechanisms and the Evidence for Folate’s Role. Adv Nutr Int Rev J 2012;3:21-38. DOI:10.3945/an.111.000992.
  43. Pompei A., Cordisco L., Amaretti A. et al. Folate Production by Bifidobacteria as a Potential Probiotic Property. Appl Environ Microbiol 2007;73:179-185. DOI:10.1128/AEM.01763-06.
  44. Strozzi G. P., Mogna L. Quantification of folic acid in human feces after administration of Bifidobacterium probiotic strains. J Clin Gastroenterol 2008;2: S179-S184.DOI:10.1097/MCG.0b013e31818087d8.
  45. Oommen A. M., Griffin J. B., Sarath G., Zempleni J. Roles for nutrients in epigenetic events. J Nutr Biochem 2005;16:747-747. DOI:10.1016/j.jnutbio.2004.08.004.
  46. Nagy-Szakal D., Ross M. C., Dowd S. E. et al. Maternal micronutrients can modify colonic mucosal microbiota maturation in murine offspring. Gut Microbes 2012;3:426-433. DOI:10.4161/gmic.20697.
  47. Macfarlane G. T., Macfarlane S. Bacteria, colonic fermentation, and gastrointestinal health. J AOAC Int 2012; 95(1): 50-60. PMID:22468341.
  48. Wong J. M., de Souza R., Kendall C. W. Colonic health: fermentation and short chain fatty acids. J Clin Gastroenterol 2006;40:235-243. DOI:10.1097/00004836-200603000-00015.
  49. Cummings J. H., Macfarlane G. T. Colonic microflora: nutrition and health. Nutrition (Burbank, Los Angeles County, Calif) 1997;13:476-478.
  50. Cummings J. H., Pomare E. W., Branch W. J. Short chain fatty acids in human large intestine, portal, hepatic and venous blood. Gut 1987;28:1221-1227.
  51. Morrison D. J., Preston T. Formation of short chain fatty acids by the gut microbiota and their impact on human metabolism. Gut Microbes 2016;7:189-200. DOI:10.1080/19490976.2015.1134082.
  52. Ye J. Improving insulin sensitivity with HDAC inhibitor. Diabetes. 2013; 62: 685-687. DOI:10.2337/db12-1354
  53. Soliman M. L., Rosenberger T. A. Acetate supplementation increases brain histone acetylation and inhibits histone deacetylase activity and expression. Mol Cell Biochem 2011;352:173-180. DOI:10.1007/s11010-011-0751-3.
  54. Soliman M. L., Smith M. D., Houdek H. M., Rosenberger TA. Acetate supplementation modulates brain histone acetylation and decreases interleukin-1β expression in a rat model of neuroinflammation. J Neuroinflammation 2012; 9: 51. DOI:10.1186/1742-2094-9-51.
  55. Wang J., Tang H., Zhang C. et al. Modulation of gut microbiota during probiotic-mediated attenuation of metabolic syndrome in high fat diet-fed mice. ISME J 2015;9:1-15.DOI:10.1038/ismej.2014.99.
  56. Fofanova T. Y., Petrosino J. F., Kellermayer R. Microbiome-Epigenome Interactions and the Environmental Origins of Inflammatory Bowel Diseases. J Pediatr Gastroenterol Nutr 2016;62:208-219. DOI:10.1097/MPG.0000000000000950.
  57. Berni Canani R., Di Costanzo M., Leone L. The epigenetic effects of butyrate: potential therapeutic implications for clinical practice. Clin Epigent 2012;4:4. DOI:10.1186/1868-7083-4-4.
  58. Tachibana K., Sakurai K., Watanabe M. et al. Associations between changes in the maternal gut microbiome and differentially methylated regions of diabetes-associated genes in fetuses: A pilot study from a birth cohort study. J Diabetes Investig. 2017; 8(4):550-553. DOI:10.1111/jdi.12598.
  59. Puddu A., Sanguineti R., Montecucco F., Viviani G. L. Evidence for the gut microbiota short-chain fatty acids as key pathophysiological molecules improving diabetes. Mediators of Inflammation 2014;162021. DOI:10.1155/2014/162021.
  60. Duranton B., Keith G., Goss. et al. Concomitant changes in polyamine pools and DNA methylation during growth inhibition of human colonic cancer cells. Exp Cell Res 1998;243:319-325.
  61. Schwiertz A. Microbiota and SCFA in lean and overweight healthy subjects. Obesity 2009;187:190-195.DOI:10.1038/oby.2009.167.
  62. Maslowski K. M., Vieira A. T., Ng A. et al. Regulation of inflammatory responses by gut microbiota and chemoattractant receptor GPR43. Nature 2009; 461:1282-1286. DOI:10.1038/nature08530.
  63. Remely M., Aumueller E., Merold C. et al. Effects of short chain fatty acid producing bacteria on epigenetic regulation of FFAR3 in type 2 diabetes and obesity. Gene 2014;537:85-92. DOI:10.1016/j.gene.2013.11.081.
  64. Louis P., Flint H. J. Diversity, metabolism and microbial ecology of butyrate-producing bacteria from the human large intestine. FEMS Microbiol Lett 2009;294:1-8. DOI:10.1111/j.1574-6968.2009.01514.x.
  65. Wang W., Chen L., Zhou R. et al. Increased proportions of Bifidobacterium and the Lactobacillus group and loss of butyrate-producing bacteria in inflammatory bowel disease. J Clin Microbiol 2014;52:398-406. DOI:10.1128/JCM.01500-13.
  66. Nugent J. L., McCoy A.N., Addamo C. J. et al. Altered tissue metabolites correlate with microbial dysbiosis in colorectal adenomas. J Proteome Res 2014; 13:1921-1929. DOI:10.1021/pr4009783.
  67. Rykova E. Y., Tsvetovskaya G. A., Sergeeva G. I. et al. Methylation-based analysis of circulating DNA for breast tumor screening. Ann N Y Acad Sci 2008;1137:232-235.
  68. Gagniere J., Raisch J., Veziant J. et al. Gut microbiota imbalance and colorectal cancer. World J Gastroenterol 2016;22:501-518. DOI:10.3748/wjg.v22.i2.501.
  69. Dickson I. Gut microbiota: Diagnosing IBD with the gut microbiome. Nat Rev Gastroenterol Hepatol 2017;14:195. DOI:10.1038/nrgastro.2017.25.
  70. Nakatsu G., Li X., Zhou H. et al. Gut mucosal microbiome across stages of colorectal carcinogenesis. Nat Commun 2015; 6: 8727. DOI:10.1038/ncomms9727.
  71. Gevers D., Kugathasan S., Knights D. et al. A Microbiome Foundation for the Study of Crohn’s Disease. Cell Host Microbe 2017;21:301-304. DOI:10.1016/j.chom.2017.02.012.
  72. Gevers D., Kugathasan S., Denson L. A. et al. The treatment-naive microbiome in new-onset Crohn’s disease. Cell Host Microbe 2014;15:382-392. DOI:10.1016/j.chom.2014.02.005.
  73. Vrieze A., Van Nood E., Holleman F. et al. Transfer of intestinal microbiota from lean donors increases insulin sensitivity in individuals with metabolic syndrome. Gastroenterology 2012;143:913-6.e7. DOI:10.1053/j.gastro.2012.06.031.

