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CLINICAL GASTROENTEROLOGY

    1. Federal State Budgetary Educational Institution of Higher Education "National Research Ogarev Mordovia State University" (430005, Saransk, Republic of Mordovia, Russia)

    Keywords: gastroesophageal reflux disease, cardiac arrhythmias, heart rate variability, autonomic nervous system

    Abstract:The study involved 57 patients with GERD, of whom 26 (45.6%) men and 31 (54.4%) women. The average age of patients is 51.4 ± 8.6 years. Among patients with GERD, the typical course of the disease was observed in 49 people (84.7%), atypical — in 8 people (15.3%). Among atypical manifestations of GERD, cardiac prevailed: 5 people (8.8%) noted the appearance of postprandial chest pain, 2 (3.5%) had complaints of palpitations and interruptions in heart function. In one patient, the clinical manifestation of GERD had a "coma in the throat." According to the endoscopic examination, esophagitis was detected in 9 patients (15.3%). Catarrhal esophagitis was diagnosed in 7 (11.9%) patients, erosive — in 2 (3.4%). The article presents an assessment of the nature of changes in vegetative and temporal parameters of heart rate variability (HRV) over a long period of time in patients with gastroesophageal reflux disease (GERD), describes their dependence on the nature of the predominant reflux, the average daily value of intraesophageal pH, exposure time of acid gastroesophageal reflux, reflux index. Women suffering from GERD are 5.4% higher (p=0.01) than men in the arithmetic mean of the RR intervals, which may indicate a relatively higher risk of various kinds of arrhythmias. Also significantly higher in women were the average values of such indicators as the adequacy of the processes of regulation and the voltage index of regulatory systems by 15.2% (p=0.04) and 24.0% (p=0.04), respectively, indicating a greater impact on the sinus node of the sympathetic division of the vegetative nervous system.

      1. Shapovalova M.M., Drobysheva E.S., Ovsyannikov E.S. et al. Otsenka kachestva zhizni bol'nyh GERB i ishemicheskoy bolezn'yu serdtsa [Evaluation of the quality of life of patients with GERD and coronary heart disease]. Sb. statey H YUbil. konf. vrachey obschey praktiki (semeynyh vrachey) YUga Rossii. 20–21 noyabrya. — 2015 [Collection of articles of the X Anniversary Conference of General Practitioners (Family Doctors) of the South of Russia. November 20–21, 2015]. Moscow, 2015, pp. 337–340.
      2. Chauhan A., Petch M. C., Schofield P. M. Cardioesophageal reflex in humans as a mechanism for «linked angina». Eur Heart J. — 1996. — V.17. — Р.407–413.
      3. Roschina. T.V. Supraezofageal'nye proyavleniya gastroezofageal'noy reflyuksnoy bolezni [Supraesophageal manifestations of gastroesophageal reflux disease]. Klinicheskie perspektivy gastroenterologii, gepatologii. — 2003. — № 1. — P.27–30.
      4. Boraeva T. T., Matveeva U.V. Sostoyanie serdechnososudistoy sistemy pri GERB u detey v Severnoy Osetii (Alanii) [The state of the cardiovascular system in children with GERD in North Ossetia (Alania)]. Materialy nauch.-prakt. konf. pediatrov i neonatologov [Materials of the scientific-practical conference of pediatricians and neonatologists]. Stavropol', 2011, pp.35–41.
      5. Kozlova I.V., Loginov S.V., Shvarts Yu. G. Gastroesophageal reflux and the degree of esopha-gitis in patients with coronary heart disease: impact on myocardial repolarization parameters and cardiac rhythm variability. Clinical medicine. 2004, no. 9, pp. 33–35.
      6. Huang CC, Chan WL, Luo JC, et al. Gastroesophageal reflux disease and atrial fibrillation: a nationwide population-based study. — PLoS One. — 2012;7:e47575.
      7. Rapoport S.I., Lakshin A.A., Rakitin B.V. et al. pH-metriya pischevoda i zheludka pri zabolevaniyah verhnih otdelov pischevaritel'nogo trakta [pH-metry of the esophagus and stomach in diseases of the upper digestive tract]. Moscow, Medpraktika. — M Publ., 2005, 208 p.
      8. Baevskiy R.M., Ivanov G.G., CHireykin L.V. et al. Heart rate variability analysis using various electrocardiographic systems. Vestnik aritmologii. 2002, no. 24, pp. 65–86.
      9. Ban A.S., Zagorodny G.M. Possible mistakes in the analysis of heart rate variability. Problemy zdorov'ya i ehkologii. 2010;3(25):119–124.
      10. Heart rate variability. Standards of measurement, physiological interpretation and clinical use. Working Group of the European Society of Cardiology and the North American Society of Stimulation and Electrophysiology. Vestnik aritmologii. 1999, no. 1, pp. 53–78.
      11. Veyn A. M., Voznesenskaya T. G., Golubev V. L. i dr. Zabolevaniya vegetativnoy nervnoy sistemy [Diseases of the autonomic nervous system]. Moscow, Meditsina Publ., 1991, 624 p.
      12. Reddy Y.M., Singh D., Nagarajan D. et al. Atrial fibrillation ablation in patients with gastroesophageal re-flux disease or irritable bowel syndrome-the heart to gut connection! J Interv Card Electrophysiol. — 2013. — V.37. — Р.259–265.
      13. Bayevsky R.N., Ivanov G.G. Cardiac Rhythm Variability: the Theoretical Aspects and the Op-portunities of Clinical Application. Ul'trazvukovaya funkcional'naya diagnostika. 2001, no.3, pp.108–127.
      14. Ryabykina G.V. Sobolev A.V. Variabel'nost' ritma serdtsa [Heart rate variability]. Moscow, Starґ Ko Publ., 1998, 200 p.
      15. Sobolev A.V. Metody analiza variabel'nosti serdechnogo ritma na dlitel'nyh promezhutkah vremeni [Methods for analyzing heart rate variability over long periods of time]. Moscow, ID «MEDPRAKTIKA-M» Publ., 2009, 172 p.
      16. Kiryachkov YU., Hmelevskiy YA. M., Vorontsova E. V. Computer analysis of heart rhythm: methods, interpretation, clinical application. Anesteziologiya i reanimatologiya. 2000, no.2, pp.56–62.
      17. Velagapudi P., Turagam M. K., Leal M. A., Kocheril A. G. Atrial fibrillation and acid reflux disease/ Clin Cardiol. — 2012. — V.35(3). — P.180–186.
     


    Full text is published :
    Eremina E. Yu., Zvereva S. I., Kozlova L. S. Parameters of heart rate variability in patients with gastroesophageal reflux disease. Experimental and Clinical Gastroenterology. 2018;157(9): 10–17. DOI: 10.31146/1682-8658-ecg-157-9-10-17.
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    1. Volgograd State Medical University, the Ministre of the Russian Federation (400131, Volgograd, Russia)
    2. Federal State Autonomous Educational Institution of Higher Education I.M. Sechenov First Moscow State Medical University of the Ministry of Healthcare of the Russian Federation (Sechenovskiy University) (119991, Moscow, Russia)

    Keywords: irritable bowel syndrome, euthyroid sick syndrome, thyroid hormones, low grade systemic inflammation, cytokines

    Abstract:The article presents the results of the study assessing the role of thyroid dysfunction and cytokine imbalance in the pathogenesis and manifestations of irritable bowel syndrome (IBS). We have found low serum triiodothyronine (T3) levels as well as normal or mildly reduced serum TSH levels in 44.78% IBS pts, thus confirming the presence of euthyroid sick syndrome. These changes in thyroid hormone levels were more frequent in IBS with constipation. Moreover, the IBS group was found to have elevated mean anti-TPO levels as compared with the controls. Thyroid imbalances were associated with moderately elevated pro-inflammatory (TNF-α, IL-1ß, IL-6, IL-8) cytokine levels and low levels of serum anti-inflammatory IL-10 cytokine as compared with the healthy subjects. Along with this, hypercytokinemia was less pronounced in IBS than in ulcerative colitis (UC). We have revealed relationship between clinical manifestations of IBS and the severity of thyroid dysfunction. Positive correlation was found between T3, free T4 and IL-8, while anti-inflammatory IL-10 cytokine was negatively correlated with free T3 levels. Our findings suggest that thyroid dysfunction and regulatory cytokines play a significant role in the pathogenesis and manifestations IBS and can be considered as an objective markers of disease severity.

      1. Abramova N.O., Pashkovskaya N.V. Current views on nonthyroidal illness syndrome in clinical practice . Vrachebnoe Delo. 2017; (1–2): 31–38. (In Russian)
      2. Babaeva A.P., Osadchuk M.A., Vidiker R.V., Kalinina E.V. et. al. Markers of systemic inflammation in pathogenesis and optimization of pharmacotherapy of irritable bowel syndrome. Experimental and Clinical Gastroenterology Journal. 2017;139(03):48–55 (In Russian)
      3. Babaeva A.R., Rodionova O.N., Vidiker R.V., Reutova E.Yu. Osobennosti narushenii neirogumoral’noy regulyatsii, tsytokinovogo i tireoidnogo statusa u bol’nykh s funktsional’nymi rasstroystvami zheludochnokishechnogo trakta. Vestnik Sankt-Peterburgskogo universiteta. 2009; 11(1): 51–57. (In Russian)
      4. Minushkin O.N. Sochetannye funktsional’nye rasstroistva zheludochno-kishechnogo trakta, ikh diagnostika i lechebnye podkhody. Meditsinsky sovet. 2015; 13: 21–26. (In Russian)
      5. Osadchuk M.A., Osadchuk M.M. Sindrom perekresta funktsional’noy dispepsii, gastroezofageal’noy refluksnoy bolezni i sindroma razdrazhennogo kishechnika: optimizatsiya terapii. RMZ “Meditsinskoe obozrenie”. 2015;28:1690–1692. (In Russian)
      6. Bashashati M, Moradi M, Sarosiek I. Interleukin-6 in irritable bowel syndrome: A systematic review and meta-analysis of IL-6 (-G174C) and circulating IL-6 levels.// Cytokine. 2017 Nov;99:132-138. doi: 10.1016/j. cyto.2017.08.017. Epub 2017 Sep 5.
      7. Bennet SMP, Palsson O, Whitehead WE, Barrow DA, Törnblom H, Öhman L, Simrén M, van Tilburg MAL. Systemic cytokines are elevated in a subset of patients with irritable bowel syndrome but largely unrelated to symptom characteristics//. Neurogastroenterol Motil. 2018 Oct;30(10):e13378. doi: 10.1111/nmo.13378. Epub 2018 May 24.
      8. De Vries E. M., Fliers E., Boelen A. The molecular basis of the non-thyroidal illness syndrome // J. Endocrinol. — 2015. — Vol. 225, N 3. — Р. 67–81.
      9. Drossman D.A., Hasler W.L. Rome IV — Functional GI disorders: disorders of gut-brain interaction. Gastroenterology 2016; 150(6): 1257–61.
      10. Farwell A. P. Nonthyroidal illness syndrome // Curr Opin Endocrinol Diabetes Obes. — 2013. — Vol. 20, № 5. — P. 478–484.
      11. Kindt S, Van Oudenhove L, Broekaert D, Kasran A, Ceuppens JL, Bossuyt X, Fischler B, Tack J. Immune dysfunction in patients with functional gastrointestinal disorders. Neurogastroenterol Motil. 2015 Apr;21(4):38998. doi:10.1111/j.1365-2982.2008.01220.x.
      12. Krysiak R, Kędzia A, Kowalcze K, Okopień B. Euthyroid sick syndrome: an important clinical problem, Рolish, 2017;70(2 pt 2):376-385.
      13. Kwakkel J., Fliers E., Boelen A. Illness-induced changes in thyroid hormone metabolism: focus on the tissue level (review article) // Neth. J. Med. — 2011. — Vol. 69, N 5. — Р. 224–228.20.
      14. Laterza L., Piscaglia A.C., Lecce S., Gasbarrini A., Stefanelli M.L. Onset of ulcerative colitis after thyrotoxicosis: a case report and review of the literature.// Eur Rev Med Pharmacol Sci. 2016;20(4):685-8.
      15. Ng Q.X., Soh A.Y.S., Loke W., Lim D.Y., Yeo W.S. The role of inflammation in irritable bowel syndrome (IBS).// J Inflamm Res. 2018 Sep 21;11:345-349. doi: 10.2147/JIR. S174982. eCollection 2018.
      16. Patel S.R., Singh A., Misra V., Misra S.P., Dwivedi M., Trivedi P. Levels of interleukins 2, 6, 8, and 10 in patients with irritable bowel syndrome. Indian J Pathol Microbiol. 2017 Jul-Sep;60(3):385-389. doi: 10.4103/IJPM. IJPM_544_16.
      17. Vara E.J., Brokstad K.A., Hausken T., Lied G.A. Altered levels of cytokines in patients with irritable bowel syndrome are not correlated with fatigue.// Int J Gen Med. 2018 Jul 6;11:285-291. doi: 10.2147/IJGM.S166600. eCollection 2018.
     


