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    1. Centre for Strategic Planning and Management of Biomedical Health Risks, 119992, Moscow, Russia
    2. L. M. Sechenov First Moscow State Medical University, 119991, Moscow, Russia

    Keywords: infl ammation bowel disease, aetiopathogenesis, commensal gut microbiota, Akkermansia muciniphila, dysfunction of local immune responses, intestinal infl ammation, probiotics, metabiotics, FMT, clinical application in IBD

    Abstract:Infl ammatory bowel disease (IBD) has increasing socio-medical and economic signifi cance for humans. Although the aetiopathogenesis of IBD is not fully established, it is believed that the imbalance of intestinal microbiota of the gastrointestinal tract and modifi cation of the intestinal immune system are the most important triggering mechanisms of risk, development and progression of IBD, their relapses and activation. Epidemiological, microbiological and immunological studies have identifi ed some pathogenic and commensal intestinal bacteria that can induce disturbances of local immune responses and predispose the risk of IBD. The review deals with the mechanism of participation of commensal intestinal anaerobic gram-negative Akkermansia muciniphila in the destruction and metabolism of the intestinal mucosa and modulation of epigenetic mechanisms, physiological, metabolic, immune and signal functions associated with the development of IBD. The use and limitations of these living bacterial commensals and their low molecular weight components and metabolites in the prevention and treatment of IBD are discussed. Challenges, limitations and potential improvement strategies using some commensal anaerobic bacteria and fecal microbiota transplantation in IBD are also considered.

      1. Ahluwalia B, Moraes L, Magnusson MK, Ohman L. Immunopathogenesis of infl ammatory bowel disease and mechanisms of biological therapies. Scandin J Gastroenterol 2018; 53(4): 379–389
      2. Kaplan GG. Th e global burden of IBD: from 2015 to 2025. Nat Rev Gastroenterol Hepatol 2015; 12(12): 720–727.
      3. Proal AD, Lindseth IA, Marshall TG. Microbe-microbe and host-microbe interactions drive microbiome dysbiosis and infl ammatory processes. Discov Med 2017; 23(124): 51–60
      4. Grigg JB, Sonnenberg GF. Host-Microbiota Interactions Shape Local and Systemic Infl ammatory Diseases. J Immunol 2017; 198(2): 564–571 jimmunol.160621
      5. Forbes JD, Van Domselaar G, Bernstein CN. Th e Gut Microbiota in Immune-Mediated Infl ammatory Diseases. Front. Microbiol 2016; 7: 1081. Doi; 10.3389/fmicb.2016.01081
      6. Hur SJ, Kang SH, Jung HS, Kim SC, Jeon HS, Kim IH, Lee JD. Review of natural products actions on cytokines in infl ammatory bowel disease. Nutr Res 2012; 32: 801–816
      7. Hold GL, Smith M, Grange C, Watt ER, El-Omar EM, Mukhopadhya I. Role of the gut microbiota in infl ammatory bowel disease pathogenesis: What have we learnt in the past 10 years? World J Gastroenterol 2014; 20(5): 1192–1210
      8. Tedjo DI, Smolinska A, Savelkoul PH, Masclee AA, Schooten FJ, Pierik MJ, et al. Th e fecal microbiota as a biomarker for disease activity in Crohn’s disease. Scientifi c Reports 2016; 6:35216. Doi: 10.1038/strep35216
      9. Shen ZH, Zhu CX, Quan YS, Yang ZY, Wu S, Luo WW, et al. Relationship between intestinal microbiota and ulcerative colitis: Mechanisms and clinical application of probiotics and fecal microbiota transplantation. World J Gastroenterol 2018; 24(1): 5–14
      10. Mijan MA, Lim BO. Diets, functional foods, and nutraceuticals as alternative therapies for infl ammatory bowel disease: Present status and future trends. World J Gastroenterol 2018; 24(25): 2673–2685
      11. Hedin CR, van der Gast CJ, Stagg AJ, Lindsay JO, Whelan K. Th e gut microbiota of siblings off ers insights into microbial pathogenesis of infl ammatory bowel disease. GUT MICROBES2017; 8(4): 359–365
      12. Moustafa A, Li W, Anderson EL, Wong EHM, Dulai PS, Sandborn WJ, et al. Genetic risk, dysbiosis, and treatment stratifi cation using host genome and gut microbiome in infl ammatory bowel disease. Clin Transl Gastroenterol 2018; 9(1): e132 doi: 10.1038/ctg.2017.58.
      13. Seregin SS, Natasha Golovchenko N, Schaf B, Chen J, Pudlo NA, Mitchell J et al. NLRP6 protects IL10–/– mice from colitis by limiting colonization of Akkermansia muciniphila. Cell Rep. 2017; 19(4): 733–745.
      14. Shi N, Li N, Duan X, Niu H. Interaction between the gut microbiome and mucosal immune system. Military Med. Res. 2017. 4:14. doi: 10.1186/s40779–017–0122–9
      15. Tailford LE, Crost EH, Kavanaugh D, Juge N. Mucin glycan foraging in the human gut microbiome. Front. Genet.2015; 6:81. doi: 10.3389/fgene.2015.00081
      16. Bansil R, Turner DS. Th e biology of mucus: Composition, synthesis and organization. Advanced Drug Delivery Reviews 2018; 124: 3–15
      17. Hooper LV, Littman DR, Macpherson AJ. Interaction between the microbiota and the immune system. Science 2012; 336: 1268–1273
      18. Selber-Hnativ S, Rukundo B, Ahmadi M, Akoubi H, Al-Bizri H, Aliu AF et al. Human Gut Microbiota: Towards an Ecology of Disease. Front Microb 2017. 17 July. Doi:10.3389/ fmicb.2017.01265
      19. Lemire P, Robertson SJ, Maughan H, Tattoli I, Streutker CJ, Platnich JM et al. Th e NLR Protein HLP6 Does not impact gut microbiota composition. Cell Reports 2017; 21:3653–3661
      20. Li N, Shi R-H. Updated review on immune factors in pathogenesis of Crohn’s disease. World J Gastroenerol 2018; 24(1): 15–22
      21. Kamada N, Nunez G. Regulation of the immune system by the resident intestinal bacteria. Gastroenterology 2014; 146(6): 1477–1488
      22. Hornef M. Pathogens, commensal symbionts, and pathobionts: discovery and functional eff ects on the host. Ilar J 2015; 56(2):159–162,
      23. Voreades N, Kozil A, Weir T L. Diet and the development of the human intestinal microbiome. Front. Microbiol. 2014; 5:494. doi: 10.3389/fmicb.2014.00494
      24. Filyk HA, Osborne LC. Th e multibiome: Th e Intestinal Ecosystem’s Infl uence on Immune Homeostasis, Health, and Diseases. EBioMedicine 2016; 13: 46–54
      25. Shenderov BA. Human microbial ecology and its role in health supporting. Metamorphoses 2014; N5: 72–80. (in Russian)
      26. Sonnenberg A, Genta RM. Low prevalence of Helicobacter pylori infection among patients with infl ammatory bowel disease. Aliment Pharmacol Th er 2012; 35: 469–476
      27. Shenderov BA, Midtvedt T. Epigenomic programing: a future way to health? Microbial ecology in Health & Disease 2014, 25: 24145– v25.24145
      28. Shenderov BA. Th e role of nutrition and symbiotic microbiota in epigenetics of chronic somatic disorders. Voprosi dietologii, 2015, 5, № 1: 22–23 (in Russian)
      29. Shenderov BA. Th e role of nutrition and symbiotic microbiota in epigenetics of chronic somatic disorders. Voprosi dietologii, 2015, 5, № 1: 22–23 (in Russian)
      30. Devaux CA, Raoult D. Th e microbiological Memory, an Epigenetic Regulator Governing the balance between good health and metaboplic disorders. Front Microbiol 2018; 9;1379. Doi;10.3389/fmicb.2018.01379
      31. Spehlmann ME, Begun AZ, Burghardt J, Lepage P, Raedler A, Schreiber S. Epidemiology of infl ammatory bowel disease in a german twin cohort: results of a nationwide study. Infl amm Bowel Dis. 2008;14: 968–976
      32. Bernstein CN, Forbes JD. Gut microbiome inn infl ammatory bowel disease and other chronic immune-mediated infl ammatory diseases. Infl am Intest Dis 2017; 2(2): 116–123
      33. Ma H-Q, Yu T-T, Zhao X-J, Zhang Yi, Zhang H-J. Fecal microbial dysbiosis in Chinese patients with infl ammatory bowel disease 2018; 24(13): 1464–1477
      34. Park JH, Peyrin-Biroulet L, Eisenhut M, Shin J I. IBD immunopathogenesis: a comprehensive review of inflammatory molecules. Autoimmun. Rev. 2017; 16: 416–426
      35. Rajilic-Stojanovic M, Shanahan F, Guarner F, de Vos WM. Phylogenetic analysis of dysbiosis in ulcerative colitis during remission. Infl amm Bowel Dis. 2013; 19(3): 481–488.
      36. Actis GC, Pellicano R. Th e pathologic galaxy modulating the genotype and phenotype of infl ammatory bowel disease: comorbidity, contiguity, and genetic and epigenetic factors. Minerva Med 2016; 107: 401–412
      37. Alipour M, Zaidi D, Valcheva R, Jovel J, Martínez I, Sergi C et al. Mucosal Barrier Depletion and Loss of Bacterial Diversity are Primary Abnormalities in Paediatric Ulcerative Colitis. J Crohns Colitis 2016; 10: 462–471
      38. Griffi n NW, Ahern PP, Cheng J, Heath A C, Ilkayeva O, Newgard C B, et al. Prior dietary practises and connections to a human gut microbial metacomminity alter responses to diet interventions. Host Microbe 2017; 21: 84–96.
      39. Barroso-Batista J, Sousa A, Lourenço M, Bergman M L, Sobra D, Demengeo J et al. Th e first steps of adaptation of Escherichia coli to the gut are dominated by soft sweeps. PLoS Genet. 2014 10: e1004182. doi: 10.1371/journal. pgen.1004182
      40. Hormannsperger G, Haller D. Molecular crosstalk of probiotic bacteria with the intestinal immune system: clinical relevance in the context of infl ammatory bowel disease. Int J Med Microbiol 2010; 300: 63–73.
      41. Vigsnaes LK, Brynskov J, Steenholdt C, Wilcks A, Licht TR. Gram-negative bacteria account for main differences between faecal microbiota from patients with ulcerative colitis and healthy controls. Benefi cial microbes. 2012; 3(4): 287–297
      42. Martin R., Miqquel S, Ulmer J, Kechaou N, Langella P, Bermúdez-Humarán LG. Role of commensal and probiotic bacteria in human health: a focus on infl ammatory bowel disease. Microbial Cell Factories 2013, 12:71
      43. Sartor RB, Wu GD. Roles for intestinal bacteria, viruses, and fungi in pathogenesis of infl ammatory bowel diseases and therapeutic approaches. Gastroenterology 2017;152(2): 327–339.
      44. Mcllroy J, Ianiro G, Mukhopadhya I, Hansen R, Hold GL. Review article: the gut microbiome in infl ammatory bowel disease-avenues for microbial management. Aliment Pharmacol Th er 2018; 47: 26–42
      45. Cani PD. Human gut microbiome: hopes, threats and promises. Gut 2018; 1–10. Doi:10.1136/gutjnl-2018–316723
      46. Donaldson GP, Lee SM, Mazmanian SK. Gut biogeography of the bacterial microbiota. Nat Rev Microbiol. 2016 Jan;14(1): 20–32.
      47. Ottman N, Reunanen J, Meijerink M, Pietilä TE, Kainulainen V, Klievink J et al. Pili-like proteins of Akkermansia muciniphila modulate host immune responses and gut barrier function. PLoS One 2017a;12: e0173004. Doi; 10.1371/ journal.pone.0173004
      48. Derrien M, Belzer C, de Vos WM. Akkermansia muciniphila and its role in regulating host functions. Microbial Pathogenesis 2016.
      49. Derrien M, Van Baarlen P, Hooiveld G, Norin E, Muller M, de Vos WM. Modulation of mucosal immune response, tolerantce, and proliferation in mice colonized by the mucin-degrader Akkermansia muciniphila. Front Microbiol 2011; 2: 166. Doi: 10.3389/fmicb.2011.00166
      50. Png CW, Linden SK, Gilshenan KS, Zoetendal EG, McSweeney CS, Sly LI, et al. Mucolytic bacteria with increased prevalence in IBD mucosa augment in vitro utilization of mucin by other bacteria. Am J Gastroenterol. 2010; 105(11): 2420–2428
      51. Plovier H, Everard A, Druart C, Depommier C, Van Matthias H, Geurts L et al. A purifi ed membrane protein from Akkermansia muciniphila or the pasteurized bacterium improves metabolism in obese and diabetic mice. Nature Med 2017; 23: 107–113
      52. Burokas A, Arboleya S, Moloney RD, Peterson VL, Murphy K, Clarke G, et al. Targeting the Microbiota-Gut-Brain Axis: Prebiotics Have Anxiolytic and Antidepressant-like Eff ects and Reverse the Impact of Chronic Stress in Mice, Biol Psychiatry. 2017/DOI:10.1016/j.biopsych.2016.12.031
      53. Wu W., Lv L, Ye J, Fang D, Guo F, Li Y et al. Protective Eff ect of Akkermkansia muciniphila against Immune-mediated Liver Injury in a Mouse Model. Front. Microbiol 2017; 8: 1804 doi:10.3389/fmicb.2017.01804
      54. Shah R, Cope JL, Nagy-Szakal D, Dowd S, Versalovic J, Hollister EB, Kellermayer R. Composition and function of the pediatric colonic mucosal microbiome in untreated patients with ulcerative colitis, Gut Microbes 2016; 7 (5): 384–396
      55. Bajer L, Kverka M, Kostovcik M, Macinga P, Dvorak J, Stehlikova Z et al. Distinct gut microbiota profi les in patients with primary sclerosing cholangitis and ulcerative colitis. World J Gastroenterol 2017; 23: 4548–4558
      56. Shang Q, Sun W, Shan X, Jiang H, Cai C, Hao J et al. Carrageenan-induced colitis is associated with decreased population of anti-infl ammatory bacterium, Akkermansia muciniphila, in the gut microbiota of C57BL/6J mice. Toxicol Lett 2017; 279: 87–95
      57. Cani PD, de Vos WM. 2017. Next-Generation Benefi cial Microbes: Th e Case of Akkermansia muciniphila. Frontiers in Microbiology, 8, 1765. article/10.3389/fmicb.2017.01765/full
      58. Tan L, Zhao S, Zhu W, Wu L, Li J, Shen M. et al, Th e Akkermansia muciniphila is a gut microbiota signature in psoriasis. Exp Dermatol. 2018; 27(2):144–149.
      59. Angriman I, Scarpa M, Castagliuolo I. Relationship between pouch microbiota and pouchitis following restorative proctocolectomy for ulcerative colitis. World J Gastroenterol 2014; 20(29): 9665–9674
      60. Zhang YJ, Li S, Gan RY, Zhou T, Xu DP, Li HB. Impacts of gut bacteria on human health and diseases. Int J Mol Sci 2015; 16: 7493–7519
      61. Ganesh BP, Klopfl eisch R, Loh G, Blaut M. Commensal Akkermansia muciniphila exacerbates gut infl ammation in Salmonella typhimurium-infected gnotobiotic mice. PLoS One. 2013; 8: e74963.
      62. Baxter NT, Zackular JP, Chen GY, Schloss PD. Structure of the gut microbiome following colonization with human feces determines colonic tumor burden. Microbiome 2014 Jun 17; 2:20. doi: 10.1186/2049–2618–2–20. eCollection.
      63. Wopereis H, Oozeer R, Knipping K, Belzer C, Knol J. Th e first thousand days – intestinal microbiology of early life: establishing a symbiosis. Pediatr Allergy Immunol 2014: 25: 428–438
      64. Mithieux G. Does Akkermansia muciniphila play a role in type 1 diabetes? Gut 2018: gutjnl-2017–315732
      65. Mendes MC, Paulino DSM, Brambilla SA, Camargo JA, Persinoti GF, Carvalheira JBC. Microbiota modifi cation by probiotic supplementation reduces colitis associated colon cancer in mice. World J Castroenterol 2018; 24(28): 1995–2008
      66. Rossen NG, Fuentes S, van der Spek MJ, Tijssen JG, Hartman JH, Duflou A et al. Findings from a randomized controlled trial of fecal transplantation for patients with ulcerative colitis. Gastroenterology 2015; 149: 110–118.
      67. Cao Y, Zhang B, Wu Y Wang O, Wang J, Shen F. Th e Value of Fecal Microbiota Transplantation in the Treatment of Ulcerative Colitis Patients: A Systematic Review and Meta-Analysis. Gastroenterology Research and Practice 2018; Article ID480961
      68. Khalili H, Chan SSM, Lochhead P, Ananthakrishnan AN, Hart AR, Chan A. Th e role of diet in the aetiopathogenesis of infl ammatory bowel diaease. Nat Rev Gastroenterol Hepatol 2018; 15: 525–535
      69. Duff W, Haskey N, Potter G, Alcorn J, Hunter P, Fowler S. Non-pharmacological therapies for infl ammatory bowel disease: Recommendations for self-care and physician guidance. World J Gastroenterol 2018; 24(28): 3055–3070