Full text is published :
Aitbaev K.A., Murkamilov I.T., Fomin V.V., Murkamilova Zh.A. INFLUENCE OF GUT MICROBIOTA ON EPIGENETICS: MECHANISMS, ROLE IN THE DEVELOPMENT OF DISEASES, DIAGNOSTIC AND THERAPEUTIC POTENTIAL. Experimental and Clinical Gastroenterology Journal. 2018;154(06):122-129
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1. Peoples’ Friendship University of Russia (Moscow, Russian Federation)
2. Volgograd State Medical University (Volgograd, Russian Federation)

Keywords: Oddi’s sphincter, dysfunction, “biliary pain”, “pancreatic pain”, diagnostics, treatment

Abstract:This article is devoted to the clinical picture, approaches to diagnosis and treatment of Oddi´s sphincter dysfunction.

• References total 15 ⇓ :: .
  1. Ivashkin V. T., Lapina T. L., red. Gastroehnterologiya: nacional’noe rukovodstvo – M.: GEHOTAR-Media, 2008. – 700 s.
  2. Kalinin A. V., Hazanov A. I., red. Gastroehnterologiya i gepatologiya: diagnostika i lechenie: rukovodstvo dlya vrachej. – M.: Miklosh, 2007. – 600 s
  3. Ivashkin V.T., red. Klinicheskie rekomendatsii. Gastroenterologiya – M.: GEOTAR-Media, 2008. – 182 s.
  4. Ivashkin V. T., Lapina T. L., Ohlobystin A. V., Bueverov A. O. Naibolee rasprostranennye zabolevaniya zheludochno-kishechnogo trakta i pecheni: sprav. dlya praktikuyushchih vrachej – M.: Litterra, 2008. – 170 s.
  5. Gastroehnterologiya i gepatologiya. Diagnostika i lechenie. Pod redakciej A. V. Kalinina, A. I. Hazanova. Rukovodstvo dlya vrachej. Izdatel’stvo MIKLOSH. M., 2007
  6. Ahmedov V. A. Prakticheskaya gastroehnterologiya. – M.: Medicinskoe informacionnoe agentstvo, 2011. 416 s.
  7. Samsonov A. A. Modern therapy of chronic cholecystitis and biliary dyskinesia. Russian medical journal. – 2009. – № 6. – P. 13–17.
  8. Zabolevaniya pecheni i zhelchevyvodyashchih putej. V. G. Radchenko i soavt. – Spb.: SpecLit, 2011. – 526 s.
  9. Anisimova E. V., Kozlova I. V., Volkov S. V. Clinical and ultrasound features of gallbladder diseases in patients with body weight deficit. Clinical medicine-2014-№ 2-p. 43–47
  10. Seliverstov P. V. Functional disorders of the biliary tract and their treatment // Vrach. – 2012-N3. – P. 9–14.
  11. Sovremennaya terapiya zabolevanij organov pishchevareniya. V. A. Maksimov i soavt. Moscow, «Adamant»», 2011.
  12. Spravochnik Vidal’. Lekarstvennye preparaty Rossii. AstraFarmServis. – 2010, S.B-1190.
  13. Cimmerman YA.S. Klinicheskaya gastroehnterologiya. M., «Gehotar-Media», 2009.
  14. Anisimova E. V., Kozlova I. V., Volkov S. V., Bozumbaev L. P. Clinical and morphological features of the liver in cholelithiasis. Astrakhan medical journal. 2012. Vol. 7. No. 3. P. 40–43.
  15. Anisimova E. V., Kozlova I. V., Volkov S. V. Features of food behavior in diseases of the gallbladder //Fundamental research. 2012. No. 7–2. P. 264–268.

Full text is published :
Khalilova U. A., Skvortsov V. V., Lunkov M. V. DIAGNOSIS AND TREATMENT OF ODDI´S SPHINCTER DYSFUNCTION. Experimental and Clinical Gastroenterology Journal. 2018;154(06):130-133
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1. Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation, Institute for regenerative medicine (Moscow, Russian Federation)

Keywords: cholelithiasis, cholangiopathy, toll-like receptors, gallstone disease, gallstones

Abstract:It is believed that gallstone formation in the biliary tree is a disease associated with alterations of the normal functioning of the organism, and often accompanied by metabolic dysfunction. Recent scientific data allow us to take a fresh look at the problem by proposing an original hypothesis about gallstone formation as a protective immunological reaction of the biliary three cells aimed to isolate exogenous microorganisms and to stop overexpression of toll-like receptors (TLR). In this paradigm, the cholelithiasis appears to be an autoimmune cholangiopathy, therapy of which is associated with the normalization of the immune status of cholangiocytes and down-regulation of its membrane receptors.