    Full text is published :
    Babaeva A. R., Osadchuk M. A., Vidiker R. V., Solodenkova K. S., Reutova E. Yu. Euthyroid sick syndrome and cytokine imbalance in pathogenesis and clinical manifestation of irritable bowel syndrome. Experimental and Clinical Gastroenterology. 2018;157(9): 18–25. DOI: 10.31146/1682-8658-ecg-157-9-18-25.
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    1. Regional clinical hospital Saratov (410053, Saratov, Russia)
    2. Saratov State Medical University named after V. I. Razumovsky (410012, Saratov, Russia)

    Keywords: obesity, chronic cholecystitis, eating behavior

    Abstract:The aim. To assess the significance of somatotype and eating behaviour for evaluation of obesity risk resulting in the development of chronic cholecystitis in men and women. Materials and methods used: The 301 patients (97 men and 204 women) suffering from chronic cholecystitis were under medical observation. The impact of somatotype and eating behaviour on obesity risk and its further development into chronic cholecystitis in men and women was analyzed. Results. 62.8% of men and 79.9% of women suffering from obesity were reported to also suffer from chronic cholecystitis, while calculous cholecystitis burdened with obesity was registered more frequently in women rather than men — 88.5% and 59.1% respectively. The increased risk of chronic cholecystitis as a result of obesity in women was proved to be associated with significant frequency of metabolic syndrome with carbohydrate metabolism disorder prevailing. Conclusion. Results of survey have proven that frequency of obesity occurrence in men of abdominal, abdominal-muscular and abnormal constitutional types doesn’t almost depend on their eating behaviour while emotional eating behaviour in men of muscular-abdominal and muscular-thoracic constitutional types is an adverse prognostic factor for obesity progression and its further development into cholecystitis. The risk of obesity and resulting chronic cholecystitis in women is mostly associated with megalosomal constitution regardless of their eating behaviour type while external and emotional eating behaviours in women of other constitutional types are considered significant risk factors.

      1. Ivashkin V.T., ed. Clinical guidelines. Gastroenterology. Moscow. GEOTAR-Media Publ., 2008; 208 p. [In Russian]
      2. Ivashkin V.T., Maev I.V., Baranskaya Ye.K. and all. Gallstone disease diagnosis and treatment: guidelines of the Russian gastroenterological association. The Russian Journal of Gastroenterology, Hepatology, Coloproctology. 2016; 26(3):64–80. [In Russian]
      3. Lazebnik L.B., Il'chenko A.A. Gallstone disease. Pathways of problem solution. Ter arkh. 2005; (2):5-10. [In Russian]
      4. Voznesenskaya T.G. Rasstrojstva pishchevogo povedeniya pri ozhirenii i ih korrekciya [Eating disorders in obesity and their correction]. Obesity and Metabolism. 2004; (2):2–6. [In Russian]
      5. Vahmistrov A.B., Voznesenskaya T.G., Posohov S.I. Klinikopsihologicheskij analiz narushenij pishchevogo povedeniya pri ozhirenii [Clinical and psychological analysis of eating disorders in obesity]. S.S. Korsakov Journal of Neurology and Psychiatry. 2001; (12):19-24. [In Russian]
      6. Dedov I.I., Mel'nichenko G.A. Ozhirenie: ehtiologiya, patogenez, klinicheskie aspekty. Rukovodstvo dlya vrachej [Obesity: etiology, pathogenesis, clinical aspects. A guide for doctors]. Moscow, Medicinskoe informacionnoe agenstvo Publ., 2004, 456 p. [In Russian]
      7. Nikityuk D.B., Nikolenko V.N., Khayrullin R.M. and all. Anthropometric method and clinical medicine. Zhurnal anatomii i gistopatologii. 2013; 2(2). [In Russian]
      8. Nikolenko, V.N., Nikityuk D.B., CHava S.V. Native constitutional anatomy in the aspect of the personificative medicine. Sechenovskij vestnik. 2013; 4 (14):9–17. [In Russian]
      9. Bunak V. V. Antropometry. Moscow, Uchpedgiz Publ., 1941, 368 p. [In Russian]
      10. Galant I. B. A new scheme of constitutional types of women. Kazanskij medicinskij zhurnal. 1927; (7):23–34. [In Russian].
     


    Full text is published :
    Zhukova E.V., Semikina T.M., Kashkina E.I., Kunitsyna M.A. Obesity and chronic cholecystitis risk in men and women with regard to their somatotype and eating behaviour. Experimental and Clinical Gastroenterology. 2018;157(9): 26–31. DOI: 10.31146/1682-8658-ecg-157-9-26-31.
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    1. Astrakhan State Medical University” of the Ministry of Health of the Russian Federation (414000, Astrakhan, Russia)

    Keywords: chronic hepatitis, liver cirrhosis, lipopolysaccharide-binding protein, soluble differentiation cluster 14, endotoxemia, portal blood flow

    Abstract:The aim of the study was to investigate the pathogenetic and diagnostic significance of changes in the concentrations of lipopolysaccharide-binding protein (LBP) and the Soluble Cluster of Differentiation 14 (sCD14) in plasma of the blood in  chronic hepatitis (CH) and liver cirrhosis (LC). Materials and methods: 54 patients with CH and 120 with LC was included in the study. Control group (CG) — 30 practically healthy donors. The concentration of LBP and sCD14 was studied in EDTA plasma by enzyme immunoassay using a commercial test — HyCult biotechnology systems (Netherlands). The study of the organs of the abdominal cavity and pulse dopplerography with color flow Doppler mapping of vessels were performed on an Ultrasound Monitor "Logic-500" (USA) with a 3.5-MHz convection sensor. Results: The mean values of LBP and sCD14 in CH and LC were significantly higher than in CG and did not differ significantly depending on the etiology of the disease. The concentration in the blood of LBP and sCD14 was influenced by the activity of CH and LC, the severity of portal hypertension and associated clinical manifestations, hepatic encephalopathy, the Child's Pugh class of severity. Reliable relationships between the studied parameters and a number of diagnostically significant ultrasound parameters of the portal blood flow (PBF) have been established. Conclusion: The study of the blood levels of LBP and sCD14 in CH and LC can be used to diagnose endotoxemia syndrome, the degree of activation of the anti-endotoxin immune response. Determination of the concentration of LBP in combination with the leading ultrasound parameters of the PBF contributes to the clarification of the degree of severity of the pathological process in the liver, allows predicting the transformation of CH to LC.

      1. Kozlova I.V., Paxomova A.L. Prakticheskaya gastroenterologiya: rukovodstvo dlya vrachej [Practical gastroenterology: a guide for doctors vol. 2.]. Moscow, Drofa Publ., 2010, 495 р. (in Russian).
      2. Komarov F.I. Osadchuk M.A., Osadchuk A.M. Prakticheskaya gastroenterologiya [Practical gastroenterology]. Moscow, MIA Publ., 2010, 480 р. (in Russian).
      3. Su G.L. Lipopolysaccharides in liver injury: molecular mechanisms of Kupffer cell activation // Am. J. Physiol. Gastrointest. Liver Physiol. — 2002. — Vol. 283. — P. 256-265.
      4. Sandler N.G., Koh C., Roque A. et al. Host Response to Translocated Microbial Products Predicts Outcomes of Patients with HBV or HCV infection // Gastroenterol. — 2011. — Vol. 141. — P. 1220–1230.
      5. Szabo G., Mandrekar P., Dolganiuc A. Innate immune response and hepatic inflammation// Semin. Liver Dis. — 2007. — Vol. 27. — P. 339–350.
      6. Levitan B.N., Umerova A.R., Larina N.N. Hronicheskaya patologiya pecheni i kishechniy mikrobiocenoz (klinikopatogeneticheskie aspekti) [Chronic liver pathology and intestinal microbiocenosis (clinical and pathogenetic aspects)]. Astrakhan, Izdatelstvo AGMA Publ., 2010, 135 p. (in Russian).
      7. Levitan B., Levitan G., Kasyanova T. Condition of immune response to lipopolysaccharides of gut microbiota in chronic viral hepatitis and liver cirrhosis. Abstracts of Falk Symposium 205: New Treatment Targets in Gut and Liver Diseases. Lucerne (Switzerland), 2016. — P. 55.
      8. Lifshitz K., Zakharova I.N., Dmitrieva Y.A. Effect of intestinal microbiome in norm and pathology on human health. Med. Sovet. 2017, no. 1. pp. 155–158.
      9. Bondarenko V.M., Likhoded V.G. Role of intestinal microflora endotoxin in human physiogy and pathology. Bull. Orenburg. nauch. Centr. UrO RAN (elektronniy zhurnal), 2012, no. 3. (in Russian).
      10. Quigley E.M., Stanton C., Murphy E.F. The gut microbiota and the liver. Pathophysiological and clinical implications // J. Hepatol. — 2013, Vol. 58, P. 1020–1027.
      11. Makoto U., Makoto M., Hayato У. Gut microbiota and host metabolism in liver cirrhosis // World J. Gastroenterol. — 2015. — Vol. 21. — P. 11597–11608.
      12. Wiest R., Lawson M., Geuking M. Pathological bacterial translocation in liver cirrhosis // J. Hepatol. — 2014, Vol. 60. — P. 197–209.
      13. Ivashkin V.T. Basic concepts and statements of fundamental immunology. Ros. J. Gastroenterol, Hepatol., Coloproctol. 2008. vol.18, no. 4, pp. 4–13.
      14. Trivedi P.J., Adams D.H. Gut — liver immunity // J. Hepatol. — 2016. — Vol. 64. — P.1187–1189.
      15. Mikurov A.A., Garbuzenko D.V. The comparative analysis of level endotoxemia at patients of the cirrhosis of the liver with the portal hypertensia. Fundament. Res. 2011, no. 6, pp. 126–128. (in Russian).
      16. Garbuzenko D.V., Mikurov A.A., Smirnov D.M. Bacterial endotoxinemia and risk of hemorrhage from oesophageal varicose veins in patients with liver cirrhosis. Clin. Med. 2012, no. 7, pp. 49–51. (in Russian).
      17. Minemura M., Shimizu Y. Gut microbiota and liver diseases // World J. Gastroenterol. — 2015. — Vol. 21. — P. 1691–1702.
      18. Miyake K. Endotoxin recognition molecules, Toll-like receptor 4-MD-2 // Semin. Immunol. — 2004. — Vol. 16, N.1. — P. 11–16.
      19. Janovey C.A., Medzhitov R. Innate immune recognition // Ann. Rev. Immunol. — 2002. — V. 20. — P.197–216.
      20. Kitchens R.L., Thompson P.A. Modulatory effects of sCD14 and LBP on LPS-host cell interactions // J. Endotoxin Res. — 2005. — V.11, N. 4. — P. 225–229.
      21. Samuilova D.S., Borovkova U.L. Lipopolysaccharidebinding protein: main functions and clinical value. Сlin. Physiol. Circulation. 2013, no. 4, pp. 5–9. (in Russian).
      22. Chen Y.Y., Lien J.M., Peng Y.S. et al. Lipopolysaccharide binding protein in cirrhotic patients with severe sepsis // J. Chin. Med. Assoc. — 2014. — Vol. 78. — P. 68–74.
      23. Guarner C., Runyon В.А., Young S. Intestinal bacterial overgrowth and bacterial translocation in cirrhotic rats with ascites // J. Hepatol. — 1997. — V. 26. — P. 1372– 1378.
      24. Albillos A., De la Hera A., Alvarez-Mon M. et al. Serum lipopolysaccharide-binding protein prediction of severe bacterial infection in cirrhotic patients with ascites // Lancet. — 2004. — Vol. 363. — P. 1608–1610.
      25. Levitan B.N., Grinberg B.A., Astahin A.V., Kolchina O.S. Issledovanie parametrov portalnogo krovotoka v norme i pri hronicheskih diffuznyh zabolevaniyah pecheni: Metodicheskie rekomendacii [Investigation of parameters of portal blood flow in normal and chronic diffuse liver diseases: Guidelines.]. Astrakhan, 2000, 25 p. (in Russian).
     