    Full text is published :
    Shenderov B. A., Yudin S. M., Zagaynova A. V., Shevyreva M. P. The role of commensal gut bacteria in the aetiopathogenesis of infl ammatory bowel disease: Akkermansia muciniphila. Experimental and Clinical Gastroenterology. 2018;159(11): 4–13. (In Russ.) DOI: 10.31146/1682-8658-ecg-159-11-4-13
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    1. Riga East clinical university hospital, Riga, Latvia
    2. Riga Stradins University, Riga, Latvia

    Abstract:The incidence of echinococcosis in European countries varies from 0.1 to 10 cases per 100,000 residents and Latvia has relatively high number of cases. The development of cystic echinococcosis is associated with the individual factors of the host organism, as well as immunological reactions and HLA DRB1 is the most polymorphic of the HLA class II genes and therefore it can be used for individual identifi cation. We can conclude that in the case of cystic echinococcosis a more severe course of a disease can be anticipated in the presence of HLA DRB1 alleles *17:01 and *04:01, DQB1 *03:02, DQA1*04:01. As well in the event of cystic echinococcosis HLA DRB1 alleles *01:01 and *15:01, DQA1 *01:01 can be considered as protective. Immunogenetic data could prove signifi cant for therapy planning in accordance with the individual characteristics of a patient, because no data on the optimal duration of therapy and whether the therapy can be terminated without facilitating the relapse of the infection are not currently available.

      1. Mosayebi M, Dalimi Asl A, Moazzeni M, Mosayebi G. Differential Genomics Output and Susceptibility of Iranian Patients with Unilocular Hydatidose. Iranian Journal of Parasitology. 2013;8(4):510–515.
      2. Eiermann TH, Bettens F, Tiberghien P, Schmitz K, Beurton I, Bresson-Hadni S, Ammann RW, Goldmann SF, Vuitton DA, Gottstein B, Kern P. HLA and alveolar echinococcosis. Tissue Antigens. 1998 Aug;52(2):124–9. PubMed PMID: 9756400.
      3. Lukmanova GI, Gumerov AA, Elicheva ZM, Lukmanova LI. [Distribution of HLA specifi city frequencies in patients with cystic echinococcosis]. Med Parazitol (Mosk). 2011 Oct-Dec;(4):14–6. Russian. PubMed PMID: 22308705.
      4. Chakhtoura M, Al-Awar G, Abdelnoor AM. Human leukocyte antigen (HLA) associations, antibody titers and circulating immune complexes in patients with cystic echinococcosis. Acta Parasitologica, 2007, 52(4), 414–418; ISSN1230–2821
      5. Hussein EM, Al-Mohammed HI, Al-Mulhim AS, Aboulmagd E. HLA class II DRB1 resistance and susceptible markers in hydatidosis Saudi patients in association to the clinical course and gender. J Egypt Soc Parasitol. 2012 Dec;42(3):573–82. PubMed PMID: 23469632.
      6. Al-Ghoury AB, El-Hamshary EM, Azazy AA, Hussein EM, Rayan HZ. HLA class II alleles: susceptibility or resistance to cystic echinococcosis in Yemeni patients. Parasitol Res. 2010 Jul;107(2):355–61. doi: 10.1007/s00436–010– 1868–0. Epub 2010 Apr 28. PubMed PMID: 20424860.
      7. Azab ME, Bishara SA, Helmy H, Oteifa NM, El-Hoseiny LM, Ramzy RM, Ahmed MA. Association of some HLA-DRB1 antigens with Echinococcus granulosus specifi c humoral immune response. J Egypt Soc Parasitol. 2004 Apr;34(1):183–96. PubMed PMID: 15125526.
      8. Yalcin E, Kiper N, Tan C, Ozcelik U, Dogru D, Cobanoglu N, Kose M, Pekcan S, Aslan AT, Ersoy F. Th e role of human leucocyte antigens in children with hydatid disease: their association with clinical condition and prognosis. Parasitol Res. 2010 Mar;106(4):795–800. doi: 10.1007/s00436–009–1719-z. Epub 2010 Jan 29. PubMed PMID: 20111876
      9. Aydinli B, Pirim I, Polat KY, Gursan N, Atamanalp SS, Ezer M, Donmez R. Association between hepatic alveolar echinococcosis and frequency of human leukocyte antigen class I and II alleles in Turkish patients. Hepatol Res. 2007 Oct;37(10):806–10. Epub 2007 Jun 15. PubMed PMID: 17573956

    Full text is published :
    Laivacuma S., Eglite J., Derovs A., Viksna L. Distribution of HLA allele frequencies in patients with cystic echinococcosis in Latvia. Experimental and Clinical Gastroenterology. 2018;159(11): 14–18. (In Russ.) DOI: 10.31146/1682-8658-ecg-159-11-14-18
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    1. St. Petersburg State Pediatric Medical University, St. Petersburg 194044, Russia
    2. I. P. Pavlov State Medical University First St. Petersburg State Medical University, St. Petersburg 197022, Russia
    3. Yu.E Veltischev Research and Clinical Institute for Pediatrics of the Pirogov Russian National Research Medical University, Moscow 125412, Russia

    Keywords: celiac disease, genotype DQ2.2, antibodies to tissue transglutaminase

    Abstract:The aim of this study was to observe the role of the genotype DQ 2.2 in patients with celiac disease (CD): serological and morphological features of celiac disease in patients with the DQ2.2 genotype Materials and methods: We examined 47 patients with СD, diagnosed according to ESPHGAN criteria. All participants were tested for antibodies to tissue transglutaminase-2 (TTG) and deamidated gliadin peptides, morphometric examination of biopsy specimens of duodenal mucosa and genotyping were carried out. Based on the results of genotyping, patients were divided into 2 groups: group 1 comprised 18 patients with the genotype DQ2.2; group of 2–29 patients with other genotypes of CD. Results: an increase of anti-TTG antibodies was observed in all patients in group 1. Moreover, a moderate increase in group 1 was 55.6%, and in the 2nd group, 27.6% (p = 0.07). A signifi cant increase of anti-TTG in group 1–44.4%, in the 2 group — 3.4% (p = 0.001). In addition, the morphological changes of the duodenal mucosa corresponding to the level of Marsh 3b were more often observed in group 1–27.8% than in 2–0% (p = 0.006). Morphometric parameters of duodenal mucosa in group 1 reveal more severe atrophic changes. Conclusion: it is expected that the detection of the genotype DQ2.2 can serve as a predictor of severe serological (a signifi cant increase of anti-TTG antibodies level) and morphological changes in CD.