• References total 55 ⇓ :: .
  1. Dyuzheva T. G., Lyundup A. V., Klabukov I. D., Chvalun S. N. et al. Prospects for tissue engineered bile duct. Genes and Cells. – 2016. – vol. 11, № 1. – P. 43–47.
  2. Gallinger Yu.I., Khrustaleva M. V. Kamni zhelchnyh protokov: klinika, diagnostika, sovremennye metody lecheniya [Bile duct stones: clinical presentation, diagnostics, modern methods of treatment]. Russian Journal of Gastroenterology, Hepatology, Coloproctology, 2006, vol. 16, no. 5, pp. 50–58.
  3. Sandblom G., Videhult P., Crona Guterstam Y., Svenner A. et al. Mortality after a cholecystectomy: a population-based study. HPB: the official journal of the International Hepato Pancreato Biliary Association. – 2015. – vol. 17, № 3. – P. 239–243.
  4. Girard R. M., Morin M. Open cholecystectomy: its morbidity and mortality as a reference standard. Canadian journal of surgery. Journal canadien de chirurgie. – 1993. – vol. 36, № 1. – P. 75–80.
  5. Escarce J. J., Shea J. A., Chen W., Qian Z. et al. Outcomes of open cholecystectomy in the elderly: a longitudinal analysis of 21,000 cases in the prelaparoscopic era. Surgery. – 1995. – vol. 117, № 2. – P. 156–164.
  6. Zimmerman Ya. S. Gastroehnterologiya [Gastroenterology]. Moscow, GEOTAR-Media Publ., 2012, 816 p.
  7. Ilchenko A. A. 10 let klassifikacii zhelchnokamennoj bolezni (CNIIG): osnovnye itogi nauchno-prakticheskogo primeneniya [10 years of gallstone disease classification (central scientific research institute of gastroenterology): highlights of scientific and practical applications]. Eksperimental’naia i klinicheskaia gastroenterologiia – Experimental & clinical gastroenterology, 2012, no. 4, pp. 3–10.
  8. Stinton L. M., Shaffer E. A. Epidemiology of gallbladder disease: cholelithiasis and cancer. Gut and liver. – 2012. – vol. 6, № 2. – pp. 172–187.
  9. Tietz P. S., LaRusso N. F. Cholangiocyte biology. Current Opinion in Gastroenterology. – 2006. – vol. 22, № 3. – pp. 279–287.
  10. Fava G., Glaser S., Francis H., Alpini G. The Immunophysiology of Biliary Epithelium. Seminars in Liver Disease. – 2005. – vol. 25, № 03. – pp. 251–264.
  11. Strazzabosco M., Fabris L., Spirli C. Pathophysiology of Cholangiopathies. Journal of Clinical Gastroenterology. – 2005. – vol. 39, № 4 Suppl 2. – pp. S90–S102.
  12. Adams D. H., Afford S. C. The role of cholangiocytes in the development of chronic inflammatory liver disease. Frontiers in bioscience: a journal and virtual library. – 2002. – vol. 7. – pp. e276–285.
  13. Chen X.-M., O’Hara S.P., LaRusso N. F. The immunobiology of cholangiocytes. Immunology and Cell Biology. – 2008. – vol. 86, № 6. – P. 497–505.
  14. Mueller T., Beutler C., Picó A. H., Shibolet O. et al. Enhanced innate immune responsiveness and intolerance to intestinal endotoxins in human biliary epithelial cells contributes to chronic cholangitis. Liver International. – 2011. – vol. 31, № 10. – P. 1574–1588.
  15. Peng Y., Yang Y., Liu Y., Nie Y. et al. Cholesterol gallstones and bile host diverse bacterial communities with potential to promote the formation of gallstones. Microbial Pathogenesis. – 2015. – vol. 83–84. – P. 57–63.
  16. Stinton L. M., Myers R. P., Shaffer E. A. Epidemiology of gallstones. Gastroenterology clinics of North America. – 2010. – vol. 39, № 2. – P. 157–169.
  17. Vítek L., Carey M. C. New pathophysiological concepts underlying pathogenesis of pigment gallstones. Clinics and research in hepatology and gastroenterology. – 2012. – vol. 36, № 2. – P. 122–129.
  18. Шаповальянц С. Г., Мыльников А. Г., Никонов А. А., Веселова В. С. Профилактика и лечение рецидивного холедохолитиаза. Анналы хирургической гепатологии. – 2013. – vol. 18, № 1. – С. 16–22.
  19. Csendes A., Csendes P., Rojas J., Sánchez M. [Results of cholecystectomy realized 10 years ago]. Revista medica de Chile. – 2000. – vol. 128, № 12. – P. 1309–1312.
  20. Paganini A. M., Lezoche E. Follow-up of 161 unselected consecutive patients treated laparoscopically for common bile duct stones. Surgical endoscopy. – 1998. – vol. 12, № 1. – P. 23–29.
  21. Pazzi P., Gamberini S., Buldrini P., Gullini S. Biliary sludge: the sluggish gallbladder. Digestive and liver disease: official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver. – 2003. – vol. 35 Suppl 3. – P. S39–45.
  22. Swidsinski A., Loening-Baucke V. Functional Structure of Intestinal Microbiota in Health and Disease. in The Human Microbiota: How Microbial Communities Affect Health and Disease, D. N. Fredricks, Ed. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2013, P. 211–254.
  23. Zvyagintseva T. D., Shargorod I. I. Sovremennye mekhanizmy razvitiya biliarnogo sladzha [Modern mechanisms of development of the biliary sludge]. Novosti mediciny i farmacii, 2012, no. 414, pp. 45–47.
  24. Janowitz P., Kratzer W., Zemmler T., Tudyka J. et al. Gallbladder sludge: spontaneous course and incidence of complications in patients without stones. Hepatology (Baltimore, Md.). – 1994. – vol. 20, № 2. – P. 291–294.
  25. Chuang Y.-H., Lan R. Y., Gershwin M. E. The immunopathology of human biliary cell epithelium. Seminars in immunopathology. – 2009. – vol. 31, № 3. – P. 323–331.
  26. Wang H. H., Liu M., Li X., Portincasa P. et al. Impaired intestinal cholecystokinin secretion, a fascinating but overlooked link between coeliac disease and cholesterol gallstone disease. European journal of clinical investigation. – 2017. – vol. 47, № 4. – P. 328–333.
  27. Kazmi H. R., Chandra A., Nigam J., Baghel K. et al. Polymorphism and Expression Profile of Cholecystokinin Type A Receptor in Relation to Gallstone Disease Susceptibility. Biochemical Genetics. – 2016. – vol. 54, № 5. – P. 665–675.
  28. Jørgensen T. Prevalence of gallstones in a Danish population. American journal of epidemiology. – 1987. – vol. 126, № 5. – P. 912–921.
  29. Friedman G. D., Kannel W. B., Dawber T. R. The epidemiology of gallbladder disease: Observations in the Framingham study. Journal of Chronic Diseases. –1966. – vol. 19, № 3. – P. 273–292.
  30. Magrupov B. A., Vervekina T. A. Analiz letal’nosti pri zhelchnokamennoj bolezni [Pathologoanatomic Analisis Dead in Patients with Cholelithiasis]. Vestnik khirurgicheskoy gastroenterologii = Journal of surgical gastroenterology, 2010, no. 8, pp. 26–33.
  31. Karlsson L., Sun S., Rao N., Venable J. et al. TLR7/9 Antagonists as Therapeutics for Immune-Mediated Inflammatory Disorders. Inflammation & Allergy-Drug Targets. – 2007. – vol. 6, № 4. – P. 223–235.
  32. Klein S. L., Flanagan K. L. Sex differences in immune responses. Nature reviews. Immunology. – 2016. – vol. 16, № 10. – P. 626–638.
  33. Gubergrits N. B., Mekki B. H. M. B. Biliarnyj sladzh: konstatirovat’ ili lechit’? [Biliary sludge: to establish a fact or to treat?]. Modern gastroenterology, 2005, vol. 4, no 24, pp. 9–19.
  34. Valdivieso V., Covarrubias C., Siegel F., Cruz F. Pregnancy and cholelithiasis: pathogenesis and natural course of gallstones diagnosed in early puerperium. Hepatology (Baltimore, Md.). – 1993. – vol. 17, № 1. – P. 1–4.
  35. Chen C. Y., Lu C. L., Huang Y. S., Tam T. N. et al. Age is one of the risk factors in developing gallstone disease in Taiwan. Age and ageing. – 1998. – vol. 27, № 4. – P. 437–441.
  36. Toledano H. The role of the heterochronic microRNA let-7 in the progression of aging. Experimental gerontology. – 2013. –vol. 48, № 7. – P. 667–670.
  37. Leitzmann M. F. A Prospective Study of Coffee Consumption and the Risk of Symptomatic Gallstone Disease in Men. JAMA. – 1999. – vol. 281, № 22. – P. 2106.
  38. Brunquell J., Morris S., Snyder A., Westerheide S. D. Coffee extract and caffeine enhance the heat shock response and promote proteostasis in an HSF-1-dependent manner in Caenorhabditis elegans. Cell stress & chaperones. – 2017. – pp. 1–11.
  39. Klabukov I. D., Lyundup A. V., Dyuzheva T. G., Tyakht A. V. Biliary microbiota and bile duct diseases. Annals of the Russian academy of medical sciences. 2017. vol. 72, no. 3, pp. 172–179
  40. Ostrow J. D. Unconjugated bilirubin and cholesterol gallstone formation. Hepatology (Baltimore, Md.). – 1990. – vol. 12, № 3 Pt 2. – P. 219S-224S.
  41. Mascia C., Maina M., Chiarpotto E., Leonarduzzi G. et al. Proinflammatory effect of cholesterol and its oxidation products on CaCo-2 human enterocyte-like cells: effective protection by epigallocatechin-3-gallate. Free Radical Biology and Medicine. – 2010. – vol. 49, № . 12, – P. 2049–2057.
  42. Nakeeb A., Comuzzie A. G., Martin L., Sonnenberg G. E. et al. Gallstones: genetics versus environment. Annals of surgery. – 2002. – vol. 235, № 6. – P. 842–849.
  43. Jimi M., Nagamitsu S. Lithogenic bile. Gastroenterologia Japonica. – 1976. – vol. 11, № 2. – P. 111–115.
  44. Sharma B. C., Agarwal D. K., Dhiman R. K., Baijal S. S. et al. Bile lithogenicity and gallbladder emptying in patients with microlithiasis: effect of bile acid therapy. Gastroenterology. – 1998. – vol. 115, № 1. – P. 124–128.
  45. Beuers U., Hohenester S., de Buy Wenniger L. J.M., Kremer A. E. et al. The biliary HCO3– umbrella: A unifying hypothesis on pathogenetic and therapeutic aspects of fibrosing cholangiopathies. Hepatology. – 2010. – vol. 52, № 4. – P. 1489–1496.
  46. Méndez-Sánchez N., Chavez-Tapia N.C., Motola-Kuba D., Sanchez-Lara K. et al. Metabolic syndrome as a risk factor for gallstone disease. World journal of gastroenterology. – 2005. – vol. 11, № 11. – P. 1653–1657.
  47. Cuevas A., Miquel J. F., Reyes M. S., Zanlungo S. et al. Diet as a Risk Factor for Cholesterol Gallstone Disease. Journal of the American College of Nutrition. –2004. – vol. 23, № 3. – P. 187–196.
  48. Ilchenko A. A. Zhelchnye kisloty v norme i pri patologii [Bile acids in health and disease]. Eksperimental’naia i klinicheskaia gastroenterologiia – Experimental & clinical gastroenterology, 2010, no. 4, pp. 3–13.
  49. Hirschfield G. M., Gershwin M. E. The immunobiology and pathophysiology of primary biliary cirrhosis. Annual review of pathology. – 2013. – vol. 8, № 1. – P. 303–330.
  50. Etminan M., Delaney J. A.C., Bressler B., Brophy J. M. Oral contraceptives and the risk of gallbladder disease: a comparative safety study. CMAJ: Canadian Medical Association journal = journal de l’Association medicale canadienne. – 2011. – vol. 183, № 8. – P. 899–904.
  51. Wang S., Wang Y., Xu J., Chen Y. Is the oral contraceptive or hormone replacement therapy a risk factor for cholelithiasis: A systematic review and meta-analysis. Medicine. – 2017. – vol. 96, № 14. – P. e6556.
  52. Shcherbinina M. B. Zabolevaniya pecheni s holestaticheskim sindromom, bolezni zhelchnogo puzyrya i ursodezoksiholevaya kislota: novye akcenty [Liver disease with cholestatic syndrome, gallbladder disease and ursodeoxycholic acid: new accents]. Modern gastroenterology. 2016;88(2):78–86.
  53. Jones H., Alpini G., Francis H. Bile acid signaling and biliary functions. Acta pharmaceutica Sinica. B. – 2015. – vol. 5, № 2. – P. 123–128.
  54. Nakanuma Y. Tutorial Review for Understanding of Cholangiopathy. International Journal of Hepatology. – 2012. – vol. 2012. – pp. 1–9.
  55. Gao W., Xiong Y., Li Q., Yang H. Inhibition of Toll-Like Receptor Signaling as a Promising Therapy for Inflammatory Diseases: A Journey from Molecular to Nano Therapeutics. Frontiers in physiology. – 2017. – vol. 8. – P. 508.