    Full text is published :
    Levitan B.N., Kasyanova T.R., Voloshina O.A.. Clinical and diagnostic significance of the lipopolysaccharide — binding protein and the soluble cluster of differentiation 14 in chronic hepatitis and liver cirrhosis. Experimental and Clinical Gastroenterology. 2018;157(9): 32–37. DOI: 10.31146/1682-8658ecg-157-9-32-37
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    1. State-funded Educational Establishment of Higher Professional Education «Volgograd State Medical University of the Ministry of Public Health of the Russian Federation» (400131, Volgograd, Russia)

    Keywords: non-alcoholic fatty liver disease, obesity, fat dysfunction, structural and functional state of the liver

    Abstract:The aim of this study was assessment of the structural and functional state of the liver in patients with non-alcoholic fatty liver disease (NAFLD) with excessive body weight and obesity of I — II degree. The study included 120 patients with NAFLD (45 to 65 years old) with diabetes mellitus type 2. Depending on the body mass index, patients were divided into four groups, comparable by sex, age, severity of chronic heart failure (myocardial infarction from 6 to 12 months earlier). Patients were examined by standard clinical and anthropometric methods, assessment of visceral obesity with bioimpedanceometry and a calculation method. Level of functional status and markers of hepatocyte damage were studied by the biochemical blood test according to standard laboratory methods. Structural state of the liver was evaluated according to ultrasound data and with calculated indices of steatosis and fibrosis of the liver. The results of the study showed that as the body mass index increases, a significantly higher incidence of hyperfermentemia transaminases and gamma glutamyltranspeptidase is determined. The level of visceral adiposity and fatty tissue dysfunction in patients with NAFLD significantly correlated with the severity of cytolysis and cholestasis, decline of bilirubinemia. Patients with heavier structural changes in the liver, both from ultrasound data and from computational methods, are prevailed among patients with obesity. In conclusion: an increase of the severity of obesity, including visceral obesity, the severity of visceral fat dysfunction in patients with NAFLD is accompanied by an increase in structural and functional disorders in the liver.

      1. Ng M, Fleming T, Robinson M, Thomson B, Graetz N, et al. Global, regional, and national prevalence of overweight and obesity in children and adults during 1980–2013: a systematic analysis for the Global Burden of Disease Study 2013. The Lancet. 2014 May. doi:10.1016/S01406736(14)60460-8.
      2. Wilson PW, D'Agostino RB, Sullivan L, Parise H, Kannel WB. Overweight and obesity as determinants of cardiovascular risk: the Framingham experience. Arch Intern Med. 2002 Sep; 162(16):1867-72. doi: 10.1001/ archinte.162.16.1867.
      3. Nguyen NT, Magno CP, Lane KT, Hinojosa MW, Lane JS. Association of hypertension, diabetes, dyslipidemia, and metabolic syndrome with obesity: findings from the National Health and Nutrition Examination Survey, 1999 to 2004. J Am Coll Surg. 2008; 207:928–934. doi: 10.1016/j.jamcollsurg.2008.08.022.
      4. Calle EE, Rodriguez C, Walker-Thurmond K, Thun MJ. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. N Engl J Med. 2003; 348(17):1625-38. doi: 10.1056/NEJMoa021423.
      5. Lubrano C, Saponara M, Barbaro G, Specchia P, Addessi E, Costantini D, Tenuta M, Di Lorenzo G, Genovesi G, Donini LM, Lenzi A, Gnessi L. Relationships between body fat distribution, epicardial fat and obstructive sleep apnea in obese patients with and without metabolic syndrome. PLoS One. 2012; 7(10):e47059. doi: 10.1371/ journal.pone.0047059.
      6. Ruhl CE, Everhart JE. Determinants of the association of overweight with elevated serum alanine aminotransferase activity in the United States. Gastroenterology. 2003; 124 (1):71–79. doi: 10.1053/gast.2003.50004.
      7. Gholam PM, Kotler DP, Flancbaum LJ. Liver pathology in morbidly obese patients undergoing Roux-en-Y gastric bypass surgery. Obes Surg. 2002; 12 (1):49–51. doi: 10.1381/096089202321144577.
      8. Petersen KF, Dufour S, Feng J, Befroy D, Dziura J, Man CD, Cobelli C, Shulman GI. Increased prevalence of insulin resistance and nonalcoholic fatty liver disease in AsianIndian men. Proc Natl Acad Sci USA. 2006; 103:18273– 18277. doi: 10.1073/pnas.0608537103.
      9. Romeo S, Kozlitina J, Xing C. Pertsemlidis A, Cox D, Pennacchio LA, Boerwinkle E, Cohen JC, Hobbs HH. Genetic variation in PNPLA3 confers susceptibility to nonalcoholic fatty liver disease. Nat Genet. 2008; 40:1461–1465. doi: 10.1038/ng.257.
      10. Browning JD, Szczepaniak LS, Dobbins R, Nuremberg P, Horton JD, Cohen JC, Grundy SM, Hobbs HH. Prevalence of hepatic steatosis in an urban population in the United States: impact of ethnicity. Hepatology. 2004; 40:1387– 1395. doi: 10.1002/hep.20466.
      11. Fabbrini E, Mohammed BS, Magkos F, Korenblat KM, Patterson BW, Klein S. Alterations in adipose tissue and hepatic lipid kinetics in obese men and women with nonalcoholic fatty liver disease. Gastroenterology. 2008; 134:424–431. doi: 10.1053/j.gastro.2007.11.038.
      12. Korenblat KM, Fabbrini E, Mohammed BS, Klein S. Liver, Muscle, and Adipose Tissue Insulin Action Is Directly Related to Intrahepatic Triglyceride Content in Obese Subjects. Gastroenterology. 2008; 134 (5):1369-1375. doi: 10.1053/j.gastro.2008.01.075.
      13. Nagle CA, Klett EL, Coleman RA. Hepatic triacylglycerol accumulation and insulin resistance. J Lipid Res. 2009; 50: 74–79. doi: 10.1194/jlr.R800053-JLR200.
      14. Weisberg SP, McCann D, Desai M, Rosenbaum M, Rudolph LL, Ferrante AWJr. Obesity is associated with macrophage accumulation in adipose tissue. J Clin Invest. 2003; 112:1796–1808. doi: 10.1172/JCI200319246.
      15. Kolak M, Westerbacka J, Velagapudi VR, Wågsäter D, Yetukuri L, Makkonen J, Rissanen A, Häkkinen AM, Lindell M, Bergholm R, Hamsten A, Eriksson P, Fisher RM, Orešic˘ M, Yki-Järvinen H. Adipose tissue inflammation and increased ceramide content characterize subjects with high liver fat content independent of obesity. Diabetes. 2007 Aug; 56(8):1960–1968. doi: 10.2337/ db07-0111.
      16. Boza C, Riquelme A, Ibanez L, Duarte I, Norero E, Viviani P, Soza A, Fernandez JI, Raddatz A, Guzman S, Arrese M. Predictors of nonalcoholic steatohepatitis (NASH) in obese patients undergoing gastric bypass. Obes Surg. 2005 Sep; 15(8):1148–53. doi: 10.1381/0960892055002347.
      17. Beymer C, Kowdley KV, Larson A, Edmonson P, Dellinger EP, Flum DR. Prevalence and predictors of asymptomatic liver disease in patients undergoing gastric bypass surgery. Arch Surg. 2003 Nov; 138(11):1240–1244. doi:10.1001/archsurg.138.11.1240.
      18. Ong JP, Elariny H, Collantes R, Younoszai A, Chandhoke V, Reines HD, Goodman Z, Younossi ZM. Predictors of nonalcoholic steatohepatitis and advanced fibrosis in morbidly obese patients. Obes Surg. 2005 Mar 1; 15(3):310–315. doi: 10.1381/0960892053576820.
      19. Diagnostika, lechenie, profilaktika ozhireniya i associirovannyh s nim zabolevanij. Nacional'nye klinicheskie rekomendacii // Rossijskij kardiologicheskij zhurnal. 2017, 164p. [In Russian].
      20. Mareev V. YU., Ageev F. T., Arutyunov G. P. Nacional'nye rekomendacii OSSN, RKO i RNMOT po diagnostike i lecheniyu HSN (chetvertyj peresmotr): utverzhdeny na Kongresse OSSN 7 dekabrya 2012 goda, na Pravlenii OSSN 31 marta 2013 i Kongresse RKO 25 sentyabrya 2013 goda // Serdechnaya nedostatochnost'. 2013, vol. 14, no. 7 (81). pp. 379-472. [In Russian].
      21. Dedov II, Shestakova MV, Mayorov AY, Vikulova OK, et al. Standards of specialized diabetes care (8th edition) Diabetes mellltus. 2017; 20(1S):1-121. doi: 10.14341/ DM20171S8. [In Russian].
      22. Lubrano C, Saponara M, Barbaro G, Specchia P, Addessi E, Costantini D, Tenuta M, Di Lorenzo G, Genovesi G, Donini LM, Lenzi A, Gnessi L. Relationships between body fat distribution, epicardial fat and obstructive sleep apnea in obese patients with and without metabolic syndrome. PLoS One. 2012; 7(10):e47059. doi: 10.1371/ journal.pone.0047059.
      23. Bedogni G, Bellentani S, Miglioli L, Masutti F, Passalacqua M, Castiglione A, Tiribelli C. The Fatty Liver Index: a simple and accurate predictor of hepatic steatosis in the general population. BMC Gastroenterology. 2006 Nov; 6: 33–38. doi: 10.1186/1471-230X-6-33.
      24. Angulo P, Hui JM, Marchesini G, Bugianesi E, George J, Farrell GC, Enders F, Saksena S, Burt AD, Bida JP, Lindor K, Sanderson SO, Lenzi M, Adams L A, Kench J, Therneau TM, Day CP. The NAFLD fibrosis score: A noninvasive system that identifies liver fibrosis in patients with NAFLD. Hepatology. 2007 Apr; 45(4): 846–854. doi: 10.1002/hep.21496.
      25. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: Insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985; 28(7): 412–9.
      26. Ergün Y. The diagnostic role of ultrasonography in liver streatosis. The Turkish Journal of Gastroenterology. 1999; 2: 96-100.
     


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    Statsenko M.E., Turkina S.V. Shilina N.N. Kosivtsova M.A., Bakumov P.A. Structural and functional features of the liver in patients with nonalcoholic fatty liver disease, depending on the severity of obesity. Experimental and Clinical Gastroenterology. 2018;157(9): 38–44. DOI: 10.31146/1682-8658ecg-157-9-38-44
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    1. Saratov State Medical University named after V. I. Razumovsky (410012, Saratov, Russia)
    2. ANO SRC "St. Petersburg Institute of Bioregulation and Gerontology" (197110, Saint Petersburg, Russia)
    3. FGBOU VO "Penza State University" (440026, Penza, Russia)

    Keywords: non-alcoholic fatty liver disease, colonocytes, morphometry, leptin, vascular endothelial growth factor, Ki-67, Bcl-2

    Abstract:Objective: To study the indicators of cellular renewal of the colon mucosa in non-alcoholic fatty liver disease (NAFLD). Materials and methods: 138 people with NAFLD and intestinal pathology were examined. The indices of proliferation (Ki-67) and apoptosis (Bcl-2) in comparison with clinical, endoscopic features of the colon and morphometric features of colonocytes expression immunopositive to leptin and the factor of vascular endothelial growth were studied. Results: It was found that changes in the intestinal mucosa and liver in NAFLD are associated with changes in the parameters of the cellular renewal of epithelial cells (the colon proliferation marker is Ki-67 and the marker of apoptosis colonocytes is Bcl-2) with changes in the production of leptin and the vascular endothelial growth factor.