      1. S. V. Belmer A. Yu., Razumovsky, A. I. Khavkin. Diseases of the intestines in children. Moscow. Medpraktika-M; 2018: Vol 1. 496 p.
      2. Husby S, Koletzko S, Korponay-Szabj IR, Mearin ML, et al. European Society for Pediatric Gastroenterology, Hepatology, and Nutrition Guidelines for the Diagnosis of Coeliac Disease. JPGN2012;54(1): 136–160. doi: 10.1097/MPG.0b013e31821a23d0.
      3. Mustalahti K, Catassi C, Reunanen A, Fabiani E, et al.; Coeliac EU Cluster, Project Epidemiology. Ann Med. 2010 Dec;42(8):587–95. doi: 10.3109/07853890.2010.505931
      4. Parzanese I, Qehajaj D, Patrinicola F., Aralica M1, et al. Celiac disease: From pathophysiology to treatment. WJGP. 2017;8(2): р27–38. doi: 10.4291/wjgp.v8.i2.27.
      5. Bai JC, Fried M, Corazza GR, Schuppan D, et al. World Gastroenterology Organisation global guidelines on celiac disease; J Clin Gastroenterol. 2013 Feb;47(2):121–6. doi: 10.1097/MCG.0b013e31827a6f83. 2012:25.
      6. Nenna R, Tiberti C, Petrarca L, Mennini M, et al. Anti-transglutaminase immunoreactivity and histological lesions of the duodenum in coeliac patients. Int Immunol. 2013;25:389–394 doi: 10.1093/intimm/dxs159.
      7. Abraham G, Rohmer A, Tye-Din JA, Inouye M. Genomic prediction of celiac disease targeting HLA-positive individuals.Genome Medicine. 2015 Jul 16;7(1):72. doi: 10.1186/ s13073–015–0196–5.
      8. Bergseng E, Dorum S, Magnus О, Nielsen A, et al. Diff erent binding motifs of the celiac disease-associated HLA molecules DQ2.5, DQ2.2, and DQ7.5 revealed by relative quantitative proteomics of endogenous peptide repertoires.Immunogenetics. 2015; 67:73–84. doi: 10.1007/s00251–014–0819–9.
      9. Karell K1, Louka AS, Moodie SJ, Ascher H, et al. HLA types in celiac disease patients not carrying the DQA1*05DQB1*02 (DQ2) heterodimer: results from the European Genetics Cluster on Celiac Disease. Hum Immunol.2003 Apr;64(4):469–77. doi:10.1016/S0198–8859(03)00027–2
      10. Almeida LM, Gandolfi L, Pratesi R, Uenishi RH, et al. Presence of DQ2.2 Associated with DQ2.5 Increases the Risk for Celiac Disease.Autoimmune Diseases. 2016 Oct. 6p doi: 10.1155/2016/5409653
      11. Murray JA, Moore SB, Van Dyke CT, Lahr BD, Dierkhising RA, et al. HLA DQ Gene Dosage and Risk and Severity of Celiac Disease. Clin Gastroenterol Hepatol. 2007 December; 5(12): 1406–1412. DOI: 10.1016/j. cgh.2007.08.013
      12. Vader W, Stepniak D, Kooy Y, Mearin L, Th ompson A, et al. Th e HLA-DQ2 gene dose eff ect in celiac disease is directly related to the magnitude and breadth of gluten-specifi c T cell responses. Proc Natl Acad Sci USA. 2003; 100:12390–12395. doi: 10.1073/pnas.2135229100
      13. Al-Toma A, Goerres MS, Meijer JW, Pena AS, et al. Human leukocyte antigen-DQ2 homozygosity and the development of refractory celiac disease and enteropathy-associated T-cell lymphoma. Clin Gastroenterol Hepatol. 2006; 4:315–319. doi: 10.1016/j.cgh.2005.12.011
      14. Alshiekh S, Zhao LP, Lernmark Å, Geraghty DE, et al. Diff erent DRB1*03:01-DQB1*02:01 haplotypes confer diff erent risk for celiac disease. HLA. 2017;90(2):95–101. doi: 10.1111/tan.13065.
      15. Novikova VP, Revnova MO, Shapovalova NS, Kalinin EJ, et al. Prevalence of autoimmune gastritis in children with celiac disease according to enzyme-linked immunosorbent assay and indirect immunofl uorescence reaction. BMJjournals.Archive of Disease in Childhood.2017;102(2):239

    Full text is published :
    Shapovalova N. S., Novikova V. P., Revnova M. O., Lapin S. V., Kholopova I. V., Khavkin A. I. The role of HLA-DQ2.2 genotype for patients with celiacia. Experimental and Clinical Gastroenterology. 2018;159(11): 19–23. (In Russ.) DOI: 10.31146/1682-8658-ecg-159-11-19-23
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    1. Federal State Educational Establishment of Higher Education “Omsk State Medical University” of the Ministry of Health of the Russian Federation, Omsk, 644099, Russia

    Keywords: Non-alcoholic fatty liver disease, fi brosis, non-invasive markers, rs738409 PNPLA3 polymorphism

    Abstract:The aim of the study was to evaluate the diagnostic signifi cance of the rs738409 C> G polymorphism of the PNPLA3 gene as a marker for the formation and progression of liver fi brosis in patients with non-alcoholic fatty disease (NAFLD). Materials and methods. An open case-control study of a group of patients with non-alcoholic fatty liver disease in the amount of 35 people was conducted. Conducted clinical, laboratory examination methods. Additionally, non-invasive serum fi brosis markers were studied: concentrations of insulin, leptin, adiponectin, matrix metalloproteinase-9 (MMP-9) and its inhibitors — tissue inhibitor of matrix metalloproteinase-1 and 2 (TIMP-1, TIMP-2). All patients underwent liver elastometry to assess the stage of fi brosis on the Metavir scale using the FibroScan apparatus (FibroScan). As a potential marker for the progression of liver fi brosis in NAFLD, PNPLA3 148M / I polymorphism (rs738409) was studied by PCR. Results. There are clinical signs that suggest that liver steatosis is more pronounced in carriers of the G allele of the PNPLA3 148M / I gene. For patients with NAFLD C / G PNPLA3 148M / I genotype, a more aggressive course of the disease with the formation of high progressive stages of fi brosis is characteristic. Conclusion. PNPLA3 148M / I polymorphism can be considered as a non-invasive marker refl ecting the formation and progression of fi brotic changes in the liver tissue in patients with NAFLD.

      1. Nonalcoholic Fatty Liver Disease and Nonalcoholic Steatohepatitis // World Gastroenterology Organisation Global Guidelines. June 2012. http://www. nafl d-nash
      2. European Association for the Study of the Liver (EASL), European Association for the Studyof Diabetes (EASD) and European Association for the Study of Obesity (EASO) Clinical Practice Guidelines for the management of non-alcoholic fatty liver disease. Journal of Hepatology. 2016;64(6):1388–1402. http://doi. org/10.1016/j.jhep.2015.11.004
      3. Sattar N., et al. Non-alcoholic fatty liver disease. BMJ. 2014;349: g4596.
      4. Jiantao Ma, Shih-Jen Hwang, Alison Pedley et al. Bi-directional analysis between fatty liver and cardiovascular disease risk factors. Journal of Hepatology. 2016;66(2):390–397. jhep.2016.09.022
      5. Angulo P., Keach J. C., Batts K. P. et al. Independed predictors of liver fi brosis in patients whis nonalcoholic steatohepatitis. Hepatology. 1999;30:1356–1362. http://
      6. Mary E. Rinella Nonalcoholic Fatty Liver Disease: A Systematic Review JAMA. 2015;313(22):2263–2273.
      7. Singh S, Allen AM, Wang Z, et al. Fibrosis progression in nonalcoholic fatty liver vs nonalcoholic steatohepatitis: a systematic review and meta-analysis of paired-biopsy studies. Clin Gastroenterol Hepatol. 2015;13(4):643–654.
      8. Pais R, Charlotte F, Fedchuk L, et al. LIDO Study Group. A systematic review of follow-up biopsies reveals disease progression in patients with non-alcoholic fatty liver. J Hepatol. 2013;59(3):550–556. jhep.2013.04.027
      9. Drapkina O. M., Ivashkin V. T. Epidemiologicheskie osobennosti nealkogol’noi zhirovoi bolezni pecheni v Rossii (Rezul’taty otkrytogo mnogotsentrovogo prospektivnogo issledovaniya-nablyudeniya DIREG L 01903). RZhGGK. 2014;24(4):32–38.
      10. Ivashkin V. T., Drapkina O. M., Maev I. V. i dr. Rasprostranennost’ nealkogol’noi zhirovoi bolezni pecheni u patsientov ambulatorno-poliklinicheskoi praktiki v Rossiiskoi Federatsii: rezul’taty issledovaniya DIREG 2. RZhGGK. 2015;6:31–41.
      11. Rohit Loomba, Nicholas Schork, Chi-Hua Chen, et al. Genetics of NAFLD in Twins Consortium Heritability of Hepatic Fibrosis and Steatosis Based on a Prospective Twin Study. Gastroenterology. 2015;149(7):1784–1793.
      12. Romeo S, Kozlitina J, Xing C et al. Genetic variation in PNPLA3 confers susceptibility to nonalcoholic fatty liver disease. Nat Genet. 2008;40:1461–1465. http://doi. org/10.1038/ng.257
      13. Huang Y, He S, Li JZ et al. A feed-forward loop amplifi es nutritional regulation of PNPLA3. Proc Natl Acad Sci USA. 2010;107(17):7892–7897. pnas.1003585107
      14. He S, McPhaul C, Li JZ et al. A sequence variation (I148M) in PNPlA3 associated with nonalcoholic fatty liver disease disrupts triglyceride hydrolysis. J Biol Chem. 2010; 285(9): 6706–6715. jbc.M109.064501
      15. Kumari M, Schoiswohl G, Chitraju C et al. Adiponutrin functions as a nutritionally regulated lysophosphatidic Acid acyltransferase. Cell Metab. 2012;15(5):691–702.
      16. Johansson L.E., Johansson L. M., Danielsson P., et al. Genetic variance in the adiponutrin gene family and childhood obesity. PLoS One. 2009;4:5327. https://doi. org/10.1371/journal.pone.0005327
      17. Li-Zhen Chen, Yong-Ning Xin, Ning Geng, et al. PNPLA3 I148M variant in nonalcoholic fatty liver disease: Demographic and ethnic characteristics and the role of the variant in nonalcoholic fatty liver fi brosis. World J Gastroenterol. 2015;21(3):794–802. https://doi. org/10.3748/wjg.v21.i3.794
      18. Sookoian S, Pirola CJ. Meta-analysis of the infl uence of I148M variant of patatin-like phospholipase domain containing 3 gene (PNPLA3) on the susceptibility and histological severity of nonalcoholic fatty liver disease. Hepatology. 2011;53:1883–1894. hep.24283
      19. Paola Dongiovanni, Benedetta Donati, Roberta FaresI148M PNPLA3 variant and progressive liver disease. World J Gastroenterol. 2013;19(41): 6969–6978.
      20. Ivashkin V. T., Drapkina O. M., Shul’pekova Yu. O. Diagnostika i lechenie nealkogol’noi zhirovoi bolezni pecheni (metodicheskie rekomendatsii) M.: OOO «Izdatel’skii dom «M–Vesti», 2009.
      21. Portincasa P. From lipid secretion to cholesterol crystallization in bile. Relevance in cholesterol gallstone disease. Ann. hepatol. 2002;1(3):121–128. https://doi. org/10.2174/1568008054064922
      22. Livzan M. A., Lapteva I. V., Krolevets T. S., Kiselev I. E. Osobennosti techeniya gastroezofageal’noi reflyuksnoi bolezni, assotsiirovannoi s ozhireniem i izbytochnoi massoi tela. Terapevticheskii arkhiv. 2016;88(2):21–27.–27
      23. Michelino Di Rosa, Lucia Malaguarnera Genetic variants in candidate genes infl uencing NAFLD progression. J Mol Med. 2012;90:105–118. s00109–011–0803-x
      24. Livzan M. A., Lapteva I. V., Miller T. S. Rol’ leptina i leptinorezistentnosti v formirovanii nealkogol’noi zhirovoi bolezni pecheni u lits s ozhireniem. Eksperimental’naya i klinicheskaya gastroenterologiya. 2014; 108(8):27–33.
      25. Livzan M. A., Krolevets T. S., Lapteva I. V., Cherkashchenko N. A. Leptinorezistentnost’ u lits s nealkogol’noi zhirovoi bolezn’yu pecheni, assotsiirovannoi s ozhireniem i izbytochnoi massoi tela. Meditsinskii sovet. 2015; 13: 58–62.