Full text is published :
Klabukov I. D., Krasilnikova O. A., Lyundup A. V., Dyuzheva T. G. IMMUNOLOGICAL CAUSES OF GALLSTONE DISEASE (ORIGINAL HYPOTHESIS). Experimental and Clinical Gastroenterology Journal. 2018;154(06):134-142
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1. Moscow Regional Research and Clinical Institute («MONIKI») (Moscow, Russian Federation)
2. A.I.Yevdokimov Moscow State University of Medicine and Dentistry (Moscow, Russian Federation)

Keywords: neuroendocrine tumors, diarrhea, lanreotide Autogel, somatostatin analogs, antiproliferative effect

Abstract:Neuroendocrine tumors (NET) are a rare, but dangerous disease, and often have malignant character. The frequency is about 35 cases at 100.000 population, with 2-5 new cases on 100.000 people a year. The majority of NET produce the active substances in various degree influencing exocrine function and motility of the gastrointestinal tract (GIT). The frequent clinical manifestation of NET is diarrhea. It is necessary to carry out a differential diagnosis of NET in patients with the persistent not stopped diarrhea and/or ulcer damage of a GIT. The purposes of treatment of NET are the elimination of primary tumor (and its metastasizes - if they are) and normalization of a hormonal background that leads to a regress of clinical symptoms. The randomized controlled studies PROMID and CLARINET with a high degree of substantiality have shown symptomatic improvement and significant anti-proliferative effect of somatostatin analogs in the treatment of NET. In the CLARINET study, the lanreotide Autogel was effective at a wide range of patients with highly - and moderate differentiated NET (Ki-67 <10%), including with primary tumor in a small intestine and pancreas, with a primary tumor of unknown localization, and with metastatic damage of a liver. Now somatostatin analogs are considered as the first line of drug treatment of patients with highly - and moderate differentiated NET of digestive tract regardless of the extent of metastatic damage of a liver.