      1. Ivashkin, V.T. Processy proliferacii i apoptoza pri patologii zheludochno-kishechnogo trakta i pecheni. Russ. Journ. of Gastroenterology, Hepatology and Coloproctology.2008; 12(6):38-43. [In Russian].
      2. Goldin R.D., Hunt N.C., Clark J. et al. Apoptotic bodies in a murine model of alcoholic liver disease: reversibilitity of ethanol-induced changes. J. Pathol. 1993; 171: 73-76.
      3. Searle J. Harmon B.V., Kerr J.F.R. The significance of cell death by apoptosis in hepatobiliary disease. J. Gastroenterol. Hepatol. 1987;2: 77-96.
      4. Coga H., Sakisaka S., Ohiski M. et al. Nuclear DNA fragmentation and expression of bcl-2 in primar biliare cirrhosis. Hepatol. 1997;25: 1077-1084.
      5. Ikeda K., Kinosshita H., Hirihashi K. et al. The ultrastructure, kinetics and intralobular distribution of apoptotic hepatocytes after portal branch ligation with special reference to their relationship to necrotic hepatocytes. Arch. Histol. Cytol. 1995;58:171-184.
      6. Nan Y.et al. Heme oxygenase-1 prevents non-alcoholic steatohepatitis through suppressing hepatocyte apoptosis in mice. Lipids health dis.2010; 9: 124.
      7. Syn W., Choi S., Diehl A. Apoptosis and Cytokines in Nonalcoholic Steatohepatitis .Clin. liver dis. 2009;1(4): 565–580.
      8. Dai Х., Wang B. Role of Gut Barrier Function in the Pathogenesis of Nonalcoholic Fatty Liver Disease. Gastroenterology Research and Practice. 2015;1-6.
      9. Lapteva E.A., Kozlova I.V. Molecular and genetic predisposing factors of comorbidity of fatty liver disease and diseases of the colon (review). Saratov J Med Sci Res.2017;13 (1):29–34. [In Russian].
      10. Tsutsumi Y., Losordo D.W. Double face of VEGF. Circulation. 2005; 112:1248-1250.
      11. Lapteva EA, Kozlova IV. Non-alcoholic fatty liver disease and intestines: interrelations and interactions.// Eksp Klin Gastroenterol. 2017; 138(2):86-91. [In Russian].
      12. Shanmugathasan M., Jothy S. Apoptosis, anoikis and their relevance to the pathobiology of colon cancer. Pathol. Int. 2000; (50)4: 273-282.
      13. Huang KW, Leu HB, Wang YJ, et al. Patients with nonalcoholic fatty liver disease have higher risk of colorectal adenoma after negative baseline colonoscopy. Colorectal Dis. 2013; 15 (7):830–5.
      14. EASL-EASD-EASO Clinical Practice Guidelines for the management of non-alcoholic fatty liver disease. Journal of Hepatology. 2016; 64:1388-1402.
      15. EASL Clinical Practical Guidelines: Management of Alcoholic Liver Disease. J Hepatol 2012; 57:399-420.
      16. Lee JH. Nonalcoholic fatty liver disease — index. EASL. 2009. Poster 59:25.
      17. Angulo P, Hui JM, Marchesini G, Bugianesi E, George J et al. The NAFLD fibrosis score: a noninvasive system that identifies liver fibrosis in patients with NAFLD. Hepatology.2007; 45(4): 846-54.
      18. Kostyuchek I.N. Metodologicheskie podhody k kolichestvennoj immunogistohimicheskoj ocenke ehkspressii markerov apoptoza i proliferacii v molochnoj zheleze [Methodological approaches to quantitative immunohistochemical evaluation of the expression of markers of apoptosis and proliferation in the mammary gland] Arhiv patologii. 2006; 1:47-48. [In Russian].
      19. Janice E. Drew. Symposium 3: Obesity-related cancers Molecular mechanisms linking adipokines to obesityrelated colon cancer: focus on leptin .//Proceedings of the Nutrition Society. 2012; 71, 175–180.
      20. Seliverstov P.V., Sitkin S.I., Radchenko V.G., Lazebnik L.B. et al. Saccharomyces boulardi modulates the composition of the gut microbiota in patients with non-alcoholic fatty liver disease, thus preventing the progression of the disease. Experimental and Clinical Gastroenterology. 2018; 150(2): 4-18.
     


    Full text is published :
    Kozlova I.V.1, Lapteva E.A.1, 3, Kvetnoy I.M. Indicators of cellular renewal of the colon mucosa in non-alcoholic fatty liver disease. Experimental and Clinical Gastroenterology. 2018;157(9): 45–50. DOI: 10.31146/1682-8658-ecg-157-9-45-50.
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    1. Samara State Medical University (443099, Samara, Russia)

    Keywords: ulcerative colitis, microbial composition, antibacterial therapy

    Abstract:Objective: The purpose of the study: optimization of diagnosis and treatment of patients with ulcerative colitis by selecting rational antibacterial therapy based on the results of microbiological examination of the microflora of the wall of the colon. Materials and methods: 35 patients with ulcerative colitis aged from 28 to 61 years who were on outpatient and inpatient treatment at the departments of coloproctology and gastroenterology of the SamSMU Clinic were examined. Collection of biopsy material of ulcerative defects of the mucous membrane of the large intestine was performed during the fibrocolonoscopy, and a pure culture of microorganisms was isolated from biopsy material using classical methods. The isolated cultures were identified using MALDI-TOF mass spectrometry. All the isolated cultures were sensitive to antibiotics by a disco-diffusion method. Results: In assessing the quantitative composition of the isolated microflora in patients with mild disease, the microflora in the wall of the colon was absent, or low titers of the sown strains (10²–10³ CFU per biopsy) were determined. In patients with an average severity and severe course of the disease in 50.0% and 53.8% of cases, respectively, a pronounced microbial contamination of the submucosal layer (the number of microorganisms 105–106 CFU per biopsy), a wide variety of species. When analyzing sensitivity to antibiotics of isolated strains, it was found that 45% of them have resistance to 1–2 groups of drugs, 33% have resistance to 3 or more groups. Only 22% of the strains were sensitive to all tested drugs. Conclusion: The eradication of a resistant flora is complex and, from our point of view, pathogenetically substantiated and requires the appointment of a combination therapy after microbiological examination of the biopsy specimen.

      1. Davydova O.E., Andreev P.S., Katorkin S.E., Ljamin A.V. et al. Microbiological investigation of biopathes of the tolstous wall tile in patients with ulcerative colitis. Lechashchij vrach. 2017; (8): 18-21. [In Russian].
      2. Vorob'ev G.I., Halif I.L. Nespecificheskie vospalitel'nye zabolevanija kishechnika [Nonspecific inflammatory bowel disease], Moscow, Miklosh Publ., 2008, 400 p. [In Russian].
      3. Tkachev A.V., Mkrtchjan L.S., Nikitina K.E. Osobennosti jepidemiologii i patogeneza vospalitel'nyh zabolevanij kishechnika: sostojanie problem [Features of epidemiology and pathogenesis of inflammatory bowel diseases: state of the problem]. Teoreticheskie voprosy mediciny — Theoretical issues of medicine. 2011; (2): 175-180. [In Russian].
      4. Zhukov B.N., Isaev V.R., Andreev P.S., Katorkin S.E., Chernov A.A. Complex treatment of nonspecific ulcerous colitis with endolymphatic therapy application. Novosti hirurgii. 2012; (2): 49-54. [In Russian].
      5. Lyagina I.A., Korneva T.K., Golovenko O.V., Veselov A.V. The characteristic of intestinal microflora in patients with ulcerative colitis. RJGHC. 2008; (2): 48-54. [In Russian].
      6. Reid K.C., Cockerill III F.R., Patel R. Clinical and Epidemiological Features of Enterococcus casseliflavus/ flavescens and Enterococcus gallinarum Bacteremia:A Report of 20 Cases. Clin. Infect. Dis. 2001 Jun; 32 (11): 1540-6.
      7. Denisov N.L., Ivashkin V.T. Local immunodefence and microbiocenosis at bowel disease. RJGHC. 2009, Vol.19. no.6, pp. 11-16. [In Russian].
      8. Lyamyn A.V., Andreev P.S., Zhestkov A.V., Zhukov B.N. Antimicrobial Resistance of Gram-negative Bacteria Isolated from Biopsy in Patients with Ulcerative Colitis. Interregional Association for Clinical Microbiology and Antimicrobial Chemotherapy (IACMAC) 2010; (4): 342346. [In Russian].
      9. Ivashkin V.T., Lapina T.L. Gastrojenterologija: nacional'noe rukovodstvo, Moscow, GJeOTAR-Media Publ, 2008, 700p. [In Russian].
      10. Ivashkin V.T., Shelygin Ju.A., Halif I.L., et al. Clinical guide of Russian Association Of Gastroenterology And Russian Association Of Coloproctology on dyagnostics and treatment of ulcerative colitis. Koloproktologija. 2017; (1): 6-31. [In Russian].
      11. Truelove S.С., Witts L.J. Cortisone in ulcerative colitis; final report on a therapeutic trial. BrMed. J; (2): 1041-8.
      12. Davydova O.E., Andreev P.S., Katorkin S.E. Jazvennyj kolit — osobennosti diagnostiki i lechenija [Ulcerative colitis — features of diagnosis and treatment]. Gastrojenterologija Sankt-Peterburga — Gastroenterology of St. Petersburg. 2017; (1): 76-77. [In Russian].
      13. Davydova O.E., Katorkin S.E., Lyamin A.V., Andreev P.S. Improvement of results of treatment of patients with ulcera-tive colitis using individual schemes of eradication therapy of conditionally pathogenic microflora, based on microbio-logical monitoring. Vrach-Aspirant. 2016; (4): 49 — 55. [In Russian].
     


    Full text is published :
    Davydova O.E., Andreev P.S., Katorkin S.E., et al. The value of the wall of the microbiota of the colon in the selection of rational antibiotic therapy in patients with ulcerative colitis. Experimental and Clinical Gastroenterology. 2018;157(9): 51–56. DOI: 10.31146/1682-8658-ecg-157-9-51-56.
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    1. South Ural state medical University (454092, Chelyabinsk, Russia)

    Keywords:comorbidity; multymorbidity; liver cirrhosis

    Abstract:The role of comorbidity in the treatment of liver cirrhosis (LC) and its complications is unknown. Purpose: studying of comorbidity in patients with LC and its impact on outcome of the disease. Materials and methods. 155 patients (women — 49,4%, men — 50,6%, mean age 52,15±12,41) were follow up for 3 year. Viral LC was diagnosed in 33.8%, alcohol LC — 22,1%, autoimmune LC-15, 6%, other causes and cryptogenic causes noted in — 28,5%. More than half of the patients had a class В of Child-Pugh (51.9%). Comorbidity was determined by Charlson and CirCom (Jepsen, 2014) scales. Results: during 3 year of observation 44 people died (28,4%): 33 (75%) patients died from LC complications; 11 (25%) patients died from causes not directly related to LC (4-cancer, 2-diabetes mellitus (DM), 1-trauma, 1-atrial fibrillation, pulmonary embolism-1, stroke-1). 44 patients (28,4%) had no comorbidities. Hypertension was noted at 26.6%, cholelithiasis — 22.1% and DM-14.9%. 41.9% of patients had 1 concomitant disease, 18.7% — 2 diseases, 10.9% — more than three. The number of comorbidities significantly increased the risk of death from causes unrelated to LC (RR: 5,000; 95% CI: 1,426-17, 532). Bilateral positive correlation (rs=0,304, p=0,00012) between the age of patients and the number of comorbidities was revealed. The analysis of the relationship between Charlson and CirCom scales confirmed their correlation at rs=0,543, p=0,0000001. Statistically significant differences of Charlson and CirCom comorbidity were found in groups of patients who died from causes unrelated to LC and lived to the end of the follow-up period (p*=0.000048, p**=0.000243). Conclusion. In patients with LC, comorbidity significantly impacts on mortality from causes unrelated to LC.