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    Krolevets T. S., Livzan M. A., Akhmedov V. A., Novikov D. G. Study of PNPLA3 gene polymorphism in patients with non-alcoholic fatty liver disease and various stages of fi brosis. Experimental and Clinical Gastroenterology. 2018;159(11): 24–32. (In Russ.) DOI: 10.31146/1682-8658-ecg-159-11-24-32
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    1. I . M. Sechenov First Moscow State Medical University (Sechenov University), 119991, Moscow, Russia
    2. St. Petersburg State Health Care Establishment the City Hospital № 40, 197706, St. Petersburg, Russia
    3. Saint Petersburg State University, 199034, St. Petersburg, Russia
    4. Center of Genetics and Reproductive Medicine “Genetico”, 119333, Moscow, Russia
    5. Center of Endosurgery and Lithotripsy, 111123, Moscow, Russia

    Keywords: trace elements, copper, Wilson disease, hepatocerebral degeneration, ATP7B, iron, HFE, hereditary hemochromatosis, molecular genetic methods, NGS

    Abstract:The aim was to study the frequency of HFE gene mutations in patients with Wilson disease (WD) as one of the possible modifi er genes. Materials and methods: There were examined 90 patients with WD. The frequency and spectrum of mutations in the HFE gene were studied using targeted NGS. Results. Mutations in the HFE gene were found in 30% patients with WD. In two patients was discovered combination of two hereditary diseases — WD and hereditary hemochromatosis, associated with metabolic disorders of copper and iron respectively.

      1. Tuluzanovskaya I. G., Juchenko N. A., Balashova M. S., Filimonov M. I., Rozina T. P., Glotov O. S., Asanov A. Yu. Wilson’s disease: intrafamilial clinical polymorphism. PEDIATRIA. 2017; 96 (6): 215–216.
      2. Belousova O.B., Okishev’ D.N., Ignatova T. M., Balashova M. S. et al. Hereditary multiple Cerebral Cavernous Malformations associated with Wilson’s Disease and Multiple Lypomatosis: case report. World Neurosurgery. – 2017. – V. 105–1034.e1–1034.e6
      3. Balashova M. S., Solov’eva O.V., Tuluzanovskaya I. G., Filimonov M. I., et al. Nablyudenie sochetaniya bolezni Vil’sona-Konovalova (BVK), nasledstvennoj neperenosimosti fruktozy i hronicheskogo gepatita C (HGC) [Observation of a combination of Wilson’s disease (WD), hereditary fructose intolerance and chronic hepatitis C (hCG)]. Rossijskij zhurnal Gastroehnterologii, Gepatologii, Koloproktologii [Russian Journal of Gastroenterology, Hepatology, Coloproctology] (prilozhenie № 49. Materialy XXII ezhegodnogo Rossijskogo kongressa “Gepatologiya segodnya” [Attachment № 49. Proc. XXII Annual Russian Congress “Hepatology Today”]). Moscow, 2017, p.26.
      4. Hordyjewska A, Popiołek Ł, Kocot J. Th e many “faces” of copper in medicine and treatment. Biometals. – V. 27.4– 2014. – P. 611–621.
      5. Steindl P. Ferenci P., Dienes H. P., Grimm G., et al. Wilson’ s disease in patients presenting with liver disease: a diagnostic challenge. Gastroenterology. –1997. –V.113(1) – P. 212–218
      6. Ala A., Walker A. P., Ashkan K., Dooley J. S., Schilsky M. L. Wilson’s disease. Lancet. – 2007. –V. 369 – P. 397–408.
      7. Maxwell K.L., Kowdley K. V. Metals and the liver. –2012– Curr Opin Gastroenterol –V.28 – P. 217
      8. Peña M. M. O., Lee J., Th iele D. J. A delicate balance: Homeostatic control of copper uptake and distribution. Journal of Nutrition. – 1999. –V.129(7) –P.1251–1260.
      9. Coff ey A. J., Durkie M., Hague S., McLay K. et al. A genetic study of Wilson’s disease in the United Kingdom. Brain: a journal of neurology– 2013. – V. 136(5). – P. 1476–1487.
      10. Poujois A., Woimant F., Samson S., Chaine P. et al. Characteristics and prevalence of Wilson’s disease: A 2013 observational population-based study in France. Clin Res Hepatol Gastroenterol. – 2017. – V.42(1) – P. 57–63
      11. O’Brien M., Kinsella K., Reilly M., Sweeney B. et al. Wilson’s disease in Ireland: increasing prevalence over 40 years. JNeurolNeurosurg Psychiatry – 2012. – V.27 – P. 83.
      12. Perri R.E., Hahn S. H., Ferber M. J., Kamath P. S. Wilson disease – keeping the bar for diagnosis raised. Hepatology (Baltimore, Md). – 2005. – V.42(4) – P. 974–974.
      13. Ivanova-Smolenskaya I. A., Ovchinnikov I. V., Karabanov A. V., Deineko N. L. et al. Th e His1069Gln mutation in the ATP7B gene in Russian patients with Wilson disease. Journal of Medical Genetics. – 1999. –V. 36(2), P. 174.
      14. Matveeva T., Zaklyazminskaya E., Polyakov A. Th e molecular-genetic analysis of ATP7B gene at the Russian patients with Wilson disease. European journal of human genetics. Ann Hum Biol. – 2016. – Vol. 43(1). – P. 1–8.
      15. Brissot P., Cavey T., Ropert M., Guggenbuhl P et al. Genetic hemochromatosis: Pathophysiology, diagnostic and therapeutic management. Presse Med. – 2017. – V.46 (12) – P. 288–295.
      16. Baranov, A. A., Kaganov, B. S., Bagaeva, M. EH., Zajnudinov, Z. M. Bolezn’ Vil’sona u detej [Wilson’s disease in children]. Voprosy sovremennoj pediatrii [Current pediatrics], 2005, 4 (2), 65–73. Мутации

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    Tuluzanovskaya I. G., Balashova M. S., Zhuchenko N. A., Glotov O. S. et al. Mutations in the HFE gene causing hereditary hemochromatosis in patients with Wilson disease. Experimental and Clinical Gastroenterology. 2018;159(11): 33–37. (In Russ.) DOI: 10.31146/1682-8658-ecg-159-11-33-37
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    1. Ryazan State Medical University, 390026, Ryazan, Russia

    Keywords: chronic pancreatitis, gene polymorphism

    Abstract:The aim of the work was the study of the polymorphism of a number of genes and their role as predisposing factors in the development of chronic pancreatitis. Materials and methods: A study of genetic polymorphisms in 35 patients with chronic pancreatitis was carried out. Patients were divided into groups. In the experimental group, 8 women and 27 men, whose mean age was 43.2 ± 5.3 years. The control group was made up of hypothetical studies according to generally accepted data for the Caucasoid race. Informed consent to participate in the study was obtained. All patients underwent standard general clinical, biochemical analyzes, as well as human genomic DNA isolated from blood leukocytes was subjected to analysis. Results: It was found that in the experimental group the frequency of gene polymorphism was higher than in the control group. Normal homozygote in the experimental group in the genotype was absent among all genes: MMP1 (–1607delG); 9MMP9 (A-8202G); TIMP-1 (C536T); IL10 (G-1082A); OPG TNFRSF11B- (mutation G1181C); P450 (3A4 CYP3A4 1A / 1B); P-450 (CYP1A1); LPL (Ser447Ter mutation), GSTP1 (mutation Ile105Val). Among heterozygous genes polymorphisms TIMP-1 (C536T), IL10 (G-1082A), LPL (mutation Ser447Ter), P450 (CYP1A1), IL10 (G-1082A) prevailed. The greatest number of pathological homozygotes was detected by MMP1, 9MMP9, P450 (3A4 CYP3A4 1A / 1B), OPG. Conclusions: A study of the genetic polymorphism of the human genome showed that there is a high risk of developing chronic pancreatitis in patients with these polymorphisms (MMP1, 9MMP9, P450 (3A4 CYP3A4 1A / 1B), OPG). Signifi cant diff erences in the frequency of occurrence of gene mutations in comparison groups were obtained. These polymorphisms are one of the factors predisposing to the development of chronic pancreatitis. The determination of gene polymorphism can be used in surgical practice, including complex diagnosis and predicting the nature of the course of chronic pancreatitis-the development of a cystic form of chronic pancreatitis.

      1. Vasiliev Yu. V. Etiopathogenetic and clinical aspects of chronic alcoholic pancreatitis. Hepatology. – 2006.- №3.- P.19-24.
      2. Tarasenko S. V., Peskov O. D., Mirov D. I., Artamonov S. V. Clinical forms of destructive pancreatitis. Russian Medical and Biological Bulletin named after academician I.P. Pavlova. – 2001. – № 3–4. – p. 40–42.
      3. Kalinin A. V. Chronic pancreatitis: prevalence, etiology, pathogenesis, classification and clinical characteristics of etiological forms. Clinical perspectives of gastroenterological hepatology. – 2006. – №6. – p. 5–15.
      4. Grigorieva I. N. Acute and chronic pancreatitis. Novosibirsk, 2010.
      5. Dorr S, Lechtenbohmer N, Rau R et al. Association of a specific haplotype across the genes MMP1 and MMP3 with radiographic joint destruction in rheumatoid arthritis. Arthritis Res Ther.-2004.-V.6.-P.199–207
      6. Tanindi A., Sahinarslan A, Elbeg S, CemriM. Relationship Between MMP-1, MMP-9, TIMP1, IL-6 and Risk Factors, Clinical Presentation, Extent and Severity of Atherosclerotic Coronary Artery Disease. Open Cardiovasc Med J. – 2011.-V.5.-P. 110–116.
      7. Konenkov VI, Shevchenko AV, Prokof’ev VF, Korolev MA, et al. Cytokine gene networks in the personalized prediction of the human health status and in the formation of high disease risk factors for implementation of preventive measures. Profilakticheskaya meditsina. 2013;16(4):19–26
      8. Tarasenko S. V., Karyukhin I. V., Rakhmaev T. S., Zaitsev O. V. Percutaneus ultrasound-guided puncture-draining interventions in treatment of patients with pancreatic cysts. Nauka molodykh (Eruditio Juvenium). 2013, No.1, pp.20–25.

    Full text is published :
    Tarasenko S. V., Natalskiy A. A., Bogomolov A. Yu., Bakonina I. V., Kadykova O. A., Andrianova K. V. Genetic polymorphisms as predisposing factors of chronic pancreatitis. Experimental and Clinical Gastroenterology. 2018;159(11): 38–43. (In Russ.) DOI: 10.31146/1682-8658-ecg-159-11-38-43
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    1. Federal State Budgetary Institution of Additional Post-graduate Education “Central State Medical Academy” Administrative Departament of the President of the Russian Federation, 121359, Moscow, Russia

    Keywords: duodenal ulcer, eradication schemes, omeprazol, clarithromycin, amoxicillin, wilprofen, levofl oxacin, pantoprazol, dazolic

    Abstract:Aim of investigation: comparative analysis of 10 schemes of eradication in patients with duodenal ulcer associated with Helicobacter pylori. Materials and methods: 10 eradication schemes were investigated at the Department of Gastroenterology for 15 years (Central state medical academy of department of presidential aff airs, Head of the Department Minushkin O. N.) 297 patients with duodenal ulcer associated with Helicobacter pylori were divided in treatment groups, as follows: 30 patients received triple therapy with omeprazol (O), clarithromycin (C) and metronidazole (M); 98 patients received triple therapy with omeprasol (O), clarithromycin (C) and amoxicillin (A): the dose of clarithromycin and the duration of treatment (5-day, 7-day, 10-day) was selected depending on the degree of Hp contamination (+, ++, +++); 68 patients received sequential therapy with omeprazol (O), clarithromycin (C) and amoxicillin (A); 117 patients received triple therapy with omeprazol (O), clarithromycin (C) and furazolidon (F) and tinidazol (T) — 57 patients or with omeprazol (O), wilprafen (W) and levofl oxacin (L) and amoxicillin (A) — 60 patients; and 50 elderly patients received half doses of O+C+A combnation or pantoprazol (P), dazolic (D) and amoxicillin (A). Esophagogastroduodenoscopy (EGS), Giemsa stain in biopsy and rapid urease test (RUT) were used to evaluate the quality of ulcer healing and effi cacy of eradication. Student`s t-criterion and Fisher`s method were used in statistical processing (Signifi cant diff erences in signifi cance level of 95%, p<0,05) Results: O+C+M scheme had the lowest effi cacy (60%). 6 of 10 schemes were eff ective: O+C+A — 80%; sequential scheme — 83% (with (F) — 93%, with (T) — 88%; with (W) 90% or (L) 80%). Discussion: Eradication effi cacy increased by 97% with day-degree contamination selection. In elderly patients half doses schemes were eff ective (O+C+A — 87% and P+D+A 90%).