• References total 36 ⇓ :: .
  1. Rossana B, Silvia R, Mariangela T, et al. Gastrointestinal neuroendocrine tumors: Searching the optimal treatment strategy – A literature review.// Crit Rev Oncol Hematol. 2016 Feb; 98: 264–274.
  2. Kuz’minov A.E., Polozkova S. A., Orel N. F., Gorbunova V. A. Neuroendocrine tumors. Effective pharmacotherapy. 2012, no.34, pp.44–48.
  3. van der Zwan JM, Trama A, Otter R, Larrañaga N, Tavilla A, Marcos-Gragera R, Dei Tos AP, Baudin E, Poston G, Links T, RARECARE WG. Rare neuroendocrine tumours: results of the surveillance of rare cancers in Europe project. Eur J Cancer. 2013 Jul; 49(11):2565–78.
  4. Yao JC, Hassan M, Phan A, Dagohoy C, Leary C, Mares JE, Abdalla EK, Fleming JB, Vauthey JN, Rashid A, Evans DB. One hundred years after “carcinoid”: epidemiology of and prognostic factors for neuroendocrine tumors in 35,825 cases in the United States. J Clin Oncol. 2008 Jun 20; 26(18):3063–72.
  5. Sandvik OM, Søreide K, Gudlaugsson E, Kvaløy JT, Søreide JA Epidemiology and classification of gastroenteropancreatic neuroendocrine neoplasms using current coding criteria. Br J Surg. 2016 Feb; 103(3):226–32.
  6. Scherübl H, Streller B, Stabenow R, Herbst H, Höpfner M, Schwertner C, Steinberg J, Eick J, Ring W, Tiwari K, Zappe SM Clinically detected gastroenteropancreatic neuroendocrine tumors are on the rise: epidemiological changes in Germany. World J Gastroenterol. 2013 Dec 21; 19(47):9012–9
  7. Tsai HJ, Wu CC, Tsai CR, Lin SF, Chen LT, Chang JS. The epidemiology of neuroendocrine tumors in Taiwan: a nation-wide cancer registry-based study. PLoS One. 2013; 8(4): e62487.
  8. Chauhan A, Yu Q, Ray N, Farooqui Z, Huang B, Durbin EB, Tucker T, Evers M, Arnold S, Anthony LB. Global burden of neuroendocrine tumors and changing incidence in Kentucky. Oncotarget. 2018 Apr 10;9(27):19245–19254. doi: 10.18632/oncotarget.24983.
  9. Dasari A, Shen C, Halperin D, Zhao B, Zhou S, Xu Y, Shih T, Yao JC. Trends in the Incidence, Prevalence, and Survival Outcomes in Patients with Neuroendocrine Tumors in the United States. JAMA Oncol. 2017 Oct 1; 3(10):1335–1342.
  10. Klöppel G. Neuroendocrine Neoplasms: Dichotomy, Origin and Classifications. Visc Med. 2017 Oct;33(5):324–330. doi: 10.1159/000481390.
  11. Klimstra D.S., Modlin I. R., Coppola D., Lloyd R. V., Suster S. The Pathologic Classification of Neuroendocrine Tumors. A review of Nomenclature, Grading, and Staging Systems.// Pancreas, 2010, 39: 707–712.3. Cives M, Strosberg J. An Update on Gastroenteropancreatic Neuroendocrine Tumors.// Oncology (Williston Park). 2014 Sep 15; 28 (9): 749–756.
  12. Vinik AI, Chaya C. Clinical Presentation and Diagnosis of Neuroendocrine Tumors.// Hematol Oncol Clin North Am. 2016 Feb; 30 (1): 21–48.
  13. Halperin DM, Shen C, Dasari A, Xu Y, Chu Y, Zhou S, Shih YT, Yao JC. Frequency of carcinoid syndrome at neuroendocrine tumour diagnosis: a population-based study. Lancet Oncol. 2017 Apr; 18(4):525–534.
  14. Boutzios G, Kaltsas G. Clinical Syndromes Related to Gastrointestinal Neuroendocrine Neoplasms. Front Horm Res. 2015;44:40–57. doi: 10.1159/000382053.
  15. Dedov I. I., Melnichenko G. A. Endocrinology: national leadership. Moscow, Geotar-media Publ., 2016, 1112 p.
  16. Pavel M, Baudin E, Couvelard A et al. Barcelona Consensus Conference participants. ENETS Consensus Guidelines for the management of patients with liver and other distant metastases from neuroendocrine neoplasms of foregut, midgut, hindgut, and unknown primary. Neuroendocrinology. 2012; 95 (2): 157–76.
  17. Clancy TE. Surgical Management of Pancreatic Neuroendocrine Tumors. Hematol Oncol Clin North Am. 2016 Feb; 30 (1): 103–18.
  18. Demirkan BH, Eriksson B. Systemic treatment of neuroendocrine tumors with hepatic metastases. Turk J Gastroenterol. 2012; 23 (5): 427–437.
  19. Shpakov A. O. Somatostatin receptors and signaling cascades coupled to them. Journal of Evolutionary Biochemistry and Physiology. 2012 48(4):329–341 ru
  20. Schally AV. Oncological applications of somatostatin analogues.// Cancer Res 1988; 1: 6977–6985.
  21. Modlin IM, Kidd M, Drozdov I, Siddique ZL, Gustafsson BI. Pharmacotherapy of neuroendocrine cancers.// Expert Opin Pharmacother 2008; 9 (15): 2617–2626.
  22. Modlin IM, Pavel M, Kidd M, Gustafsson BI. Review article: somatostatin analogues in the treatment of gastroenteropancreatic neuroendocrine (carcinoid) tumours.// Aliment Pharmacol Ther. 2010 Jan 15; 31 (2): 169–188.
  23. Orlova R. V., Novik A. V. Modern approaches of medicinal treatment of generalized forms of neuroendocrine tumors. Symptomatic therapy of syndromes in neuroendocrine neoplasias. Practical oncology. 2005;6(4):240–246.
  24. Karakaxas D, Gazouli M, Liakakos T, et al. Pancreatic neuroendocrine tumors: current opinions on a rare, but potentially curable neoplasm.// Eur J Gastroenterol Hepatol. 2014; 26 (8): 826–35.
  25. Rinke A, Muller HH, Schade-Brittinger C, et al. Placebo-controlled, double-blind, prospective, randomized study on the effect of octreotide LAR in the control of tumor growth in patients with metastatic neuroendocrine midgut tumors: a report from the PROMID Study Group.// J Clin Oncol, 2009; 27: 4656–4663.
  26. Caplin ME, Pavel M, Ćwikła JB, Phan AT, Raderer M, Sedláčková E, Cadiot G, Wolin EM, Capdevila J, Wall L, Rindi G, Langley A, Martinez S, Blumberg J, Ruszniewski P CLARINET Investigators. Lanreotide in metastatic enteropancreatic neuroendocrine tumors.// New Engl J Med, 2014; 371: 224–233. doi: 10.1056/NEJMoa1316158.
  27. Buil-Bruna N, Dehez M, Manon A, Nguyen TX, Trocóniz IF. Establishing the Quantitative Relationship Between Lanreotide Autogel®, Chromogranin A, and Progression-Free Survival in Patients with Nonfunctioning Gastroenteropancreatic Neuroendocrine Tumors. AAPS J. 2016 May;18(3):703–12. doi: 10.1208/s12248–016–9884–3.
  28. Caplin ME, Pavel M, Ćwikła JB, Phan AT, Raderer M, Sedláčková E, Cadiot G, Wolin EM, Capdevila J, Wall L, Rindi G, Langley A, Martinez S, Gomez-Panzani E, Ruszniewski P CLARINET Investigators. Anti-tumour effects of lanreotide for pancreatic and intestinal neuroendocrine tumours: the CLARINET open-label extension study. Endocr Relat Cancer. 2016 Mar;23(3):191–9. doi: 10.1530/ERC-15–0490.
  29. Wolin EM, Pavel M, Cwikla JB, Phan AT, Raderer M, Sedlackova E. Final progression-free survival analyses for lanreotide autogel/depot 120 mg in metastatic enteropancreatic neuroendocrine tumors: the CLARINET extension study. J Clin Oncol. 2017, Vol. 35, no. 15_suppl: 4089–4089. DOI: 10.1200/JCO.2017.35.15_suppl.4089
  30. Phan AT, Caplin ME, Pavel ME, Cwikla J B, Raderer M, Sedláčková E, Cadiot G, Wolin EM, Capdevila J, Wall L, Rindi G, Langley A, Gomez-Panzani E, Ruszniewski PB. Effects of lanreotide Depot/Autogel in pancreatic neuroendocrine tumors: a subgroup analysis from the CLARINET study. J Clin Oncol. 2015. Vol. 33, no. 3_suppl:233–233. DOI: 10.1200/jco.2015.33.3_suppl.233
  31. Cwikla JB, Wolin EM, Pavel M, Phan AT, Raderer M, Sedláčková E, Cadiot G, Capdevila J, Rindi G, Lombard-Bohas C, Liyanage N, Truong Thanh X–M, Ruszniewski P, Caplin M. Ann Oncol. 2017. Vol. 28, Issue suppl_5, https://doi.org/10.1093/annonc/mdx368.023
  32. Massironi S, Conte D, Rossi RE. Somatostatin analogues in functioning gastroenteropancreatic neuroendocrine tumours: literature review, clinical recommendations and schedules.// Scand J Gastroenterol. 2016; 51 (5): 513–523.
  33. Saif MW. Lanreotide for the treatment of gastroenteropancreatic neuroendocrine tumors.// Expert Opin Pharmacother. 2016;17 (3): 443–456.
  34. Kos-Kudła B. Treatment of neuroendocrine tumors: new recommendations based on the CLARINET study.// Contemp Oncol (Pozn). 2015;19 (5): 345–9.
  35. Mehrvarz Sarshekeh A, Halperin DM, Dasari A. Update on management of midgut neuroendocrine tumors. Int J Endocrine Oncol. 2016;3(2):175–189. doi:10.2217/ije-2015–0004.

Full text is published :
Ilovayskaya I. A. DIARRHEA AS A CLINICAL MARKER OF NEUROENDOCRINE TUMORS. Experimental and Clinical Gastroenterology Journal. 2018;154(06):143-149
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1. North-western State Medical University n. a. I. I. Mechnikov (St. Petersburg, Russian Federation)
2. Federal State Autonomous Educational Institution of Higher Education I. M. Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation (Moscow, Russian Federation)

Keywords: ursodeoxycholic acid, Grinterol®, cytolysis syndrome, cholestasis syndrome

Abstract:The influence of therapy with ursodeoxycholic acid Grinterol® on the clinical and biochemical parameters of patients with hepatobiliary pathology under conditions of real polyclinic practice was studied. The study involved 300 centers in 25 cities of the Russian Federation. The number of participants was 10213 patients. The study included patients with non-alcoholic fatty liver disease, alcoholic liver disease, chronic viral hepatitis, drug damage to the liver, cirrhosis, сholecystitis with biliary sludge. An assessment of the dynamics of clinical symptoms and biochemical markers of hepatic cytolysis and cholestasis demonstrated the high clinical effectiveness of therapy with Grinterol®, safety and the minimum side effects in all the examined groups. According to the results of the study, the use of the medicinal preparation Grinterol® seems very appropriate for the treatment of diseases of the hepatobiliary system.