      1. Verbovoy A.F., Tsanava I.A., Verbovaya N.I. Meditsina XXI veka: v fokuse komorbidnost' [Medicine of the 21st Century: Comorbidity in Focus] Universitetskaya meditsina Urala — Ural University Medicine. 2017, no.2, pp. 27–31. (In Russ.)
      2. Tarlovskaya Ye.I., Problem of polymorbidity — challenge tо modern medicine. Therapy. 2017, vol. 3, no. 2, pp. 4–14. (In Russ.)
      3. Oganov R.G., Denisov I.N., Simanenkov V.I., et al. COMORBIDITIES IN PRACTICE. CLINICAL GUIDELINES. Cardiovascular Therapy and Prevention. 2017;16(6):5-56. (In Russ.) https://doi.org/10.15829/17288800-2017-6-5-56.
      4. Andrews J.C., Schunemann H.J., Oxman A.D., Pottie K., Meerpohl J.J., Coello P.A. et al. GRADE guidelines: Going from evidence to recommendation—determinants of a recommendation’s direction and strength.//J.Clin. Epidemiol. — 2013.—№ 66. — С.726–35. https://doi. org/10.1016/j.jclinepi.2013.02.003
      5. de Franchis R Portal Hypertension VI. Proceedings of the Sixth Baveno Consensus Workshop: Stratifying Risk and Individualizing Care. Switzeland: Springer; 2016. https:// doi.org/10.1007/978-3-319-23018-4
      6. Oganov R.G., Drapkina O.M. POLYMORBIDITY: SPECIFICS OF CO-DEVELOPMENT AND CONCOMITANCE OF SEVERAL DISEASES IN ONE PATIENT. Cardiovascular Therapy and Prevention. 2016;15(4):4-9. (In Russ.) https://doi.org/10.15829/17288800-2016-4-4-9.
      7. Benfante A., Basile M., Battaglia S., Spatafora M., Scichilone N. Use of ICS/LABA (extra-fine and non-extrafine) in elderly asthmatics // Ther. Clin. Risk Manag. — 2016. — № 12. — С. 1553–62. https://doi.org/10.2147/ tcrm.s103709.
      8. Jepsen P., Vilstrup H., Andersen PK., Lash T.L., Sørensen H.T. Comorbidity and Survival of Danish Cirrhosis Patients: A Nationwide Population-Based Cohort Study. //Hepatology. — 2008. — V.48, № 1. — С. 214-220. https://doi.org/10.1002/hep.22341.
      9. Nguyen T.A., De Shazo J.P., Thacker L.R., Puri P., Sanyal A.J. The Worsening Profile of Alcoholic Hepatitis in the United States. //Alcohol Clin Exp Res. — 2016. — V. 40, № 6. — С. 1295–1303. https://doi.org/10.1111/acer.13069.
      10. Kalaitzakis E, Gunnarsdottir SA, Josefsson A, Björnsson E. Increased risk for malignant neoplasms among patients with cirrhosis. //Clin Gastroenterol Hepatol. — 2011. — 9. — С. 168-174. https://doi.org/10.1016/j.cgh.2010.10.014
      11. Sørensen H.T, Friis S, Olsen J.H, Thulstrup A.M, Mellemkjær L, Linet M. et al. Risk of liver and other types of cancer in patients with cirrhosis: a nation-wide cohort study in Denmark. //Hepatology. — 1998. — 28. — С. 921925. https://doi.org/10.1097/00042737-199812000-00017.
      12. Cabibbo G., Palmeri L., Palmeri S., Craxì A. Should cirrhosis change our attitude towards treating nonhepatic cancer? //Liver Int. —2012. — 32. — С. 21–27. https://doi.org/10.1111/j.1478-3231.2011.02629.x.
      13. Gundling F, Seidl H, Schmidtler F, Löffler N, Strassen I, Wolf P. et al. Extrahepatic cancer in liver cirrhosis: a retrospective study of prevalence, complication rate after specific oncological treatment, follow-up and prognostic predictors of outcome in 354 patients with cirrhosis. //J Gasrroenterol. — 2010. — V.48, № 10. — С. 2931–2938. https://doi.org/10.1055/s-0030-1267658.
      14. Holzmann M.J, Carlsson A.C, Hammar N., Ivert T., Walldius G,. Jungner I. et al. Chronic kidney disease and 10-year risk of cardiovascular death. //Eur J Prev Cardiol. — 2015 [Epub ahead of print] https://doi. org/10.1177/2047487315614491.
      15. Pesanti EL. Immunologic defects and vaccination in patients with chronic renal failure. //Infect Dis Clin North Am. — 2001. — V.15, № 3. — С. 813–32. https:// doi.org/10.1016/s0891-5520(05)70174-4.
      16. Berzigotti A., Albillos A., Villanueva C., Genescà J., Ardevol A., Augustin S., et al. Effects of an intensive lifestyle intervention program on portal hypertension in patients with cirrhosis and obesity: The SportDiet study. //Hepatology. — 2017. — V. 65, № 4. — С. 1293– 1305. https://doi.org/10.1002/hep.28992.
      17. Trombetta M., Spiazzi G., Zoppini G., Muggeo M. Review article: type 2 diabetes and chronic liver disease in the — V.22, № 2. — С. 24–7. https://doi.org/10.1111/ i1365-2036.2005.02590.x.
      18. Jepsen P., Vilstrup H., Lash T.L. Development and validation of a comorbidity scoring system for patients with cirrhosis.// Gastroenterology. 2014. — № 146. — С. 147–156. https://doi.org/10.1053/j. gastro.2013.09.019.
      19. Wlazlo N., van Greevenbroek M.M, Curvers J., Schoon E.J,. Friederich P., Twisk J.W. et al. Diabetes mellitus at the time of diagnosis of cirrhosis is associated with higher incidence of spontaneous bacterial peritonitis, but not with increased mortality. //Clin Sci (Lond). — 2013. — V. 125. — С. 341-348. https://doi.org/10.1042/ CS20120596.
      20. Quintana J.O., García-Compean D., González J.A., Pérez J.Z., González F.J., Espinosa L.E. et al. The impact of diabetes mellitus in mortality of patients with compensated liver cirrhosis-a prospective study. //Ann Hepatol. — 2011. — № 10. — С. 56–62.
      21. Charlson M.E., Pompei P., Ales K.L. A new method of classifying prognostic comorbidity in longitudinal studies: development and validation. //Chronic Dis. — 1987. — V.40, № 5. — С.373–83 https://doi. org/10.1016/0021-9681(87)90171-8.
      22. Fortin M., Bravo G., Hudon C., Vanasse A., Lapointe L. Prevalence of multimorbidity among adults seen in family practice. Ann Fam Med. 2005; 3: 223–228. https:// doi.org/10.1370/afm.272.
      23. Feudjo-Tepie M. A., Le Roux G., Beach K. J., Bennett D., Robinson N. J. Comorbidities of Idiopathic Thrombocytopenic Purpura: A Population-Based Study. //Advances in Hematology. — 2009. — № 2009. — С. 1–12. https://doi.org/10.1155/2009/963506.
      24. Bueverov A.O. The natural course and therapy options of alcoholic liver disease. High tech medicine. 2016, Vol. 3, no.1, pp. 18–25.
      25. Mikheyeva O.M. Pechen' i lekarstvennyy metabolizm [Liver and drug metabolism]. Experimental and clinical gastroenterology. 2011, no. 1, pp. 121–124.
     


    Full text is published :
    Olevskaya E.R., Dolgushina A.I., Tarasov A.N., Khihkhlova A.O. Comorbidity patients with liver cirrhosis: effect on course and outcome. Experimental and Clinical Gastroenterology. 2018;157(9): 57–63. DOI: 10.31146/1682-8658-ecg-157-9-57-63.
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    1. Kharkiv National Medical University (61022, Kharkiv, Ukraine)

    Keywords: chronic pancreatitis, arterial hypertension, polymorphism of VDR gene, osteoporosis

    Abstract:The aim of the research: to establish diagnostic and prognostic values of chromosomal aberrations in the gene of vitamin D receptors in the combined course of chronic pancreatitis and arterial hypertension. Materials and methods: For this research, two groups of patients were created — the main one — 70 patients with chronic pancreatitis and arterial hypertension and a comparison group — 40 persons with isolated course of chronic pancreatitis. Results: The prevalence of B-allelic polymorphism of this gene was established. The comorbidity of chronic pancreatitis and arterial hypertension in 51.4% of cases occurs against the pathological (ВВ-genotype) polymorphism of the VDR gene, which means early development of complications. With В-allelic polymorphism of the VDR gene, favorable conditions for the development of osteopenic conditions (32.9%) are created, which causes their early diagnosis and treatment.

      1. Global health risks: mortality and burden of disease attributable to selected major risks [Электронный ресурс]: WHO Library Cataloguing-in-Publication Data.2009. — 62 p.
      2. Kovalenko V.M., Kornats’ki V.M. Regional’ni osoblyvosti rivnya zdorov”ya Ukrainy. Analitychno-statystychnyi posibnyk — rekomendovanyi dlya kardiologiv, revmatologiv, terapevtiv, organizatoram OZ ta likariv zagal’noy praktyky. Kyiv, 2011, 168 p.
      3. 2013 ESH/ESC Guidelines for them anagement of arterial hypertension / The Task Force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC) // Journal of Hypertension. — P.1281 — 1357.
      4. Zhuravleva L.V. Sovremennaya strategiya lecheniya arteryal'noy gypertenzii. Metodycheskie ukazaniya dlya vrachey. Har'kov, HNMU Publ., 2013, pp. 3–4.
      5. Sydorchuk L.P. Kliniko-demografichna harakterystyka hvoryh z essentsial'noy arterial'noy gipertenziey zalezhno vid polimorfizmu geniv. Serce i sudyny. 2008, no. 4 (24), pp. 54–66.
      6. Tseluyko V.O., Peletskaya O.V. Vliyaniye typa I/D polimorfizma gena angiotenzinprevrashhayushhego fermenta na klynycheskoe techenie gypertonicheskoy bolezni. Ukr. kardyolog. Zhurnal. 2008, no. 1, pp. 33–36.
      7. Conwell D.L. Chronic Pancreatitis: Making the Diagnosis / D. L. Conwell, U. Bechien // Clin. Gastroenterol. Hepatol. 2012. — № 10.— P. 1088—1095.
      8. The Spanish Pancreatic Club recommendations for the diagnosis and treatment of chronic pancreatitis: part 1 (diagnosis). Pancreatology. 2013 Jan-Feb;13(1):8-17. doi: 10.1016. — j.pan.2012.11.309. Epub 2012 Nov 27.
      9. Kovalenko V.M. Hvoroby sistemy krovoobigu yak medyko-sotsial'na i suspil'no-politychna problema. Analitychno-statystychnyi posibnyk. Kyiv, 2014, 279 p.
      10. Kocher H. M. Chronic pancreatitis / H. M. Kocher // Am. Fam. Physician. — 2008. — Vol. 77, № 5. — P. 661–662.
      11. Ratsional'naya diagnostika i farmakoterapiya zabolevanyi vnutrennih organov / Pod red. A.N. Belovola, G.D. Fadeenko, O.Ja. Babaka // Spravochnik vracha «Semeynyy vrach, terapevt». Kiev, OOO «Byblyoteka «Zdorov'e Ukrainy» Publ., 2013, 438 p.
      12. Tkach S.M. Prakticheskie podhody k diagnostike hronicheskogo pankreatita. Suchasna gastroenterologiya. 2013, no. 1 (69), pp. 136–146.
      13. Babinets' L.S., Galabits'ka I.M. Patogenetychni aspekty klinichnogo perebigu hronichnogo pankreatytu: rol' pro — i antioksidantnogo status. Zdorov’ya Ukrainy, 2016, no. 1 (39), pp. 49_51.
      14. Hills C.E., Younis M.Y., Bennett J. et al. Calcium — Sensing Receptor Activation Increases Cell-Cell Adhesion and b-Cell Function // Cell Physiol. Biochem. — 2012. — Vol. 30(3). — P. 575–586.
      15. Ross A. C. Institute of Medicine (US) Committee to Review Dietary Reference Intakes for Vitamin D and Calcium / A. C. Ross, C. L. Taylor, A. L. Yaktine [et al.] // Dietary Reference Intakes for Calcium and Vitamin D. — 2011. — Washington (DC): National Academies Press (US); 2011. Available from: http://www.ncbi.nlm.nih. gov/books/NBK56070.
      16. Kunes J., Zicha J. The interaction of genetic and environmental factors in the etiology of hypertension. // Physiol Res. 2009;58 Suppl 2:S33-41.
      17. Bang D. Cardiovascular Disease Prevalence in Patients with Osteoarthritis, Gout, or Both / D.Bang, J.Xu, R.Keenan, V.Pike, R.Lehmann, C.Tenner, D.Crittenden, M.Pillinger, S. Krasnokutsky // Bulletinofthe Hospital Joint Disease (2013). 2016 Vol. 74. — S. 2. P.113–118.
      18. Prentice R. L. Health risks and benefits from calcium and vitamin D supplementation: Women's Health Initiative clinical trial and cohort study / R. L. Prentice, M. B. Pettinger, R. D. Jackson [et al.] // Osteoporos Int. — 2013. — Vol. 24 (2). — P. 567–580.
      19. Bernstein C.N., Leslie W.D. The pathophysiology of bone disease in gastrointestinal disease // Eur. J. Gastroenterol. Hepatol. — 2013. — Vol. 15(8). — P. 857–864.
      20. Povoroznyuka V.V., Pludovs'ki P. Defitsit ta nedostatnist' vitaminu D: epidemiologiya, diagnostyka, profilaktyka ta likuvannya. Donets'k, 2014, 262 p.
      21. Duggan S.N., O’Sullivan M., Hamilton S. et al. Patients with chronic pancreatitis are at increased risk for osteoporosis // Pancreas. — 2012. — Vol. 41(7). — P. 1119–1124.
     