      1. Shulpekowa Yu. O. Use of rabeprasol in practice of gastroenterologist //Medical Sovet, 2016, № 14, S.26–31.
      2. Pimanov S. I., Makarenko E. V. Optimized eradication protocols: recommendations of the American gastroenterologist board, Maastricht v/Florentine and Toronto consensuses.// Medical Sovet, 2017, № 15, S.10–17.
      3. Haastrup H.F, Paulsen M.S, Christensen R. D. et al. Medical and non-predictors of intiating long-term use of proton pump inhibitors: a nationwide cohort study of fi rst-time users during a 10-year period. Aliment Pharmacol Th er, 2016 Jul, 44(1): 78–87.
      4. Sugimoto M, Sahara S, Ichikawa H. et al. Four-timesdayle dosing of rabeprazole with sitafl oxacin, high-dose amoxicillin, or both for metronidasole-ressistant infection with Helicobacter pylori in Japan//Helicobacter, 2016, may 23 {Epub ahead of print}.
      5. Stanghellin V. et al. Gastroduodenal disorders //Gastroenterology 2016, 150, S.1380–1392.
      6. Sugano K. et al. Kyoto global consensus report on Helicobacter pylori gastritis //Gut, 2015, 64, S.1353–1367.
      7. Zhang Z., et al. Infl uence of effl ux pump inhibitors on the multidrugs resistance of Helicobacter pylori. Word. J. Gastroenterol. 2012, Mar 14, 16 (10). S.1279–1284.
      8. Minushkin O.N, Zverkov I.V, Ostrovskaya A. I. Hepatoprottctors of vegetable orgin in therapy of drugs-induced hepatitis // Medical Sovet, 2016, № 14, S.48–52.

    Full text is published :
    Zverkov I. V., Maslovskii L. V. Comparative eff ectiveness of diff erent eradication schemes in the treatment of peptic ulcer disease associated with Helicobacter pylori. Experimental and Clinical Gastroenterology. 2018;159(11): 44–47. (In Russ.) DOI: 10.31146/1682-8658-ecg-159-11-44-47
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    1. Kazan (Volga region) Federal University, Kazan, Russia
    2. Kazan State Medical University, Kazan, Russia

    Keywords: gut microbiota, H. pylori, metagenome, eradication therapy, shotgun sequencing

    Abstract:The aim of the study: to evaluate the composition of gut microbiota in H. pylori-negative and H. pylori-positive patients, as well as to assess the infl uence of H. pylori eradication therapy on the gut microbiota composition immediately after and one month after completion of therapy. Materials and methods: stool samples from 93 H. pylori-positive and 42 H. pylori-negative (control group) patients were used for analysis. Stool samples immediately after and one month after completion of therapy were collected from 93 and 14 patients, respectively. Gut microbiota composition assessment including the evaluation of alpha diversity (Shannon index) was performed by shotgun sequencing. Results: Firmicutes (56,73±21,81)%, Bacteroidetes (35,97±23,65)%, Actinobacteria (2,42±4,24)%, Proteobacteria (2,37±7,00)%, Verrucomicrobia (0,94±2,54)% were the most represented bacterial phyla in the gut microbiota of H. pylori-positive patients before the eradication therapy. Immediately after eradication therapy the number of Verrucomicrobia and Actinobacteria bacterial phyla decreased, and, conversely, the representation of Proteobacteria phylum increased. In 4 weeks the representation of these phyla did not diff er from the initial level. Representation of Firmicutes phylum had a tendency to decrease immediately after the completion of eradication therapy; there was a further decrease in their representation in a month. Bacterial genera: Bacteroides (15,1±17,32)%, Prevotella (14,07±21,60)%, Eubacterium (13,79±10,49)%, Faecalibacterium (6,26±5,85)%, Ruminococcus (5,61±6,00)%, Subdoligranulum (5,34±5,77)%, Butyrivibrio (4,57±13,26)% were predominat in the gut microbiota in H. pylori-positive patients before the treatment. Immediately after therapy the representation of almost all these genera decreased, except Bacteroides which representation increased. The abundance of Escherichia and Klebsiella bacterial genera also increased. One month after the therapy a tendency to return to initial composition was observed for most of bacterial genera. Conclusion: thus, H. pylori eradication therapy aff ects the gut microbiota composition. Some changes persist for one month after completion of therapy.

      1. Malfertheiner P., Megraud F., O’Morain C.A., et al. Management of Helicobacter pylori infection-the Maastricht V/Florence Consensus Report // Gut. – 2017. – Vol. 66 (1). – Р. 6–30.
      2. Sugano K., Tack J., Kuipers E. J., et al. Kyoto global consensus report on Helicobacter pylori gastritis // Gut. – 2015. – Vol. 64 (9). – P. 1353–67.
      3. Chey W.D., Leontiadis G. I., Howden C. W., Moss S. F. ACG Clinical Guideline: Treatment of Helicobacter pylori Infection // Am J Gastroenterol. – 2017. – Vol. 112 (2). – P. 212–239.
      4. Ivashkin V. T., Mayev I. V., Lapina T. L., Sheptulin A. A., et al. Diagnostics and treatment of Helicobacter pylori infection in adults: Clinical guidelines of the Russian gastroenterological association. Russian Journal of Gastroenterology, Hepatology, Coloproctology. 2018;28(1):55–70. (In Russ.) https://doi. org/10.22416/1382–4376–2018–28–1–55–70
      5. IARC/WHO. Helicobacter pylori eradication as a strategy for preventing gastric cancer. International Agency for Research on Cancer/ World Health Organisation. – 2014. pdfs/pr227_E.pdf/
      6. Herrero R., Park J. Y., Forman D. The fight against gastric cancer – the IARC Working Group report // Best Pract Res Clin Gastroenterol. – 2014. – Vol. 28 (6). – P. 1107–14.
      7. Fock K. M., Graham D. Y., Malfertheiner P. Helicobacter pylori research: historical insights and future directions // Nat Rev Gastroenterol Hepatol. – 2013. – Vol. 10 (8). – P. 495–500.
      8. Yu S., Yang M., Nam K. T. Mouse models of gastric carcinogenesis // J Gastric Cancer. – 2014. – Vol. 14 (2). – P. 67–86.
      9. Li W. Q., Ma J. L., Zhang L., et al. Eff ects of Helicobacterpylori treatment on gastric cancer incidence and mortality in subgroups // J Natl Cancer Inst. – 2014. – Vol. 106 (7).
      10. Kamada T., Kurose H., Yamanaka Y., et al. Relationship between gastroesophageal junction adenocarcinoma and Helicobacter pylori infection in Japan // Digestion. – 2012. – Vol. 85 (4). – P. 256–60.
      11. Wong B. C., Lam S. K., Wong W. M., et al. Helicobacter pylori eradication to prevent gastric cancer in a highrisk region of China: a randomized controlled trial // JAMA. – 2004. – Vol. 291 (2). – P. 187–94.
      12. Rugge M., Genta R. M., Graham D. Y., et al. Chronicles of a cancer foretold: 35 years of gastric cancer risk assessment // Gut. – 2016. – Vol. 65 (5). – P. 721–725.
      13. Ma J. L., Zhang L., Brown L. M., et al. Fift een-year eff ects of Helicobacter pylori, garlic, and vitamin treatments on gastric cancer incidence and mortality // J Natl Cancer Inst. – 2012. – Vol. 104 (6). – P. 488–492.
      14. Wang J., Xu L., Shi R., et al. Gastric atrophy and intestinal metaplasia before and aft er Helicobacter pylori eradication: a meta-analysis // Digestion. – 2011. – Vol. 83 (4). – P. 253–60.
      15. Rokkas T., Pistiolas D., Sechopoulos P., et al. Th e longterm impact of Helicobacter pylori eradication on gastric histology: a systematic review and meta-analysis // Helicobacter. – 2007. – Vol. 12 (suppl 2). – P. 32–8.
      16. Kong Y. J., Yi H. G., Dai J. C., Wei M. X. Histological changes of gastric mucosa aft er Helicobacter pylori eradication: a systematic review and meta-analysis // World J Gastroenterol. – 2014. – Vol. 20. – P. 5903–5911.
      17. Ford A. C., Forman D., Hunt R. H., et al. Helicobacter pylori eradication therapy to prevent gastric cancer in healthy asymptomatic infected individuals: systematic review and meta-analysis of randomised controlled trials // BMJ. – 2014. – Vol. 348. – P. g3174.
      18. de Martel C., Forman D., Plummer M. Gastric cancer: epidemiology and risk factors // Gastroenterol Clin North Am. – 2013. – Vol. 42 (2). – P. 219–240.
      19. Ferlay J., Steliarova-Foucher E., Lortet-Tieulent J., et al. Cancer incidence and mortality patterns in Europe: estimates for 40 countries in 2012 // Eur J Cancer. – 2013. – Vol. 49 (6). – P. 1374–1403.
      20. Wang Z., Graham D. Y., Khan A., et al. Incidence of gastric cancer in the USA during 1999 to 2013: a 50-state analysis // Int J Epidemiol. – 2018. – Vol. 47 (3). – P. 966–975.
      21. Torre L. A., Siegel R. L., Ward E. M., Jemal A. Global Cancer Incidence and Mortality Rates and Trends – An Update // Cancer Epidemiol Biomarkers Prev. – 2016. – Vol. 25 (1). – P. 16–27.
      22. Ivashkin V. T., Sheptulin A. A., Mayev I. V., et al. Diagnostics and treatment of peptic ulcer: clinical guidelines of the Russian gastroenterological Association. Russian Journal of Gastroenterology, Hepatology, Coloproctology. 2016;26(6):40–54. (In Russ.) https://doi. org/10.22416/1382–4376–2016–26–6–40–54
      23. Lazebnik L. B., Tkachenko E. I., Abdulganiyeva D. I., et al. VI national guidelines for the diagnosis and treatment of acid-related and helicobacter pylori-associated diseases (VI Moscow agreement). Experimental and Clinical Gastroenterology Journal. 2017;138(02):03–21
      24. WHO. Global priority list of antibiotic-resistant bacteria to guide research, discovery, and development of new antibiotics. (17.09.2018).
      25. Yuan Y., Ford A. C., Khan K. J., et al. Optimum duration of regimens for Helicobacter pylori eradication // Cochrane Database Syst Rev. – 2013. – Vol. 11 (12). CD008337.
      26. Calvet X., García N., López T., et al. A meta-analysis of short versus long therapy with a proton pump inhibitor, clarithromycin and either metronidazole or amoxycillin for treating Helicobacter pylori infection // Aliment Pharmacol Th er. – 2000. – Vol. 14 (5). – P. 603–9.
      27. Ford A., Moayyedi P. How can the current strategies for Helicobacter pylori eradication therapy be improved? // Can J Gastroenterol. – 2003. – Vol. 17 (Suppl B). – P. 36B-40B.
      28. Flores H. B., Salvana A., Ang E. L.R., et al. Duration of proton-pump inhibitor-based triple therapy for Helicobacter pylori eradication: a meta-analysis // Gastroenterology. – 2010. – Vol. 138 (5, Suppl 1). – P. 340
      29. Antonopoulos D. A., Huse S. M., Morrison HG, et al. Reproducible community dynamics of the gastrointestinal microbiota following antibiotic perturbation // Infect Immun. – 2009. – Vol. 77 (6). – P. 2367–75.
      30. Dethlefsen L., Huse S., Sogin M. L., Relman D. A. Th e pervasive eff ects of an antibiotic on the human gut microbiota, as revealed by deep 16S rRNA sequencing // PLoS Biol. – 2008. – Vol. 6 (11). – P. e280.
      31. Jernberg C., Löfmark S., Edlund C., Jansson J. K. Longterm ecological impacts of antibiotic administration on the human intestinal microbiota // ISME J. – 2007. – Vol. 1. – P. 56–66.
      32. Dethlefsen L., Relman D. A. Incomplete recovery and individualized responses of the human distal gut microbiota to repeated antibiotic perturbation // Proc Natl Acad Sci USA. – 2011. – Vol. 108 (Suppl 1). – P. 4554–61.
      33. Antunes L. C., Han J., Ferreira R. B., et al. Effect of antibiotic treatment on the intestinal metabolome // Antimicrob Agents Chemother. – 2011. – Vol. 55 (4). – P. 1494–503.
      34. Adamsson I., Edlund C., Nord C. E. Impact of treatment of Helicobacter pylori on the normal gastrointestinal microfl ora // Clin Microbiol Infect. – 2000. – Vol. 6. – P. 175–7.
      35. Jakobsson H., Wreiber K., Fall K., et al. Macrolide resistance in the normal microbiota aft er Helicobacter pylori treatment // Scand J Infect Dis. – 2007. – Vol. 39. – P. 757–63.
      36. Sullivan A., Edlund C., Nord, C. E. Eff ect of antimicrobial agents on the ecological balance of human microfl ora // Lancet Infect. Dis. – 2001. – Vol. 1 (2). – P. 101–14.
      37. Bengtsson-Palme J., Angelin M., Huss M., et al. Th e Human Gut Microbiome as a Transporter of Antibiotic Resistance Genes between Continents // Antimicrob Agents Chemother. – 2015. – Vol. 59 (10). – P. 6551–60.
      38. Smillie C. S., Smith M. B., Friedman J., et al. Ecology drives a global network of gene exchange connecting the human microbiome // Nature. – 2011. – Vol. 30, 480 (7376). – P. 241–4
      39. Ivashkin V. T., Maev I. V., Lapina T. L., Sheptulin A. A. et al. Recommendations of the Russian Gastroenterological Association for the diagnosis and treatment of Helicobacter pylori infection in adults. koloproktologii. Russian Journal of Gastroenterology, Hepatology, Coloproctology. 2012;22(1):87–89. (In Russ.)
      40. 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. 646–64.
      41. Zhang B.W., Li M., Ma L. C., Wei F. W. A widely applicable protocol for DNA isolation from fecal samples // Biochem. Genetics. – 2006. – Vol. 44 (11–12). – P. 494–503.
      42. Mitra S., Förster-Fromme K., Damms-Machado A., et al. Analysis of the intestinal microbiota using SOLiD16S rRNA gene sequencing and SOLiD shotgun sequencing // BMC Genomics. – 2013. – Vol. 14 (Suppl 5). – P. S16.
      43. Langmead B., Trapnell C., Pop M. Ultrafast and memory effi cient alignment of short DNA sequences to the human genome // Genome Biol. – 2009. – Vol. 10 (3). – P. R25.
      44. Truong D.T., Franzosa E. A., Tickle T.L, et al. MetaPhlAn2 for enhanced metagenomic taxonomic profi ling // Nat Methods. – 2015. – Vol. 12 (10). – P. 902–3.
      45. Bordin D. S., Embutnieks Yu.V., Vologzhanina L. G., Il’chishina T.A. et al. European Registry on the management of Helicobacter pylori infection (Hp-EuReg): analysis of 2360 patients receiving fi rst-line therapy in Russia. Terapevticheskiy arkhiv (Th erapeutic archive). 1018;2(90):35–42
      46. Ivashkin V. T., Mayev I. V., Sheptulin A. A., Lapina T. L., et al. Diagnosis and treatment of the functional dyspepsia: clinical guidelines of the Russian Gastroenterological Association. Russian Journal of Gastroenterology, Hepatology, Coloproctology. 2017;27(1):50–61. (In Russ.)–4376–2017– 27–1–50–61
      47. Ley R.E., Bäckhed F., Turnbaugh P., et al. Obesity alters gut microbial ecology // Proc Natl Acad Sci USA. – 2005. – Vol. 102(31). – P. 11070–11075.
      48. Ley R.E., Turnbaugh P. J., Klein S., Gordon J. I. Microbial ecology: human gut microbes associated with obesity // Nature. – 2006. – Vol. 444 (7122). – P. 1022–1023.
      49. Myllyluoma E., Ahlroos T., Veijola L., et al. Effects of anti-Helicobacter pylori treatment and probiotic supplementation on intestinal microbiota // Int. J. Antimicrob. Agents. – 2007. – Vol. 29 (1). – P. 66–72.
      50. Bühling A., Radun D., Müller W. A., Malfertheiner P. Infl uence of anti-Helicobacter triple-therapy with metronidazole, omeprazole and clarithromycin on intestinal microfl ora // Aliment. Pharmacol. Th er. – 2001. – Vol. 15 (9). – P. 1445–52.
      51. Lou J.G., Chen J., Huang X. L., Zhao Z. Y. Changes in the intestinal microfl ora of children with Helicobacter pylori infection and aft er Helicobacter pylori eradication therapy // Chin. Med. J. – 2007. – Vol. 120 (10). – P. 929–31.
      52. Yang Y.J., Sheu B. S. Probiotics-containing yogurts suppress Helicobacter pylori load and modify immune response and intestinal microbiota in the Helicobacter pylori-infected children // Helicobacter. – 2012. – Vol. 17 (4). – P. 297–304.
      53. Eckburg P.B., Bik E. M., Bernstein C. N. et al. Diversity of the human intestinal microbial fl ora // Science. – 2005. – Vol. 308 (5728). – P. 1635–1638.
      54. Yanagi H., Tsuda A., Matsushima M., et al. Changes in the gut microbiota composition and the plasma ghrelin level in patients with Helicobacter pylori-infected patients with eradication therapy // BMJ Open Gastro. – 2017. – P. 4 e000182.
      55. Yap T.W., Gan H. M., Lee Y. P., et al. Helicobacter pylori Eradication Causes Perturbation of the Human Gut Microbiome in Young Adults // PLoS One. – 2016. – Vol. 18; 11 (3). – P. e0151893.
      56. Jakobsson H.E., Jernberg C., Andersson A.F, et al. ShortTerm antibiotic treatment has diff ering long-term impacts on the human throat and gut microbiome // PLoS One. – 2010. – Vol. 5(3). – P. e9836.