• References total 23 ⇓ :: .
  1. Grinevich V. B., Sas E. I. Physiological effects of bile acids. RMJ. Medical review. 2017. No. 2, Pp. 87–91. (in Russian)
  2. Lapina TL, Kartavenko IM. Ursodeoxycholic acid: effect on the mucosa of the upper gastrointestinal tract. Ros Zhurn Gastroenterologii Gepatologii Koloproktologii. 2007; no. 17(6), pp. 51–7. (In Russian)
  3. I. I. Chukaeva, N. V. Orlova. Clinical management of patient with refractory gastroesophageal reflux disease. Medicinskij alfavit 2017, vol. 2 no. 34 pp 22–27 (In Russian)
  4. McQuaid KR, Laine L, Fennerty MB, Souza R, Spechler SJ. Systematic review: the role of bile acids in the pathogenesis of gastro-oesophageal reflux disease and related neoplasia. Aliment Pharmacol Ther., 2011 Jul, 34(2): 146–65.
  5. Banerjee B, Shaheen NJ, Martinez JA et al. Clinical Study of Ursodeoxycholic Acid in Barrett’s Esophagus Patients. Cancer Prev Res (Phila), 2016 Feb 23. pii: canprevres.0276.2015.
  6. Ilchenko А. А. Bolezni zhelchnogo puzyrya i zhelchnykh putej [Diseases of the gallbladder and biliary tracts], Meditsinskoe informatsionnoe agentstvo, 2011, p. 880 (in Russian)
  7. Wijaya I. The Role of Ursodeoxycholic Acid in Acute Viral Hepatitis: an Evidence-based Case Report. Acta Med Indones., 2015 Oct, 47(4): 352–7.
  8. Rejzis А.R., Matanina N. V., Nikitina T. S., et al. Primenenie preparatov ursodezoksikholevoj kisloty (Ursosana) v lechenii ostrykh i khronicheskikh virusnykh gepatitov [The use of drugs ursodeoxycholic acid (ursosan) in the treatment of acute and chronic viral hepatitis], informatsionnoe pis’mo FGUN CNIIE Rospotrebnadzora, 2006, pp. 1–19 (in Russian)
  9. T.L. Lapina, I. M. Kartavenko, V. T. Ivashkin Pathogenic and therapeutic role of bile acids at reflux-gastritis, Russian Journal of Gastroenterology, Hepatology, Coloproctology, 2016 vol. 25, no. 1, pp. 86–93 (in Russian)
  10. Mehtiyev S.N., Mehtiyev O. A. Algorithm for the management of patients with functional disorders of the biliary tract. Lechaschiy Vrach, 2013, no. 4, pp. 52–59. (in Russian)
  11. O. N. Minushkin, L. V. Maslovsky, O. A. Eremenko, O. F. Shaposhnikova, M. S. Makarova. Biliary sludge as the initial stage of cholelithiasis. Therapy and prevention, Meditsinskiy Sovet, 2017, no. 5, pp. 65–69 (in Russian).
  12. Lazebnik L.B. et al. Nonalcoholic fatty liver disease: clinic, diagnostics, treatment, Eksperimental’naya i Klinicheskaya Gastroenterologiya 2017; 138 (2), pp. 22–37 (in Russian)
  13. Bojtsov S. А., Chuchalin А. G. Dispansernoe nablyudenie bol’nykh khronicheskimi neinfektsionnymi zabolevaniyami i patsientov s vysokim riskom ikh razvitiya [Clinical follow-up of patients with chronic non-infectious diseases and patients at high risk of their development], Moscow, 2014, p. 112 (In Russian)
  14. A.A. Shipovskaya, O. P. Dudanova. Intrahepatic cholestasis in nonalcoholic fatty liver disease. Therapeutic Archive, 2018, vol. 90, no. 2, pp. 69–74 (in Russian)
  15. Kazyulin A. N. Place of ursodeoxycholic acid in the therapy of non-alcoholic fatty liver disease at different stages: steatosis, steatohepatitis, fibrosis / cirrhosis, RMJ. 2017. No. 17. pp. 1248–1257 (in Russian)
  16. Oh B, Choi WS, Park SB, Cho B, Yang YJ, Lee ES, Lee JH. Efficacy and safety of ursodeoxycholic acid composite on fatigued patients with elevated liver function and/or fatty liver: a multi-centre, randomised, double-blinded, placebo-controlled trial. Int J Clin Pract., 2016 Apr, 70(4): 302–11.
  17. Plevris J. N., Hayes P. C., Bouchier I. A. D. Ursodeoxycholic acid in the treatment of alcoholic liver disease. Gastroenterol // Hepatol. 1991; 3: 6536–6541
  18. Roma M.G., Toledo F. D., Boaglio A. C. et al. Ursodeoxycholic acid in cholestasis: linking action mechanisms to therapeutic applications // Clin. Sci. (Lond.). 2011. Vol. 121. № 12. P. 523–544.
  19. Landar’ L. N., CHudakov N. V. Alcoholic liver disease, therapeutic treatment, Nauka i obrazovanie: sokhranyaya proshloe, sozdayom budushhee, 2018, pp. 210–214. (in Russian)
  20. V. M. Makhov, L. N. Ugryumova, A. A. Balakhonov, Z. A. Mamieva Ursodezoksiholevaja acid: therapist’s view, Meditsinskiy Sovet, 2017. No. 5. Pp. 112–116 (in Russian)
  21. Vertkin A.L., Torubarov S. F. Alkogol’-assotsiirovannye sostoianiia v klinike vnutrennikh boleznei. Opredelenie, taktika vedeniia. Ambulatornyi priem. 2017; 1 (3): 57–62. (in Russian)
  22. O. N. Minushkin, I. V. Zverkov, Yu. S. Skibina. Some approaches to treatment of patients with chronic (biliary) reflux gastritis, Medical Alphabet, 2017, vol. 2, no. 19, pp. 28–31. (in Russian)
  23. Polunina Т. Е. Biliary dysfunction. Rome Consensus IV. Therapy. 2017;6(16), pp. 100–112. (in Russian)

Full text is published :
Oreshko L.S., Makhov V.M., Balakhonov A.A. EFFECT OF THERAPY WITH URSODEOXYCHOLIC ACID PREPARATION GRINTEROL® ON THE CLINICAL AND BIOCHEMICAL PARAMETERS OF PATIENTS WITH HEPATOBILIARY PATHOLOGY. RESULTS OF THE OBSERVATIONAL STUDY IN 2016-2017. Experimental and Clinical Gastroenterology Journal. 2018;154(06):150-159
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1. “Russian Medical Academy of Continuing Professional Education” Russian Federation Ministry of Health (Moscow, Russian Federation)
2. First Moscow state medical University. I. M. Sechenov Russian Ministry Of Health (Moscow, Russian Federation)

Keywords: СYР2С19, Helicobacter pylori, eradication therapy, proton pump inhibitors

Abstract:The clinical situation in which the dependence of the result of Н. pylori eradication therapy on the genotype СYР2С19 controlling the metabolism rate of proton pump inhibitors is described. When carrying the allele variant СUR2С19 * 17 (homo-, heterozygote), a person refers to the “fast metabolizers” of this group of drugs. In view of this anti-Helicobacter therapy can not be achieved in the proper amount.