    Full text is published :
    Pasieshvili L.M., Viun T.I. Сhromosome aberration as a possible mechanism of early complications in the combined course of chronic pancreatitis and hypertensive disease. Experimental and Clinical Gastroenterology. 2018;157(9): 64–68. DOI: 10.31146/1682-8658-ecg-157-9-64-68.
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    1. "Izhevsk State Medical Academy" (426034, Izhevsk, Russia)

    Keywords: ulcer disease, chronic duodenal insufficiency, duodenogastric reflux, motor-evacuation function of the stomach and duodenum

    Abstract:The purpose: to study the peculiarities of motor and evacuation functions of the stomach and duodenum in patients with peptic ulcer with associated chronic duodenal insufficiency (СDI). Materials and methods. The complex examination was carried out by 160 patients with ulcer disease (UD) with concomitant CDI (group 1) and 104 patients with no concomitant CDI (2nd group). The verification of UD was carried out by clinical and fibrogastroduodenoscopy studies. In the definition of CDI contrast duodenography and fibrogastroduodenoscopy were used. The evaluation of the motor-evacuation function (MEF) of the stomach and duodenum was carried out with the help of the peripheral electrogastroenterograph. Results of the study. In patients with UD with associated HDI before meals were identified bradygastria (75%) and hypertension (67%) of the stomach, and after eating the parameters of the electrical activity of the stomach in frequency and amplitude were decreased. We revealed hypokinesia (74%) and hypertension (52%) of duodenum on an empty stomach, postprandial frequency of it decreases compared with a thorough examination. The duodenogastric reflux is revealed in the fasting phase of the study. A segmenting and peristaltic contractions of the duodenum are slowed down, which is manifested in a decrease in the evacuation function of stomach and duodenum. Before meals in patients with UD without accompanying HDI were identified hypertension of the stomach (15%) and duodenum (68,95%), after a meal the indices of electrical activity of the stomach and duodenum were increased. In patients with duodenum ulcer of 1 group the electrical activity of duodenum before meals was corresponded to hyperkinetic (98.2%) and hypertensive (62.3%) type of the curve. The eating in patients of this group increases the peristaltic contractions of the longitudinal muscle layer of the duodenum, thereby accelerating the evacuation of the chyme without mixing it and disrupting the digestion process. In patients with duodenal ulcer without accompanying HDI before meals were identified the hypertension of the stomach (15%) and duodenum (68.95%), coordinated work of stomach and duodenum, as well as evacuation of food chyme were preserved. The conclusion. In patients with ulcer disease of stomach and duodenum with accompanying duodenal insufficiency, there was a violation of motor and evacuation activity of the stomach and duodenum both on an empty stomach and after eating, which adversely affects the course of ulcer disease.

      1. Zvyagintseva T.D., Shargorod I.I. Chronic duodenal obstruction and the principles of conservative therapy // Gastroenterology.2011, no.2, pp. 5–7.
      2. Ugolev A.M. Enterinovaya (kishechnaya gormonal'naya) sistema [Enteric (intestinal hormonal) system]. SPb, Science Publ., 1978, 314 p.
      3. Levin MD, Korshun Z., Mendelson G. Motor function of the duodenum in norm and with some diseases (hypothesis). Therapeutic archive. 2016, no.4, pp. 68–74.
      4. Lazebnik L.B., Guseinadze M.K., Li I.A. Epidemiology of peptic ulcer of the stomach and duodenum. Therapeutic Archive. 2007, no.2, pp. 12–15.
      5. Lapina T.L. Peptic ulcer: opportunities on the threshold of a new century. Consilium medicum. 2000, no.7, pp. 275–279.
      6. Kolesnikova E.A., Dmitrienko M.A., Nikulin Yu.A. Primeneniye meditsinskoy tekhniki pri funktsional'noy diagnostike v gastroenterologii [The use of medical equipment in functional diagnostics in gastroenterology]. St. Petersburg, 2006, 104 p.
      7. Smirnova G.O., Siluyanov S.V., Stupina V.A. Perifericheskaya elektroenterografiya v klinicheskoy praktike [Peripheral electroencephalography in clinical practic]. Moscow, GEM Publ., 2009, 20 p.
      8. Sheptulin A.A. Disturbance of gastric motility and modern possibilities of their pathogenetic therapy. Ros. Journal of Gastroenterology, Hepatology, Coloproctology. 2010, no.5, pp. 49–54.
      9. Maev I.V., Samsonov A.A. Khronicheskiy duodenit [Chronic duodenitis]. Moscow, GOU VUNMTS MH and SR RF, 2005, 160 p.
      10. Ettinger A.P. Fundamentals of the regulation of electrical and motor activity of the gastrointestinal tract. RZHGK. 1998, no. 4, pp. 13–17.
      11. Vakhrushev Ya.M., Busygina M.S. Features of the clinical course of peptic ulcer with concomitant duodenal insufficiency. Archive of internal medicine. 2016, no.4, pp. 30–34.
      12. Vakhrushev Ya.M., Busygina M.S. Gastro-duodenal motor activity of patients with peptic ulcer with concomitant duodenal insufficiency // Proceedings of the Izhevsk State Medical Academy. 2015, no.2, pp. 51–52.
     


    Full text is published :
    Vahrushev Ya.M., Busygina M.S., Zelenin V.A. The motor and evacuation function of the stomach and duodenum in patients with ulcer deseas with associated chronic duodenal incufficiensy. Experimental and Clinical Gastroenterology. 2018;157(9): 69–75. DOI: 10.31146/1682-8658-ecg-157-9-69-75.
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    1. Saratov State Medical University named after V. I. Razumovsky (410012, Saratov, Russia)

    Keywords: Rheumatoid arthritis, pharmacoepidemiology, adverse events, disease-modifying antirheumatic drugs; glucocorticosteroids, nonsteroidal anti-inflammatory drugs

    Abstract:Aim. Analysis of gastroenterological adverse events of rheumatoid arthritis (RA) pharmacotherapy and measures for their prevention and correction. Materials and methods. An open pharmacoepidemiological prospective study was conducted based on the analysis of 230 medical records of patients with diagnosis of RA in the specialized department. Results of the study. Adverse events from the digestive system were developed in 52,2% patients taking diseasemodifying antirheumatic drugs (DMARDs). The largest number of adverse events were registered for the methotrexate use. The average dose of methotrexate that led to adverse events was 15±7,1 mg per week. Correction of folate deficiency with the use of methotrexate was performed only in 84,4% of patients. NSAIDs-gastropathy was developed in 25,5% cases using of nonsteroidal anti-inflammatory drugs (NSAIDs)/ All patients taking NSAIDs and/or glucocorticosteroids received proton pump inhibitors. Conclusion. For the treatment of RA used DMARDs, NSAIDs, glucocorticosteroids. Adverse events are developing in most patients. Most often adverse events occured from the digestive system.

      1. Nasonov E.L. (Eds). Klinicheskie rekomendatsii. Revmatologiya [Clinical guidelines. Rheumatology]. Moscow, GEHOTАR-Media Publ., 2008, pp. 25–71. [In Russian].
      2. Nasonov E.L. (Eds). Klinicheskie rekomendatsii. Revmatologiya [Clinical guidelines. Rheumatology]. Moscow, GEHOTАR-Media Publ., 2010, pp. 90–230. [In Russian].
      3. Folomeeva O.M., Galushko E.A., Erdes S.F. Prevalence of rheumatic diseases in adult populations of Russian Federation and USA. Rheumatology Science and Practice. 2008;46(4):4–13. https://doi.org/10.14412/19954484-2008-529 [In Russian].
      4. Balabanova R.M., Erdes S.F. Trends in the prevalence of rheumatic diseases in ICD-10 in the adult population of the Russian Federation over 2000–2010. Rheumatology Science and Practice. 2012;50(3):10–12. https://doi. org/10.14412/1995-4484-2012-702.
      5. Nyberg F., Askling J., Berglind N. et al. Using epidemiological registry data to provide background rates as context for adverse events in a rheumatoid arthritis drug development program: a coordinated approach // Pharmacoepidemiology and Drug Safety. — 2015. — Vol.24. — P. 1121–1132.
      6. Gabriel S.E., Michaud K. Epidemiological studies in incidence, prevalence, mortality, and comorbidity of the rheumatic diseases // Arthritis Research and Therapy. — 2009. — Vol.11. — doi 10.1186/ar2669.
      7. Kuusalo L., Puolakka K., Kautiainen H. et al. High Burden of Adverse Events is Associated with Reduced Remission Rates in Early Rheumatoid Arthritis // Clinical Rheumatology. — 2017. Vol.37. — P. 1–6.
      8. MacDonald T. Morant S., Robinson G. et al. Association of upper gastrointestinal toxicity of non-steroidal antiinflammatory drugs with continued exposure: cohort study // British Medical Journal. — 1997. — Vol.315 — P. 1333–1337.
      9. Garcia Rodriguez L., Hernandez-Diaz S. The risk of upper gastrointestinal complications associated with nonsteroidal anti-inflammatory drugs, glucocorticoids, acetaminophen and combinations of these agents // Arthritis Research and Therapy. — 2001. — Vol.3 — P. 98–101.
      10. Ramiro S., Gaujoux-Viala C., Nam J.L. et al. Safety of synthetic and biological DMARDs: a systematic literature review informing the 2013 update of the EULAR recommendations for management of rheumatoid arthritis // Annals Rheumatic Disease. — 2014. — Vol.73. — P. 529–535.
      11. Lampropoulos C., Orfanos P., Bournia V. et al. Adverse events and infections in patients with rheumatoid arthritis treated with conventional drugs or biologic agents: a real world study // Clinical and Experimental Rheumatology. — 2015. — Vol.33. — P. 216–224.
      12. Ruxandra E., Ioana C., Dana G. Particularities of treatment with conventional synthetic diseasemodifying antirheumatic drugs (DMARDs) in a group of patients with rheumatoid arthritis // Farmacia. — 2017. — Vol. 65. — P. 479–484.
      13. Cannon G., Holden W., Juhaeri J. et al. Adverse events with disease modifying antirheumatic drugs (DMARD): a cohort study of leflunomide compared with other DMARD. Rheumatology. — 2014. — Vol.31. — P. 1906–1911.
      14. Prabha M., Rani A., Balasubramanian M., Ramya J. Prescribing pattern and adverse drug reactions monitoring in patients with rheumatoid arthritis in a tertiary care hospital // International Journal of Basic and Clinical Pharmacology. — 2016. — Vol.5. — P. 805–809.
      15. Machado-Alba J., Ruiz A., Machado-Duque M. Adverse drug reactions associated with the use of diseasemodifying anti-rheumatic drugs in patients with rheumatoid arthritis // Revista Panamericana de Salud Publica. — 2014. — Vol.36. — P. 396–401.
      16. Muravyev Y.V. How is folic acid to be used in rheumatoid arthritis during methotrexate treatment? Rheumatology Science and Practice. 2013;51(2):201–204. https://doi. org/10.14412/1995-4484-2013-649.
      17. Ortiz Z., Shea B., Suarez-Almazor M. et al. The efficacy of folic acid and folinic acid in reducing methotrexate gastrointestinal toxicity in rheumatoid arthritis. A metaanalysis of randomized controlled trials // Rheumatology. — 1998. — Vol. 25. — P. 36–43.
      18. Federal'nyye klinicheskiye rekomendatsii po revmatologii [Federal clinical guidelines for rheumatology]. http:// rheumatolog.ru/ru/nauka/klinicheskie-rekomendacii/ [in Russia].
      19. Smolen J., Lamdewe R., Breedveld F. et al. EULAR recommendations for the management of rheumatoid anti-rheumatic drugs // Annals Rheumatic Disease. — 2010. — Vol.69. — P. 964–97
      20. Smolen J., Lamdewe R., Breedveld F. et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2013 update // Annals Rheumatic Disease. — 2014. — Vol.73. — P. 492–509.
      21. Muravyev Y.V., Denisov L.N., Alekseyeva A.V., Muravyeva N.V., Shakhramanova E.L., Kasumova K.A., Gukasyan D.A., Dydykina I.S., Lebedeva V.V., Nasonov E.L. 4-WEEK OPEN-LABEL CONTROLLED RANDOMIZED COMPARATIVE STUDY OF THE INJECTABLE AND TABLETTED FORMULATIONS OF METHOTREXATE IN RHEUMATOID ARTHRITIS. Rheumatology Science and Practice. 2011;49(5):58–61. https://doi. org/10.14412/1995-4484-2011-1462.
      22. Karateev A.E. NSAID GASTROPATHY: CHANGES OVER 12 YEARS. Rheumatology Science and Practice. 2011;49(3):20–24. https://doi.org/10.14412/1995-44842011-568.
      23. Wolfe M., Lichtenstein D., Singh G. Gastrointestinal toxicity of nonsteroidal antiinflammatory drugs // New England of Journal Medicine. — 1999. — Vol. 340. — P. 1888–1899.
      24. Christina A., Griffith J., Kaplan C. et al. A Retrospective Analysis of Corticosteroid Utilization Before Initiation of Biologic DMARDs Among Patients with Rheumatoid Arthritis in the United States // Rheumatology and Therapy. — doi.org/10.1007/s40744-017-0089-8.
      25. Karateev A.E., Nasonov E.L., Ivashkin V.T., et al. RATIONAL USE OF NONSTEROIDAL ANTIINFLAMMATORY DRUGS. CLINICAL GUIDELINES. Rheumatology Science and Practice. 2018;56:1–29. https://doi.org/10.14412/1995-4484-2018-1-29.
      26. Hoes J., Jacobs J., Boers M. et al. EULAR evidence-based recommendations on the management of systemic glucocorticoid therapy in rheumatic diseases // Annals Rheumatic Disease. — 2007. — Vol.66. — P. 1560–1567.
     