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    Safina D. D., Abdulkhakov S. R., Markelova M. I., Grigoryeva T. V. et al. Changes in the taxonomic composition of the intestinal microbiota under the infl uence of Helicobacter pylori eradication therapy. Experimental and Clinical Gastroenterology. 2018;159(11): 48–61. (In Russ.) DOI: 10.31146/1682-8658-ecg-159-11-48-61
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    1. Federal research center “Krasnoyarsk scientifi c center” Siberian branch of the Russian Academy of Sciences Research Institute of Medical Problems of the North, Krasnoyarsk 660022, Russia
    2. Krasnoyarsk regional clinical cancer center named. A. I. Kryzhanovsky, Krasnoyarsk 660022, Russia

    Keywords: neutrophilic granulocytes; chemiluminescence; rectal cancer

    Abstract:The purpose of our work is to study the spontaneous and induced chemiluminescent activity of neutrophilic granulocytes (NG) in patients with rectal cancer in dynamics. Materials and methods. The study included 56 patients with rectal cancer. At the fi rst stage there were 9 people, in the II stage 19 people, on the III 17 and at the IV stage 11 patients. The object of study are neutrophilic granulocytes isolated from venous blood. The control group consisted of 112 healthy blood donors. The intensity of synthesis of active oxygen species of NG was determined by the method of chemiluminescence analysis. Results. The study showed a signifi cant increase in the intensity of spontaneous and induced luminescence and the area under the curve of spontaneous chemiluminescence in the II–IV stages of the disease. When studying zymosan-induced chemiluminescence, the area under the curve is increased in all groups of patients, while in patients at stage IV the total production of ROS is signifi cantly higher than in stages I and II. On the 7th day after the surgical treatment, the intensity of spontaneous chemiluminescence remains elevated only in patients at the IV stage of the rectal cancer. The intensity of induced chemiluminescence and the area under the curve of spontaneous and induced luminescence are increased at all stages of the disease with respect to control. The activation index was increased in patients at all stages of with rectal cancer both before and after surgery. Сonclusion. As a result of the study, an increase in the intensity of ROS synthesis in patients with rectal cancer was revealed. The total production of reactive oxygen species is higher in the late stage of the disease. An increase in the activation index of neutrophils in all stages of the RPC characterizes the metabolic capabilities of neutrophils to the enhanced synthesis of ROS in functional activation.

      1. Gordeev S. S., Barsukov Yu.A., Tkachev S. I. et al. Locally advanced (fi xed & tethered) rectal cancer: defi nitions, classifi cations, current treatment options. HERALD of the Moscow Cancer Society. 2014, no.2, pp.2–6.
      2. Balkanov A. S., Gurov A. N., Katuntseva N. A., Belousova E. A. Incidence of rectal cancer in the population of the moscow region in 2010–2014. Almanac of Clinical Medicine. 2016;44(5):599–605. (In Russ.) https://doi. org/10.18786/2072–0505–2016–44–5–599–605
      3. Райков Н.С., Чупин Р.Н ., Попов И. Н. и соавт. Рак прямой кишки // Тюменский медицинский журнал. –2010. –№ 3–4. – С. 75–77.
      4. Нестерова И. В., Ковалева С. В., Чудилова Г. А. и соавт. Двойственная роль нейтрофильных гранулоцитов в реализации противоопухолевой защиты // Иммунология. –2012. –№ 5. – С. 281–285.
      5. Maltseva V. N., Safronova V. G. Ambiguity role of neutrophils in oncogenesis. Tsitologiya. 2009;51(6): 467–474.
      6. Fridlender Z. G., Albelda S. M. Tumor-associated neutrophils: frend or foe? // Carcinogenesis. –2012. –Vol.33, no. 5. –Р. 949–955.
      7. Finisguerra V., Di Conza G., Di Matteo M. et аl. MET is required for the recruitment of anti-tumoral neutrophils // Nature. –2015. –Vol. 522, no. 7556. –P. 349–353.
      8. Swierczak A., Mouchemore K. A., Hamilton J. A., Anderson R. L. Neutrophils: important contributors to tumor progression and metastasis // Cancer Metastasis Rev. –2015. –Vol. 34(4), – Р.735–751.
      9. Gracheva T. A. Sovershenstvovanie khemilyuminestsentnogo metoda issledovaniya funktsional`noy aktivnosti fagotsitiruyushchikh kletok [Improvement of a chemiluminescent method of research of functional activity of fagotsitis cells]. Klinicheskaya Laboratornaya Diagnostika. 2008, no.2, pp.54–55
      10. Di Carlo E., Forni G., Lollini P. L., Colomobo M. P. et al. Th e intriguing role of polymorphonuclear neutrophils in antitumor reactions // Blood. – 2001. –Vol. 97(2): – Р. 339–345.
      11. Kit O. I., Frantsiyants E. M., Nikipelova E. A., Komarova E. F. Condition of free radical processes in the tissue of a malignant tumor of the colon. Siberian medical review. 2014; № 1: 30–34. DOI 10.20333/25000136–2014– 1–30–34
      12. Prestwich R. J., Errington F., Hatfi eld Р., Roodman D. G. Th e immune system – is it relevant to саnсеr development, progression and treatment? // Clin. Oncol. –2008. – Vol. 20. –Р. 101–112.
      13. Kolenchukova O. A., Savchenko A. A., Smirnova S. V. Features of luminol- and lucigenin-induced chemiluminescence of neutrophilic granulocytes in patients with chronic rhinosinusitis. Medical Immunology. (Russia) 2010;12(4–5):437–440. (In Russ.) https://doi. org/10.15789/1563–0625–2010–4–5–437–440
      14. Schins R. Р. F., Воrm Р. J. А., Van Schooten F. J. Neutropihis and respiratory tract DNA damage and mutagenesis: а review // Mutagenesis. –2006. –Vol. 21. –Р. 225–236.
      15. Smirnova O. V., Manchuk V. T., Agilova Y. N. Characteristics of neutrophil chemiluminescence in patients with type g multiple myeloma at diff erent stages of the disease. Medical Immunology (Russia). 2015;17(6):579–584. (In Russ.)–0625–2015– 6–579–584
      16. Smirnova O. V., Titova N. M., Elmanova N. G. Features chemiluminescent activity of neutrophilic granulocytes of patients with obstructive jaundice of benign origin. Russian Journal of Immunology (RJI). 2015;9(2–1): 313–315
      17. Smirnova O. V., Manchuk V. T., Agilova Yu. N. Th e role of non-specifi c immunity in the progression of myelomic disease. Modern problems of science and education. 2014, no.2, 515 p.