• References total 6 ⇓ :: .
  1. И.В. Маев, Ю. А. Кучерявый, Д. Н. Андреев «Причины неэффективности антигеликобактерной терапии». РЖГК. -2013. - Т. 23. -№ 6. - с. 62-72
  2. «Актуальные вопросы оказания медицинской помощи больным с кислотозависимыми заболеваниями в клинической практике». Медицинский алфавит № 19 (316) 2017. Практическая гастроэнтерология. - Том № 2. - стр. 11
  3. Сычев Д.А. «Фармакогенетическое тестирование: клиническая интерпретация результатов»2011. стр.48
  4. Malfertheiner P., Megraud F., O’Morain C.A. et al. Management of Helicobacter pylori infection - the Maastricht IV/ Florence Consensus Report // Gut. 2012. Vol. 61. № 5. P. 646-664
  5. С. И. Пиманов, Е. В. Макаренко. Рекомендации Маастрихт V/Флорентийского консенсуса по лечению хеликобактерной инфекции. ConsiliumMedicum. 2017; 8.1: 8-27
  6. Ивашкин В. Т., Маев И. В., Лапина Т. Л., Шептулин А. А., Трухманов А. С., Абдулхаков Р. А. и др. Лечение инфекции Helicobacter pylori: мейнстрим и новации // Российский журнал гастроэнтеролии, гепатолии, колопроктологии. 2017. № 27(4). С. 4-21

Full text is published :
Bojko E.N., Denisenko N.P., Grishina E.A., Ryzhikova K.A. et al. THE INFLUENCE OF GENE POLYMORPHISMS СУР2С19 ON THE EFFECTIVENESS OF ERADICATION THERAPY OF H. PYLORI. Experimental and Clinical Gastroenterology Journal. 2018;154(06):160-163
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1. State funded medical institution “City clinical hospital № 15 named after O. M. Filatov” Department of healthcare of Moscow. (Moscow, Russian Federation)
2. State funded institution of higher professional education “Moscow State Medical and Dental University of A. I. Evdokimov” (Moscow, Russian Federation)

Keywords:rapidly progressing glomerulonephritis, mixed cryoglobulinemia, nephrotic and nephritic syndrome, systemic vasculitis, chronic viral hepatitis C, pulse-therapy, immunosuppressive therapy

Abstract:The present study demonstrates severe course of glomerulonephritis with underlying nephrotic and acute nephritic syndrome with rapidly progressing kidney failure and skin lesion associated with chronic viral hepatitis C. Unfortunately despite the combined immunosuppressive therapy the patient still had azotemia and the nephrotic syndrome was progressing. It was impossible to conduct antiviral therapy because of acute kidney damage, as the clearance of the pegylated interferon decreases under kidney failure. The therapy by monoclonal antibodies to CD20 was not discussed. Kidney damage remains the main cause of death of patients with mixed cryoglobulinemia. The presented clinical case emphasizes the urgency of the problem of extrahepatic aspect of chronic viral hepatitis C and proves the role of lymphotropic chronic viral hepatitis C in the mechanism of the development of rapidly progressing glomerulonephritis. The development of the scheme of modern antiviral therapy and relapse prevention is needed.

• References total 18 ⇓ :: .
  1. Cacoub P., Costedoat Chalumeau N., Lidove O., Alric L. Cryoglobulinemia vasculitis // Curr. Opin. Rheumatol. –2002; 14: 29.
  2. Bushueva N. In. Krel P. E., Isaeva E. I., etc. Markers of hepatitis C virus in liver tissue, serum, and mononuclear peripheral blood cells of patients With chronic hepatitis C and extrahepatic manifestations of chronic HCV infection // Russian journal of Hepatology, gastroenterology, Coloproctology. –2005. – Vol. XV. – № 2. – P. 73–79.
  3. Prakticheskaya gepatologiya // Pod. redak. N. A. Muhina. –M. 2004. –S. 162–164.).
  4. Charles E. D., Dustin L. B. Hepatitis C virus induced cryoglobulinemia // Kindey Int. –2009; 76 (8): 818–824.
  5. Engels E. A., Chatterjee N., Cerhan J. R. Hepatitis C virus infection and Non-Hodgkin lymphoma: result of the NCI-seer multi-center case control study / International of cancer. 2004; 111 (1): 76–80
  6. Saadoun D., Landau D. A., Calabrese L. H. et al. Hepatitis C- associated mixed cryoglobulinemia: a crossroad between autoimmunity and lymphoproliferation // Rheumatology. 2007; 46: 1234–1242/
  7. Kozlovskaya, L, B., Mukhin N. A. Gordovskaya N. B. etc. risk Factors of progression of cryoglobulinemias glomerulonephritis associated with hepatitis C virus // Clinical medicine. –2001. – № 4. – P. 32–35.
  8. Milovanova S. Yu., Ignatova M. T., Nekrasova T. P. and others. Features of the course of chronic hepatitis C with cryoglobulinemia / / Russian journal of gastroenterology, Hepatology and proctology, Coloproctology. –2005. – Vol. XV – № 5. – P. 48–51.
  9. Charles E. D., Dustin L. B. Hepatitis C virus induced cryoglobulinemia. Kindey Int. 2009; 76 (8): 818–824.
  10. Ferii C. Mixed cryoglobulinemia. Orphanet J Rare. 2008; 3:25
  11. Kozlovskaya L. V., Gordovskaya N. B., Malyshko Y. Y. Cryoglobulinemia kidney disease: course and treatment // Nephrology and dialysis. 2002. Vol. 4. № 1: 4–8.
  12. Muhin N. Ah. Kozlovskaya L. V., Malyshko E. Yu. Cryoglobulinemic nephritis associated with chronic infection of hepatitis C virus // Ter archive. 2000; 6: 1–5
  13. Tegai S. V., Lopatina, T. N., Kocmankova E. N. etc. kidney disease associated with hepatitis b and C. Med Consilium.2002; vol. 4. № 7: 337–341.
  14. Muhin N. A. Nefrologiya // Nacional’noe rukovodstvo kratkoe izdanie. -Moskva.-2015g.-s 597
  15. Kozlovskaya L. V., Gordovskyaa N. B., Malyshko, E. Y., S. V. Tegay, Korotchaeva, Yu. Varshavsky V. A., Miroshnichenko N. G., Milovanova Yu. S., etc. Cryoglobulinemic kidney disease: course and treatment // Nephrology and dialysis. -T4. – № 1.-2002. – P. 4–8.
  16. Saadoun D., Rigon M. R., Sene D. et al. Rituximab plus Peg-interferon –alfa/ribavirin compared with Peginterferon-alfa/ribavirin in hepatitis C-related mixed cryoglobulinemia. Blood.2010; 116:326–334.
  17. EASL Recommendation on Treatment of Hepatitis C2015. European Association for the Study of the Liver. J. of Hepatology. 2015 Jul; 63(1): 199–236
  18. Dunaeva N. V., Karaev V. E., Vorob’eva O.A., Mazing A. V., Lapin S. V., Smirnov A. V. Protivovirusnaya terapiya hronicheskogo gepatita S, oslozhnennogo sistemnym krioglobulinemicheskim vaskulitom // ZHurnal Inektologii. Original’noe issledovanie. -Tom 8.-№ 2.-2016. –S.40–47.

Full text is published :
Sagynbaeva V.E., Lazebnik L.B., Golovanova E.V. RAPIDLY PROGRESSING GLOMERULONEPHRITIS WITH THE DEVELOPMENT OF SYSTEMIC CRYOGLOBULINEMIC VASCULITIS ASSOCIATED WITH CHRONIC VIRAL HEPATITIS C. Experimental and Clinical Gastroenterology Journal. 2018;154(06):164-169
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1. “Polyclinic № 3” of Affairs Management for the President of Russian Federation (Moscow, Russian Federation)

Keywords:medical metaphors, gastronomic medical terms, gastronomic medical metaphors

Abstract:In the article are collected “gastronomic” Russian- and the English-speaking medical metaphors connected with digestive system. Terms are grouped on nozologic and organic sign. The diseases having “gastronomic” symptoms are shortly outlined.