    Full text is published :
    Reshetko O.V., Levitan A.I., Suleymanova R.R. Gastrosafety of rheumatoid arthritis pharmacotherapy. Experimental and Clinical Gastroenterology. 2018;157(9): 76–80. DOI: 10.31146/1682-8658-ecg-157-9-76-80.
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    1. Federal State Budgetary Educational Institution of Higher Education “Petrozavodsk State University” (PetrSU) (185910, the Republic of Karelia, Petrozavodsk, Russia)
    2. Institute of Biology of Karelian Research Centre Russian Academy of Sciences (IB KarRC RAS) (185910, the Republic of Karelia, Petrozavodsk, Russia)

    Keywords: non-alcoholic fatty liver disease, hepatic steatosis, apoptosis, cytokeratin-18, tumor necrotic factor-alpha

    Abstract:The aim of the research was to assess the severity of hepatocyte apoptosis in early form of non-alcoholic fatty liver disease (NAFLD) — liver steatosis (LS). Materials and methods. Total of 83 patients of LS were examined: men 42 (50.6%), women — 41 (49.4%) at the age of 52.4 ± 12.3 years. The diagnosis of the LS was established on the basis of clinical, laboratory data, the results of ultrasound liver examination and histological examination of liver biopsy specimens. Blood plasma levels of cytokeratin-18 (CK-18) (apoptosis marker) («TPS ELISA test system», Biotech, Sweden), tumor necrotic factor alpha (TNF-α) («Human TNFα Platinum ELISA test system», "EBioscience", Austria), insulin («Insulin TEST system», USA) were examined by ELISA. The HOMA index, the NAFLD fibrosis score (NAFLD FS) were calculated. The histological activity and fibrosis were evaluated using the Brunt method. Statistics were analyzed using the "StatGraphics 2.1" , using the Mann-Whitney U test, Spearman's rank correlation analysis. Results. High content of CK-18 was found in patients with hepatic steatosis compared with that in healthy individuals — 184.4±64.6 U/l versus 90.1±37.2 U/l (p=0.030). A significant increase of laboratory markers of intrahepatic cholestasis, HOMA-IR, TNF-α, cholesterol, low-density lipoproteins, triglycerides, glucose and NAFLD FS were revealed in patients with liver steatosis relative to the control. The level of CK-18 correlated only with cholesterol in LS — r=+0,70 (p=0,004). Conclusion. An increased CK-18 level of hepatocyte apoptosis marker was detected in an early form of NAFLD — liver steatosis, indicating the risk of progression of this disease. The close relationship between the content of CK-18 and the level of cholesterol in the blood confirmed the role of the latter in the development of hepatocyte apoptosis. Therapy is aimed at arresting hepatocyte apoptosis and normalization of cholesterol levels, appropriate for the earliest form of NAFLD — liver steatosis.

      1. Ivashkin V.T., Mayevskaya M.V., Pavlov Ch.S., Tikhonov I.N., et al. Diagnostics and treatment of non-alcoholic fatty liver disease: clinical guidelines of the Russian Scientific Liver Society and the Russian gastroenterological association. Ross z gastroenterol gepatol koloproktol 2016; 26(2):24-42.
      2. Lazebnik L.B., Radchenko V.G., Golovanova E.V., Zvenigorodskaya L.A., Konev Yu. V. et al. Nonalcoholic fatty liver disease: diagnostic, symptoms, treatment guidelines were approved by the xv gastroenterological scientific society of russia in 2015. Experimental and Clinical Gastroenterology. 2015; 119(7):85–97.
      3. Ivashkin V.T., Drapkina O.M., Mayev I.V., Trukhmanov A.S., et al. Prevalence of non-alcoholic fatty liver disease in out-patients of the Russian Federation: DIREG 2 study results. Ross z gastroenterol gepatol koloproktol 2016; 25(6):31-41.
      4. Guicciardi M. E., Gores G. J. Apoptosis as a mechanism for liver disease progression. // Semin. Liver Dis. — 2010. — Vol. 30 (4). — P. 402–410.
      5. Aida Y., Abe H., Tomita Y., Nagano T., Seki N., Sugita T., Itagaki M. et al. Serum cytokeratin 18 fragment level as a noninvasive biomarker for non-alcoholic fatty liver disease. // Int. J. Clin. Exp. Med. — 2014. — Vol. 7. — P. 4191–4198
      6. Arab J. P., Hernández-Rocha C., Morales C., Vargas J. I., Solís N., Pizarro M. et al. Serum cytokeratin-18 fragment levels as noninvasive marker of nonalcoholic steatohepatitis in the chilean population. // Gastroenterol. Hepatol. — 2017. — Vol. 40 (6). — P. 388–394.
      7. Shen J., Chan H. L.-Y., Wong G. L.-H., Choi P. C.L., Chan L. W-H., Chim A. M.-L.et al. Non-invasive diagnosis of nonalcoholic steatohepatitis by combined serum biomarkers. // J. Hepatol. — 2012. — Vol. 56. — P. 1363–1370.
      8. Wu G., Li H., Fang Q., Zhang J., Zhang M., Zhang L. et al. Complementary Role of Fibroblast Growth Factor 21 and Cytokeratin 18 in Monitoring the Different Stages of Nonalcoholic Fatty Liver Disease. // Sci. Rep. — 2017. — Vol. 7 (1). — P. 5095.
      9. Angulo P., Hui J. M., Marchesini G., Bugianesi E., George J., Farrell G. C. et al. The NAFLD fibrosis score: a noninvasive system that identifies liver fibrosis in patients with NAFLD. // Hepatology. — 2007. — Vol. 45 (4). — P. 846–54.
      10. Brunt E. M., Janney C. G., Di Bisceqlie A. M., Neuschwander-Tetri B. A., Bacon B. R. Nonalcoholic steatohepatitis: a proposal for grading and staging the histological lesions. // Am. J. Gastroenterol. — 1999. — Vol. 94 (9). — P. 2467–2474.
      11. Canbay A., Feldstein A. E., Higuchi H., Werneburg N., Grambihler A., Bronk S. F. et al. Kupffer cell engulfment of apoptotic bodies stimulates death ligand and cytokine expression // Hepatology. — 2003. — Vol. 38 (5). — P. 1188–1198.
      12. Cusi K., Chang Z., Harrison S., Lomonaco R., Bril F., Orsak B. et al. Limited value of plasma cytokeratin-18 as a biomarker for NASH and fibrosis in patients with non-alco¬holic fatty liver disease. // J. Hepatol. — 2014. — Vol. 60. — P. 167–174.
      13. Ioannou G. N. The Role of Cholesterol in the Pathogenesis of NASH. // Trends Endocrinol. Metab. — 2016. — Vol. 27 (2). — P. 84–95.
      14. Wang K. Molecular mechanisms of hepatic apoptosis. // Cell Death Dis. — 2014. — Vol. 5 (1). — P. e996.
     


    Full text is published :
    Dudanova O. P., Shipovskaya A. A., Kurbatova I. V. Apoptosis of hepatocytes in the early form of non-alcoholic fatty liver disease. Experimental and Clinical Gastroenterology. 2018;157(9): 81–85. DOI: 10.31146/1682-8658-ecg-157-9-81-85.
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    1. Federal State Budgetary Institution “Almazov National Medical Research Centre” of the Ministry of Health of the Russian Federation (197341, Saint-Petersburg, Russia)
    2. Federal State Budgetary Educational Institution of Higher Education “Academician I.P. Pavlov First St. Petersburg State Medical University” of the Ministry of Healthcare of Russian Federation (197022, Saint-Petersburg, Russia)

    Keywords: Non-alcoholic fatty liver disease, type 2 diabetes mellitus; obesity; adipocytokines; leptin; adiponectin; glucagon-like peptide-1; ghrelin; incretinomimetics; galectin-3, markers of fibrosis: glucagon-like peptide-1 receptors agonists

    Abstract:Therapy of glucagon-like peptide 1 receptors agonists (aGLP1) liraglutide within 24 weeks led to considerable weight reduction, a circle of a waist, HbA1c, TG, AST and increase in HDLP at patients with type 2 diabetes mellitus (2TDM) and multiple manifestations of metabolic syndrome (obesity, dyslipidemia, hypertension) in real clinical practice. Effects of therapy liraglutide on the markers of fibrosis and a scale estimating risk of its progression were ambiguous and depended on various predictors. Decrease in the index of fibrosis on therapy aGLP1 depended on a floor and extent of increase in HDLP. Dynamics galectin-3 depended on weight reduction and its significant decrease is noted only at patients with loss weight ≥ 5%. Initial levels of incretin (GIP and GLP1) acted as predictors of decrease in PIIINP. Further researches on big cohorts of patients with obesity, a metabolic syndrome and 2TDM are necessary for definition of groups of the patients capable it is essential to reduce risk of a progression of fibrosis on therapy aGLP1