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    Smirnova O. V., Kasparov E. V., Perepechay Ya. I., Versenev A. A., Laletin I. A. Features of nonspecifi c immunity in the progression of colorectal cancer. Experimental and Clinical Gastroenterology. 2018;159(11): 62–67. (In Russ.) DOI: 10.31146/1682-8658-ecg-159-11-62-67
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    1. Novosibirsk State Medical University, Ministry of Health of Russia, Novosibirsk, Russia

    Keywords: syndrome of excessive bacterial growth, infl ammatory bowel disease, hydrogen respiratory test

    Abstract:Research objective: to study the frequency of gastrointestinal symptoms in patients with infl ammatory bowel disease (IBD) depending on the presence of the small intestinal bacterial overgrowth (SIBO). Materials and methods of the study: The study included 152 patients with IBD. All patients would be given a hydrogen breath test (VDT) with lactulose to diagnose SIBO. The analysis of gastrointestinal symptoms in patients depending on the presence of SIBO, as well as the dynamics of symptoms after its correction was carried out. Results: The frequency of SIBO in patients with IBD was 48%. Patients with SIBO were more likely to have symptoms: diarrhea, bloating, fl atulence, weakness, whining and irritability. After a 2-week course of correction of SIBO, patients had a decrease in the frequency of these symptoms. Conclusion: The data obtained indicate a high frequency of SIBO in patients with IBD. SIBO is associated with symptoms that may accompany an acute attack of the IBD. The diagnosis of SIBO should be included in routine practice in patients with acute attack of IBD for selection of adequate therapy, which will include correction of microbiota disorders and will not lead to inappropriate change of basic therapy.

      1. Lane E.P., Zisman T. L., Suskind D. L. Microbiota in infl ammatory bowel diseases: modern and therapeutic fi ndings. Jay was Infl amed by RES, 2017, vol.10, pp. 63–73. doi: 10.2147/JIR.S116088.
      2. Osipenko M. F., Skalinskaya M. I., Kulygina Y. A., Kholin S. I., Krasner Ya. A. What we know about the bacterial overgrowth syndrome. Medical Council, 2016, № 09, pp. 70–74. doi: 10.21518/2079–701X-2016–9
      3. Kulygina Yu.A., Osipenko M. F., Skalinskaya M. I., Palchunova K. D. Th e prevalence of bacterial overgrowth syndrome and its associated factors in patients with infl ammatory bowel diseases (according to the data of the Novosibirsk registry. Terapevticheskii arkhiv, 2017, № 2, pp. 15–19. doi: 10.17116/terarkh201789215–19
      4. Kverka M. Tlaskalová-Hogenová H. Intestinal Microbiota: Facts and Fiction, Digestive Diseases, 2017, vol. 35, pp. 139–147. doi: 10.1159/000449095
      5. Fava F., Danese S. Intestinal microbiota in infl ammatory bowel disease: Friend of foe? World J Gastroenterol, 2011, vol. 17(5), pp. 557–566. doi: org/10.3748/wjg.v17.i5.557.
      6. Andrei M., Gologan S., Stoicescu A., Ionescu M., Nicolaie T., Diculescu M. Small Intestinal Bacterial Overgrowth Syndrome Prevalence in Romanian Patients with Infl ammatory Bowel Disease. Current Health Sciences Journal. 2016; 42(2); 151–156. doi: org/10.1093/ecco-jcc/ jjv215.
      7. Rubio-Tapia A., Barton S. H., Rosenblatt J. E., Murray J. A. Prevalence of small intestine bacterial overgrowth diagnosed by quantitative culture of intestinal aspirate in celiac disease. J Clin Gastroenterol, 2009, vol. 43, pp. 157–161. doi: org/10.1097/mcg.0b013e/3191557e67
      8. Pande C., Kumar A., Sarin S. K. Small-intestinal bacterial overgrowth in cirrhosis is related to the severity of liver disease. Aliment Pharmacol Th er, 2009, vol. 29, pp. 1273–1281. doi: 10.1111/j.1365–036.2009.03994.
      9. Runyon B. A. Pathogenesis of spontaneous bacterial peritonitis. UpToDate on line, 18.1. Wellesley, 2010, pp. 1517– 1541. doi: org/10.1016/b978–1–4160–6189–2.00091–3.
      10. Klaus J., Spaniol U., Adler G., Mason R. A., Reinshagen M., Tirpitz C. Small intestinal bacterial overgrowth mimicking acute fl are as a pitfall in patients with Crohn’s Disease. BMC Gastroenterol, 200, vol. 9, pp. 61. doi: org/10.1186/1471–230x-9–61.
      11. Castiglione F., Del Vecchio B. G., Rispo A. et al. Orocecal transit time and bacterial overgrowth in patients with Crohn’s disease. J Clin Gastroenterol, 2000, vol, 31, n.1, pp. 63–66. PMID: 10914780
      12. Rutgeerts P., Ghoos Y., Vantrappen G. et al. Ileal dysfunction and bacterial overgrowth in patients with Crohn’s disease. Eur J Clin Invest, 1981, vol. 11, no. 3, pp. 199–206.
      13. Wigg A.J., Roberts-Th omson I.C., Dymock R. B. et al. Th e role of small intestinal bacterialovergrowth, intestinal permeability, endotoxaemia, and tumour necrosis factor alpha in the pathogenesis of non-alcoholic steatohepatitis. Gut, 2001, vol. 48, no. 2, pp. 206–11.PMID:11156641
      14. Fialho A.., Th ota P., McCullough A. J. et al. Small Intestinal BacterialOvergrowth Is Associated with Non-Alcoholic Fatty Liver Disease. J Gastrointestin Liver Dis, 2016, vol. 25, no. 2, pp. 159–165. doi: 10.15403/ jgld.2014.1121.252.iwg.

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    Kulygina Yu. A., Osipenko M. F., Lukinov V. L., Lukashova L. V., Pomogaeva A. P. The bacterial overgrowth syndrome in the small intestine and gastrointestinal symptoms in patients with infl ammatory bowel diseases depending on the presence of smal-intestinal bacterial overgrowth syndrome. Experimental and Clinical Gastroenterology. 2018;159(11): 68–74. (In Russ.) DOI: 10.31146/1682-8658-ecg-159-11-68-74
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    1. Novosibirsk State Medical University,
    2. Institute of Chemical Biology and Fundamental Medicine of the SB RAS
    3. GBUZ NSO "City infectious diseases clinical hospital № 1", Novosibirsk, Russia
    4. State Research Center of Virology and Biotechnology Vector, Koltsovo, Novosibirsk region
    5. Siberian state MEDICAL University of Minzdrav of Russia, Tomsk, Russia

    Keywords: acute viral gastroenteritis, noroviruses, rotaviruses, astroviruses, epidemiology, clinical and laboratory manifestations, polymerase chain reaction, pregnant women, synbiotic

    Abstract:Objective: to determine the epidemiological, clinical and laboratory features of viral acute gastroenteritis (AGE) in hospitalized pregnant women and to evaluate of the eff ectiveness of synbiotics in the treatment of AGE in pregnant women. Materials and methods: The study involved 482 adult patients with AGE hospitalized from February to June 2017, including 103 pregnant women aged from 21 to 37 years. Along with the generally accepted diagnostic methods, feces were studied by PCR using a set of original specifi c primers to detect rotaviruses of group A and group C, noroviruses of the second gene group (HNoV GII) and astroviruses. Identifi ed virus isolates were genotyped. Results: out of 103 pregnant women with AGE, more than half of cases (53.3%) accounted for viral AGE: norovirus — 51.4% of cases, rotavirus — 1.9%. Astrovirus infection was not registered. Noroviruses of new genotypes GII.P17 / GII.17 and GII. P16 / GII.2, and rotavirus genotype G9P were detected in pregnant women with AGE. In noroviral AGE, the food route of transmission prevailed, the leading factors of transmission were salads and dairy products. The disease proceeded in moderate form and had clinical features characteristic of norovirus infection. In pregnant women with AGE of norovirus etiology and unspecifi ed etiology, using of synbiotic “Normobact” in the combined therapy, the earlier arrest of diarrhea was noted comparing with patients receiving only pathogenetic therapy (p <0.05). Conclusion: the established high frequency of viral AGE in pregnant women shows the need for introducing into clinical practice universal test systems for diagnosing the most common viral pathogens in order to improve therapy. The eff ectiveness of synbiotic “Normobact” in pregnant women with viral OGE was shown in terms of earlier stopping diarrhea, which makes it possible to recommend it as part of complex therapy.

      1. O sostoyanii sanitarno-epidemiologicheskogo blagopoluchiya naseleniya v Rossiyskoy Federatsii v 2017 godu [On the state of sanitary and epidemiological well-being of the population in the Russian Federation in 2017] State Report. Federal Service for Supervision of Consumer Rights Protection and Human Welfare, 2018, 268 p.
      2. Shrestha A, Bajracharya AM, Subedi H et al. Multidrug resistance and extended spectrum beta lactamase producing Gram negative bacteria from chicken meat in Bharatpur Metropolitan, Nepal. BMC Res Notes. 2017;10(1):574.
      3. Puzari M, Sharma M, Chetia P. Emergence of antibiotic resistant Shigella species: A matter of concern. J Infect Public Health. 2017. S1876–0341(17)30260–5.
      4. Desselberger U. Global issues related to enteric viral infections. Virus disease. 2014; 25(2): 147–9.
      5. Oude Munnink BB, van der Hoek L. Viruses Causing Gastroenteritis: Th e Known, Th e New and Th ose Beyond. Viruses. 2016; 8(2): 42.
      6. Zhang Z, Lai S, Yu J, et al. Etiology of acute diarrhea in the elderly in China: A six-year observational study. PLoS One. 2017; 12(3): e0173881.
      7. Bruun T, Salamanca BV, Bekkevold T, et al. Norwegian Enhanced Pediatric Immunisation Surveillance (NorEPIS) Network. Burden of Rotavirus Disease in Norway: Using National Registries for Public Health Research. Pediatr Infect Dis J. 2016; 35(4):396–400.
      8. O sostoyanii sanitarno-epidemiologicheskogo blagopoluchiya naseleniya v Rossiyskoy Federatsii v 2017 godu [On the state of sanitary and epidemiological well-being of the population in the Russian Federation in 2016] State Report. Federal Service for Supervision of Consumer Rights Protection and Human Welfare, 2017, 200 p.
      9. Yokoyama Y, Asahara T, Nomoto K, et al. Eff ects of Synbiotics to Prevent Postoperative Infectious Complications in Highly Invasive Abdominal Surgery. Ann Nutr Metab. 2017;71 Suppl 1:23–30.
      10. Gurry T. Synbiotic approaches to human health and well-being. Microb Biotechnol. 2017;10(5):1070–1073.
      11. Kukkonen K., Savilahti E., Haahtela T., et al. Long-term safety and impact on infection rates of postnatal probiotic and prebiotic (synbiotic) treatment: randomized, double-blind, placebo-controlled trial // Pediatrics. 2008; 122 (1): 8–12.
      12. Picard C., Fioramonti J., Francois A., et al. Review article: bifi dobacteria as probiotic agents – physiological eff ects and clinical benefi ts // Aliment. Pharmacol. Th er. 2005;22 (6): 495–512.
      13. A. I. Havkin, 2009. Probiotic food and the body's natural defense system. Russian medical journal, 17 (4): 241–245.
      14. Borovik T. E., Yacik S. P. and N. N. Semenova, 2012. Th e effectiveness of synbiotic Normobact in the postoperative period in children with chronic obstructive pyelonephritis. Eff ective pharmacotherapy, (29): 52–56.
      15. Bondarenko V. M., Gracheva N. M., Maculevich T. V. and A. A. Vorobev, 2003. Microecological changes of the intestine and their correction with the help of therapeutic and prophylactic drugs. Journal gastroenterology hepatology coloproctology, 4: 66–76.
      16. Lei WT, Shih PC, Liu SJ, et al. Eff ect of Probiotics and Prebiotics on Immune Response to Infl uenza Vaccination in Adults: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Nutrients. 2017;9(11). pii: E1175.
      17. Kim J, Choi SH, Kim YJ, et al. Clinical Eff ect of IRT-5 Probiotics on Immune Modulation of Autoimmunity or Alloimmunity in the Eye. Nutrients. 2017;9(11). pii: E1166.
      18. Guarino A., Ashkenazi Sh., Gendrel D. et al. European Society for Paediatric Gastroenterology, Hepatology, and Nutrition/European Society for Paediatric Infectious Diseases Evidence-based Guidelines for the Management of Acute Gastroenteritis in Children in Europe // JPGN. 2014; 59 (1):132–152.
      19. Glass I, Parashar UD, Estes MK, Norovirus Gastroenteritis. N Engl J Med. 2009; 361(18): 1776–1785
      20. Krasnova E. I., Kapustin D. V., Khokhlova N. I., Zhirakovskaia E. V. et al. Acute norovirus gastroenteritis in adults. Experimental and Clinical Gastroenterology. 2017;145(09):25–29