• References total 32 ⇓ :: .
  1. Kole A., Chandakole D. Strawberry Tongue // N Engl J Med 2015;373:467.
  2. Rogers R.S., Bruce A. J. The tongue in clinical diagnosis.// J Eur Acad Dermatol Venereol. 2004;18(3):254-259.
  3. Viswanath V., Nair S., Chavan N., Torsekar R. “Caviar tongue”. // Indian journal of dermatology, venereology and leprology 2011;77(1):78-79.
  4. Lee H.J., Jo D. Y. Images in clinical medicine. A smooth, shiny tongue. // N Engl J Med. 2009;360: e8.
  5. Terry S.I., Hanchard B. Gastrology: the use of culinary terms in medicine. // Br Med J. 1979; 2(6205): 1636-1639.
  6. Stadler J., Hölscher A. H., Feussner H., et al. The “steakhouse syndrome”. Primary and definitive diagnosis and therapy”. // Surgical Endoscopy 1989;3(4):195-198.
  7. Benjamin S.B., Gerhardt D. C., Castell D. O. High amplitude, peristaltic esophageal contractions associated with chest pain and/or dysphagia. // Gastroenterology 1979;77(3):478-83.
  8. Chen Y.M., Ott Dh., Hewson E. G., et al. Diffuse esophageal spasm: radiographic and manometric correlation. // Radiology 1989:170:807-810.
  9. Patela N.C., Caicedo R. A. Esophageal infections: an update. // Curr Opin Pediatr 2015;27:642-648.
  10. British Society of Gastroenterology Endoscopy Committee. Non-variceal upper gastrointestinal haemorrhage: guidelines. // Gut. 2002;51 Suppl 4: iv1-6.
  11. Jabbari M., Cherry R., Lough J. O., et al. Gastric antrovascular ectasia: the watermelon stomach. // Gastroenterology 1984;87:1165-1170.
  12. Joffe S.N., Lee F. D., Blumgart L. H. Duodenitis. // Clin Gastroenterol 1978;7:635-650.
  13. Arutyunov A. G., Burkov S. G., Okoyemov M. N., Nikiforov P. A. Gastrointestinal endoscopy in out-patient practice. Moscow, Print-Atel’e Publ., 2008, 104 p.
  14. Shaoul R., Enav B., Steiner Z., et al. Clinical presentation of pyloric stenosis: the change is in our hands. // Isr Med Assoc J. 2004;6:134-137.
  15. Chhabra M.K., Mongia A. K. Cascade stomach: a case report. // Int Surg J. 2016;3(2):1005-1008.
  16. Kundukulam S. S. Tea pot stomach. // Indian Journal of Gastroenterology 2010;(6):249-249.
  17. Maeda E., Oryu M., Tani J., et al. Characteristic waffle-like appearance of gastric linitis plastica: A case report. // Oncol Lett. 2015; 9(1):262-264.
  18. Hofmann W., Aufenanger J., Hoffmann G. Laboratory diagnostic pathways: clinical manual of screening methods and stepwise diagnosis. Ed. 1-st. Walter de Gruyter GmbH & Co KG. 2016, 221.
  19. Bayraktar U.D., Seren S., Bayraktar Y. Hepatic venous outflow obstruction: three similar syndromes. // World J Gastroenterol. 2007;13(13):1912-1927.
  20. Rab S.M., Alam N., Hoda A. N., et al. Amoebic liver abscess: Some unique presentations. // Am J Med 1967;43(5):811-816.
  21. Lardière-Deguelte S., Ragot E., Amroun K., et al. Hepatic abscess: diagnosis and management. // J Visc Surg. 2015;152(4):231-43.
  22. Talluri S.K., Nuthakki H., Tadakamalla A., et al. Chylous ascites. // N Am J Med Sci. 2011; 3(9):438-440.
  23. Dairi S., Demeusy А., Sill A. M., et al. Implications of gallbladder cholesterolosis and cholesterol polyps? // Journal of surgical research 2016;200(2):467-472.
  24. Ilchenko A. A., Orlova Yu. N. Diffuse thickening of the gallbladder wall. Clinical significance. Experimental and Clinical Gastroenterology Journal. 2010, no. 10, pp. 04–14
  25. Lohr J., Dominguez-Munoz E., Rosendahl J., et al. United European Gastroenterology evidence based guidelines for the diagnosis and therapy of chronic pancreatitis (HaPanEU). // United European Gastroenterology Journal 2017;5(2):153-199
  26. Harper M. Congenital steatorrhoea due to defect of the pancreas. // Med J Aust 1949;1(5):137-141
  27. Cera S. M. Intestinal intussusception. // Clin сolon rectal surg. 2008;21(2):106-113
  28. Morozov D. A., Gorodkov S. Yu., Filippov Yu.V., Staroverova G. A. Invagination of the intestine: is it possible to conduct conservative treatment regardless of the duration of the disease? Russian Journal of Pediatric Surgery, Anesthesiology and Reanimatology. 2012;2(4):17–20.
  29. Alexakis L. C. Cholera - «Rice water stools». // Pan Afr Med J. 2017;26:147
  30. Stephens I., Levine M. Management of typhoid fever in children. // Pediatric infectious disease journal. 2002;21(2):157-159
  31. Kumar K., Kumar A. Gastronomic pathology. // Journal of general internal medicine 1994;9(4):207
  32. Roche C.J., O’Keeffe D.P., Lee W. K., et al. Selections from the buffet of food signs in radiology. // RadioGraphics 2002;22:1369-1384

Full text is published :
Burkov S. G., Golubev N. N. ASSOCIATIVE SYMPTOMS OF DISEASES IN GASTROENTEROLOGY. Experimental and Clinical Gastroenterology Journal. 2018;154(06):170-173
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1. North-western State Medical University n. a. I. I. Mechnikov (St. Petersburg, Russian Federation)

Abstract:The 19th Congress of the Gastroenterological Scientific Society of Russia (GSSR - NOGR) and the 20th Anniversary International Slavic-Baltic Scientific Forum "St. Petersburg - Gastro-2018" took place in St. Petersburg, on May 16-18, 2018 as a friendly event to the Russian Scientific Medical Society of Physicians. About 2000 delegates from 23 countries took part in the work of the Congress and Forum, the scientific program of which covered a wide range of issues of diagnosis, treatment, and prevention of the most important diseases of the digestive organs and comorbidities. Within the framework of the Congress and Forum, seven plenary sessions were held on the following issues: “Gastroenterology and nutrition in the 21st century: from fundamental knowledge to clinical perspectives”, “Efficacy and safety of modern pharmacotherapy and diet therapy of diseases of the digestive organs”, “Modern approaches to patient management with functional and organic diseases of the gastrointestinal tract "," Current approaches to the management of patients with dyspepsia and Helicobacter pylori-associated diseases "," Microbiota and its role in the pathogen ese and sanogenesis of diseases ”,“ Diseases of internal organs through the microbiotology prism ”“ Actual gastroenterology for the practicing physician ”. The article is in Russian.

Full text is published :
Sitkin S. I., Seliverstov P. V. A REPORT OF THE XIX CONGRESS OF THE GASTROENTEROLOGICAL SCIENTIFIC SOCIETY OF RUSSIA. Experimental and Clinical Gastroenterology Journal. 2018;154(06):174-175
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