      1. Shen J., Goyal A., Sperling L. The emerging epidemic of obesity, diabetes, and the metabolic syndrome in china. Cardiology Research and Practice. — 2012. — 178–675.
      2. Younossi Z.M., Koenig A.B., Abdelatif D. et al. Global epidemiology of nonalcoholic fatty liver disease-metaanalytic assessment of prevalence, incidence, and outcomes. Hepatology. — 2016. —64. — 73–84.
      3. Dam-Larsen S., Franzmann M., Andersen I.B. et al. Long term prognosis of fatty liver: risk of chronic liver disease and death. Gut. — 2004. —53.—750–5.
      4. Dyson J.K., Anstee Q.M., McPherson S. Non-alcoholic fatty liver disease: a practical approach to diagnosis and staging. Frontline Gastroenterol. — 2014. —5(3). — 211–218.
      5. Wong V.W., Wong G.L., Choi P.C. et al. Disease progression of non-alcoholic fatty liver disease: a prospective study with paired liver biopsies at 3 years. Gut. — 2010. — 59.  — 969–74.
      6. The Diagnosis and Management of Non-alcoholic Fatty Liver Disease: Practice Guideline by the American Gastroenterological Association, American Association for the Study of Liver Diseases, and American College of Gastroenterology. Gastroenterology — 2012. — 142. — 1592–1609.
      7. Lee J.H., Kim D., Kim H.J. et al. Hepatic steatosis index: a simple screening tool refl ecting nonalcoholic fatty liver disease. Digestive and Liver Disease. — 2010. — 42(7). — 503–8.
      8. Dvorak K., Stritesky J., Petrtyl J. et al. Use of non-invasive parameters of nonalcoholic steatohepatitis and liver fi brosis in daily practice-an exploratory casecontrol study. PLOS One. — 2014. — 9(10):e111551. doi: 10.1371/journal. pone.0111551.
      9. Torres D.M., Harrison S.A. Nonalcoholic Fatty Liver Disease. In.: Sleisenger and Fordtran’s Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, Management / ed. by Mark Feldman, Lawrence S Friedman, Laurence J Brandt. — 10th ed. 2015.
      10. Angulo P., Hui J.M., Marchesini G. et al. The NAFLD fi brosis score: a noninvasive system that identifi es liver fi brosis in patients with NAFLD. Hepatology. — 2007. — 45. — 846–54.
      11. Loaeza-del-Castillo A., Paz-Pineda F., OviedoCardenas E. at al. AST to platelet ratio index (APRI) for the noninvasive evaluation of liver fibrosis. Annals of Hepatology. — 2008. — 7(4). — 350–357.
      12. Shah A.G., Lydecker A., Murray K. et al. Comparison of noninvasive markers of fi brosis in patients with nonalcoholic fatty liver disease. Clinical Gastroenterology and Hepatology. — 2009. — 7 (10). — 1104–12.
      13. McPherson S., Anstee Q.M., Henderson E. et al. Are simple noninvasive scoring systems for fi brosis reliable in patients with NAFLD and normal ALT levels. European Journal of Gastroenterology & Hepatology. — 2013. — 25. — 652–658.
      14. Shiiya T., Nakazato M., Mizuta M. et al. Plasma ghrelin levels in lean and obese humans and the effect of glucose on ghrelin secretion The Journal of Clinical Endocrinology and Metabolism. — 2002. — 87(1). — 240–244.
      15. Crujeiras A.B., Goyenechea E., Abete I. et al. Weight regain after a diet-induced loss is predicted by higher baseline leptin and lower ghrelin plasma levels. Journal Of Clinical Endocrinology And Metabolism. — 2010. — 95(11). — 5037–5044.
      16. Finan B., Müller T.D., Clemmensen C. Reappraisal of GIP Pharmacology for Metabolic Diseases. Trends in Molecular Medicine. — May 2016. — Vol. 22 № 5. — 1–8.
      17. Buechler С., Haber E.M., Rein-Fischboeck L., Aslanidis C. Adipokines in Liver Cirrhosis International Journal of Molecular Sciences. — 2017. — 18. —1392.
      18. Marchesini G., Pagotto U., Bugianesi E. et al. Low ghrelin concentrations in nonalcoholic fatty liver disease arerelated to insulin resistance. The Journal of Clinical Endocrinology and Metabolism. — 2003. — 8(12). — 5674–9.
      19. Armstrong M. J., Barton D., Gaunt P. et al. Liraglutide efficacy and action in non-alcoholic steatohepatitis (LEAN): study protocol for a phase II multicentre, double-blinded, randomised, controlled trial. BMJ Open. — 2013. — 4. — 3(11). 2013;3:e003995. doi:10.1136/ bmjopen-2013 — 003995.
      20. Mykhalchyshyn G., Kobyliak N., Bodnar P. Diagnostic accuracy of acyl-ghrelin and it association with nonalcoholic fatty liver disease in type 2 diabetic patients Journal of Diabetes and Metabolic Disorders. — 2015. — Vol. 19, № 14. — 44.
      21. Tanwar S., Trembling P.M., Guha I.N. et al. Validation of terminal peptide of procollagen III for the detection and assessment of nonalcoholic steatohepatitis in patients with nonalcoholic fatty liver disease. Hepatology. — 2013. — 57(1). — 103–11.
      22. Wang Н., Lafdil F., Wang L. et al. Tissue inhibitor of metalloproteinase 1 (TIMP-1) deficiency exacerbates carbon tetrachloride-induced liver injury and fibrosis in mice: involvement of hepatocyte STAT3 in TIMP-1 production. Cell & Bioscience. — 2011. — 1. — 14.
      23. Chiba Y., Sugawara D., Tanaka Y. et al. The Evaluation of Procollagen Type III N-Terminal Peptide(P IIIP) As a Marker of Fatty Liver Change in Obese Children and Adolescents. Endocrine Society's 98th Annual Meeting and Expo, April 1–4, 2016 — Boston. Presentation Number: FRI-001 Date of Presentation: April 1, 2016.
      24. Chalasani N., Younossi Z., Lavine J.E. et al; American Gastroenterological Association, American Association for the Study of Liver Diseases, American College of Gastroenterology. The diagnosis and management of non-alcoholic fatty liver disease: practice guideline by the American Gastroenterological Association, American Association for the Study of Liver Diseases, and American College of Gastroenterology. Gastroenterology. — 2012. — 142. — 1592–609.
      25. Yoneda M., Sumida Y. Current and future pharmacological therapies for NAFLD/NASH. Journal of Gastroenterology. — 2018. — 53. — 362–376.
      26. Barb D., Portillo-Sanchez P., Cusi K. Pharmacological management of nonalcoholic fatty liver disease. Metabolism clinical and Experimental 65. — 2016. — 1183–1195.
      27. Abdul-Ghani M., DeFronzo R.A. Is It Time to Change the Type 2 Diabetes Treatment Paradigm? Yes! GLP-1 Ras Should Replace Metformin in the Type 2 Diabetes Algorithm Diabetes Care. — 2017. — 40. — 1121–1127.
      28. Pappachan J.M. , Babu S., Krishnan B.,Ravindran M. Non-alcoholic Fatty Liver Disease: A Clinical Update. Journal of Clinical and Translational Hepatology. — 2017. — December 28; 5(4). — 384–393.
      29. Armstrong MJ, Barton D, Gaunt P, et al. Liraglutide efficacy and action in non-alcoholic steatohepatitis (LEAN): study protocol for a phase II multicentre, double-blinded, randomised, controlled trial. BMJ Open 2013;3:e003995. doi:10.1136/bmjopen-2013 — 003995.
      30. Eguchi Y. et al. Pilot study of liraglutide effects in nonalcoholic steatohepatitis and non-alcoholic fatty liver disease with glucose intolerance in Japanese patients (LEAN-J). Hepatology Research. — 2014 doi: 10.1111/ hepr.12351.
      31. Belyaeva O.D., Bazhenova E.A., Berezina A.V., et al. Adiponectin levels, lipid profile and glucose metabolism in patients with abdominal obesity. Arterial Hypertension. 2009; 15(3):309–314.
      32. Tikhonenko E.V., Tsoy U.A., Vasilieva E.Yu., Babenko A. Yu. Characteristics of eating behavior and the level of hormones regulating the appetite in patients with type 2 diabetes mellitus and body mass index more than 35. Obesity and metabolism. 2018; 15(1): 30–38. https://doi. org/10.14341/omet2018130–38.
      33. Takaki А., Kawai D., Yamamoto К. Multiple Hits, Including Oxidative Stress, as Pathogenesis and Treatment Target in Non-Alcoholic Steatohepatitis (NASH). International Journal of Molecular Sciences. — 2013. — October14 (10). — 20704–20728.
      34. Babenko A.Yu., Tikhonenko E.V., Shlyahto E.V. Predictors of efficacy of glucagon-like peptide-1 receptor agonist therapy in patients with type 2 diabetes and obesity. Obesity and metabolism. 2018;15(4) (in print).
      35. Amato M.C., Giordano C., Pitrone M., Galluzzo A. A Cut-off points of the visceral adiposity index (VAI) identifying a visceral adipose dysfunction associated with cardiometabolic risk in a Caucasian Sicilian population. Lipids Health Dis. — 2011. — № 10. — 183.
     


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    Babenko A.Yu., Laevskaya M.Yu., Trofimova A.Yu., Simanenkova A.V. et al. Dynamics of markers of hepatic fibrosis on therapy liraglutide at patients with type 2 diabetes mellitus in combination with a metabolic syndrome. Experimental and Clinical Gastroenterology. 2018;157(9): 86–94. DOI: 10.31146/1682-8658-ecg-157-9-86-94.
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    1. Saratov State Medical University named after V. I. Razumovsky (410012, Saratov, Russia)

    Keywords:sarcoidosis, pathology of digestive organs

    Abstract:Methods of retrospective analysis analyzed the case histories of 85 patients that hospitalized in the pulmonology department of the Saratov City Clinical Hospital No.8 in 2015-2017 with sarcoidosis of the intrathoracic lymph nodes and lungs. Pathology of the gastrointestinal tract was detected in 28% of cases. The most frequent disease was chronic gastroduodenitis, in the most cases it was asymptomatic. The revealed pathology of the gastrointestinal tract was not associated with drug therapy of sarcoidosis of the intrathoracic lymph nodes and lungs. Perhaps the described combinations can be considered as a manifestation of the comorbidity of diseases of the gastrointestinal tract and bronchopulmonary system.

      1. Chuchalin A.G., Vizel A.A., Ilkovich M.M., Avdreev S.N., et al. Diagnosis and treatment of sarcoidosis. Sammary of federal conciliative clinical recommendation. part І. Classification, etiopathogenesis, clinic. The Bulletin of Contemporary Clinical Medicine. 2014, Vol.7, no. 4, pp. 62–70.
      2. Chuchalin A.G., Vizel A.A., Ilkovich M.M., Avdreev S.N., et al. Diagnosis and treatment of sarcoidosis. Sammary of federal conciliative clinical recommendation (part ІІ. diagnosis, treatment, prognosis). The Bulletin of Contemporary Clinical Medicine. 2014, Vol. 7, no. 5, pp. 73–81.
      3. Vizel A.A., Vizel I.Yu. Epidemiology of sarcoidosis in the Russian Federation. The Bulletin of Contemporary Clinical Medicine. 2017, Vol.10, no. 5, pp. 66–73.
      4. Mortaz E, Adcock IM, Barnes PJ. Sarcoidosis: Role of non-tuberculosis mycobacteria and Mycobacterium tuberculosis // Int. J. Mycobacteriol. 2014. 3 (4). Р. 225–229.
      5. Iannuzzi MC. Advances in the genetics of sarcoidosis.// Proc. Am. Thorac. 2007. 4 (5).Р. 457–60.
      6. Chernikov A.Yu., Zemlyanskikh L.G. Fenotipy sarkoidoza. Pulmonologiya. 2012, no. 5, pp. 53–55.
      7. Vizel A.A., Amirov N.B. Sarcoidosis and digestive system organs involvement. The Bulletin of Contemporary Clinical Medicine. 2010, Vol. 3, no. 1, pp. 43–50.
      8. Surattanont F, Mandel B, Wolinsky F et al. Bilateral parotid swelling caused by sarcoidosis //J. Am. Dent. Assoc. 2002. No. 133(6). Р. 738–744.
      9. Munker M., Sharma O. Fatal gastrointestinal hemorrhage in sarcoidosis. A previously unreported occurrence // Sarcoidosis. 2007; 4 (5): 457-60.
      10. Medvedev A.V. Gastroezofagealno-reflyuksnaya bolezn u bolnykh sarkoidozom legkikh i vnutrigrudnykh limfaticheskikh uzlov. Evraziyskiy Nauchnyy Zhurnal. 2016, no. 6. (http://www.gastroscan.ru/literature/ authors/9237).
      11. Maev I.V., Andreyev D.N., Kucheryavyy Yu.A. Gastric sarcoidosis. Сlinical medicine. 2014, no 3, pp. 21–27.
      12. Akinyemi E, Rohewal U, Tangorra M, Abdullah M. Gastric sarcoidosis. // J. Natl. Med. Assoc. 2006; 98 (6): 948–9.
      13. Nomata M, Ikushima S, Awano N et al. Upper gastrointestinal sarcoidosis: report of three cases. // Intern. Med. 2012; 51 (13): 1689–94.
      14. Hernandez CJ, Gonzalez BS. Pulmonary and gastric sarcoidosis: report of one case. // Rev. Med. Chil. 2009. Vol. 137. No.7. P. 923–927.
      15. Mayev I.V., Penkina T.V., Dicheva D.T., Andreyev D.N. Generalizovannyy sarkoidoz. Klinicheskaya gepatologiya. 2012, Vol. 92, no. 11, pp. 37–39.
      16. Mayev I.V., Pavlov Ch.S., Diyeva D.T., Penkina T.V., Andreev D.N. Portal hypertension as a clinical manifestation of hepatic lesions in sarcoidosis. Сlinical medicine. 2012, Vol. 90, no. 11, pp. 64–67.
      17. Baroni RH, Pedrosa I, Tavernaraki E et al. Pancreatic sarcoidosis: MRI features //J. Magn. Reson. Imaging. 2004. № 20(5). Р. 889–893.
      18. Romboli E, Campana D, Piscitelli L et al. Pancreatic involvement in systemic sarcoidosis // A case report Dig. Liver Dis. 2004. No. 36 (3). Р. 222–227.
      19. Fordice J, Katras T, Jackson RE et al. Massive splenomegaly in sarcoidosis //South Med. J. 1992. Vol. 85. No. 7. P. 775– 778.
      20. Vizel A.A., Vizel I.Yu. Sarcoidosis as pathology of bloodmaking organs and immune system from literature data to authors' observations. Pacific Medical Journal. 2011, no. 2, pp. 18–23.
      21. Baughman R, Lower EE. Treatment of sarcoidosis // Clin. Rev. Allergy Immunol. 2015.49 (1). Р 79–92.
     


    Full text is published :
    Shapovalova T.G., Shashina M.M., Ryabova A.Yu., Arhangelskaya E.E.et al. Pathology of digestive organs in group of patients with sarcoidosis: a vision of the pulmonary physician. Experimental and Clinical Gastroenterology. 2018;157(9): 95–100. DOI: 10.31146/1682-8658ecg-157-9-95-100.
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