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    Krasnova E. I., Kapustin D. V., Khokhlova N. I., Zhirakovskaia E. V. et al. Acute viral gastroenteritis in pregnant women. Experimental and Clinical Gastroenterology. 2018;159(11): 75–82. (In Russ.) DOI: 10.31146/16828658-ecg-159-11-75-82
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    1. Novosibirsk state medical university, Krasnyi prospect, 52, Novosibirsk 630091, Russia

    Keywords: senile asthenic syndrome, opisthorchosis, hepatobiliary system, laennec

    Abstract:The article deals with some features of clinical course, diagnostics, treatment of the senile asthenic syndrome in patients with chronic opisthorchosis and hepatobiliary damage. Values of a life style, a role of etiotropny and pathogenic therapy are shown. Separately the role of application of laennec as an important factor of pathogenetic and anti-aging medicine is considered.

      1. Lazebnik L. B., Drozdov V. I. Diseases of the digestive organs in the elderly. Moscow, Anakharsis Publ. 2003, 207 p.
      2. Lazebnik L. B. Cholelithiasis. Ways to solve the problem. Ter. Arh. 2005, no. 2, pp. 5–9.
      3. Ilnitskiy A. N., Prashchayeu K. I. Frailty as the concept of modern gerontology. GERONTOLOGY. 2013;1(1):5–16.
      4. Rockwood K. Frailti defi ned by defi cit accumulation and geriatric medicine defi ned by frailty // Clin. Geriatr. Med. – 2011 – № 27(1) – p.7–26
      5. Yao X. Infl ammation and immune system alterations in frailty II Clin. Geriatr. Med. – 2011 – #27(1) – p. 79–87
      6. Pal'tsev A. I. Zabolevaniya organov pishchevareniya pri khronicheskom opistorkhoze [Diseases of the digestive organs in chronic opisthorchiasis]. Novosibirsk. 1995, 147 p.
      7. Frankl V. E. [Suff ering from the meaninglessness of life. Actual psychotherapy] Siberian university Publ. 2008, 69 p.
      8. Paltsev A. I. Features of lesion of the gastrointestinal tract in opisthorchiasis. In the book: Gastroenterology. Edited by L. B. Lazebnik and P. L. Shcherbakov. Diseases of adults. – A guide for doctors.
      9. Skulachev V. P., Skulachev M. V., Fenyuk B. A. Zhizn' bez starosti. [Life without old age] Moscow, Eksmo Publ., 2013, 11 p.
      10. Ilnitsky A. N., Maximov V. A., Karimova I. M., Pozdnyakova N. M. Antivozrastnaya meditsina: voprosy gepatologii. Posobiye dlya vrachey. [Anti-aging medicine: issues of hepatology. Manual for doctors]. Moscow, 2016, 38 p.

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    Paltsev A. I. Senile asthenic syndrome in patients with hepatobiliary damage of opisthorchosis etiology. Experimental and Clinical Gastroenterology. 2018;159(11): 93–98. (In Russ.) DOI: 10.31146/1682-8658-ecg-159-11-93-98
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    1. GBU the MСRC named after A. S. Loginov DZ Moscow, 111123 Moscow, Russia
    2. Peoples ' friendship University of Russia, Moscow, Russia
    3. National research Mordovian state University. N. P. Ogaryov, Saransk, Russia

    Keywords: mucous membrane of the gastrointestinal tract, autoimmune component, immune system of the gastrointestinal tract, M-cells

    Abstract:The mucous membrane of the gastrointestinal tract is an extensive information and communication system that quickly reacts to both external and internal factors of the body, ensuring the maintenance of homeostasis of tissue and blood. The aim of the study was to determine the factors that ensure the appearance of an autoimmune component in damage to the pancreas in rats. Material: manipulations were performed on white Wistar rats weighing 190,0–230,0.Immunization of animals was carried out according to the standard scheme. There were 4 intraperitoneal injections of 2 ml of pancreatic tissue homogenate. Total antibodies (at) to parietal cells (PC) (Parietal Cell antibodies, IgG, IgA, IgM) were determined in plasma by enzyme immunoassay. The animals were divided into one control group and fi ve experimental groups (6 groups of 5 rats in total). Experimental groups: 1st-immunization of intact animals (IM) according to the above scheme. 2nd-acute pancreatitis (AP); 3rd group AP+ IM; 4th-chronic pancreatitis (CP); 5th group-CP+IM. With AP and CP, there is an autoimmune component that interferes with the restoration of damaged pancreatic tissue. Experimental studies have shown that the presence of acute infl ammation, accompanied by full blood vessels, hyperemia, edema, hypoxia, necrosis, death of a large number of cells, the release of cellular elements that are endogenous antigens. Infl ammation of the pancreas stimulates the immune system of the gastrointestinal tract. In addition, factors contributing to the development of an autoimmune reaction are: alcohol, infection: bacterial, viral and/or parasitic.

      1. Yaglov V. V. Yaglova N. V. Itogi i perspektivy izucheniya diff uznoy endokrinnoy epitelialnoy sistemy. Klinicheskaya i eksperimentalnaya morfologiya. 2012. № 3. p.3
      2. Aruin L. I. Zverkov I. V. Vinogradov V. A. Endokrinnyye kletki zheludochno-kishechnogo trakta. Klinicheskaya meditsina. 1987, no. 6, p. 2231.
      3. Kvetnoy I. M. APUD-SISTEMA (strukturno-funktsionalnaya organizatsiya. biologicheskoye znacheniye v norme i patologii). Uspekhi fi ziologicheskikh nauk. 1987, vol. 18. no. 1, p. 84–102.
      4. Aleshin B. V. Problema neyroendokrinnykh kletok i gipotezy “Diff uznoy endokrinnoy sistemy.” Uspekhi sovremennoy biologii. 1984, vol. 98, no. 1(4), p.116–133.
      5. Korotko G. F. Fiziologiya sistemy pishchevareniya. OOO BK “Gruppa B” Krasnodar. 2009, 608 p.
      6. Sapin M. R. Immunnyye struktury pishchevaritelnoy sistemy. Meditsina. 1987, 224 p.
      7. Kononov A. V. Mestnyy immunnyy otvet na infektsiyu Helicobacter pylori. Rossiyskiy zhurnal gastroenterologii. gepatologii. koloproktologii. 1999, no.2, pp.15–22.
      8. Jang MH, Kweon MN, Iwatani K, Yamamoto M, Terahara K, Sasakawa C, Suzuki T, Nochi T, Yokota Y, Rennert PD, et al. Intestinal villous M cells: an antigen entry site in the mucosal epithelium. Proc Nat AcadSci U S A 2004; 101:6110–5; PMID:15071180; http:// [PMC free article] [PubMed] [Cross Ref]
      9. Kyd JM, Cripps AW. Functional diff erences between M cells and enterocytes in sampling luminal antigens. Vaccine 2008; 26:6221–4; PMID:18852006; http://dx.doi. org/10.1016/j.vaccine.2008.09.061 [PubMed] [Cross Ref]
      10. Miller H, Zhang J, Kuolee R, Patel GB, Chen W. Intestinal M cells: the fallible sentinels? World J Gastroenterol: WJG 2007; 13:1477–86; PMID:17461437; http://dx.doi .org/10.3748/wjg.v13.i10.1477 [PMC free article] [PubMed] [Cross Ref]Жуков Н.А., Гусаров А. И. Иммунологические аспекты кишечного дисбактериоза // Терапевтический архив. 1980. – Т. 52, № 2. – С. 23–27.
      11. Proshchina A. E., Savelyev S. V. Immunogistokhimicheskoye issledovaniye raspredeleniya A- i B- kletok v raznykh tipakh ostrovkov Langergansa podzheludochnoy zhelezy cheloveka. Byulleten eksperimentalnoy biologii i meditsiny. 2013, Vol. 155, no.6, p.763. http://www.iramn. ru/journal/bebm/2013/bbm1306.htm
      12. Trubitsyna I. E. Vorobyeva N. N. Chikunova B. Z. Kryukova N. B. Autoimmunnyy komponent pri alkogolnom povrezhdenii pecheni u krys. Eksperimentalnaya i klinicheskaya gastroenterologiya. 2012, no. 12, p.52–54.
      13. Trubitsina I. E. Abdulatipova Z. M. Vasnev O. S. et al. Cerotonin v razvitii i podderzhanii vospalitelnoy reaktsii v slizistoy obolochke zheludka u krys. Fundamentalnyye issledovaniya. 2014, no.10–2, pp. 380–385.
      14. Trubitsyna I. E., Smirnova A. V., Chikunova B. Z., Sokolov D. V. Patogeneticheskoye obosnovaniye korrektsii morfologicheskikh izmeneniy i disbalansa tsitokinov v eksperimentalnoy modeli yazvy zheludka. Lecheniye i profi laktika. 2015, no. 3 (15), pp. 63–68.
      15. Trubitsyna I. E., Smirnova A. V., Chikunova B. Z., Sokolov D. V. Patogeneticheskoye obosnovaniye korrektsii morfologicheskikh izmeneniy i disbalansa tsitokinov v eksperimentalnoy modeli yazvy zheludka. Lecheniye i profi laktika. 2015, no. 3 (15), pp. 63–68.
      16. Trubitsyna I., Onischenko N., Lyundup A., Knyazev O., Parfenov A., Vinocurova L., Orlova Yu., Abdulatipova Z., Ruchkina I., Smirnova A. Иммуномодулирующий эффект аллогенных мезенхимальных стволовых клеток костного мозга крыс// В книге: Abstracts for Cell Technologies at Th e Edge: Research & Practice (CTERP) 2016. С. 121.

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    Trubitsyna I. E., Ruchkin I. N., Mikhailovа S. F., Efremov L. I. et al. MALT-the mucous membrane system of the gastrointestinal tract. Experimental and Clinical Gastroenterology. 2018;159(11): 83–87. (In Russ.) DOI: 10.31146/1682-8658-ecg-159-11-83-87
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    1. Pirogov Russian National Research Medical University (RNRMU), Moscow, Russia
    2. Peoples Friendship University of Russia (RUDN), Moscow 117198, Russia

    Keywords: stomach, colon, motor activity, serotonin

    Abstract:Trial objective: study the mechanism of multidirectional eff ect of Serotonin adipinate on gastric and colon motor activity. Materials and methods: experiments were carried out on Wistar rats (N83) in surgical anesthesia. An electromyogram and hydrostatic pressure in the cavities of organs was registered using an amplifi er BioAmp ML132 (Adinstruments, Australia), an analog-to-digital converter Maclab 8e (Adinstruments, Australia), a computer Масintosh Performa 6400/180 and a software program Chart 4.2.3. Trial fi ndings: it was established that intra-arterial injection of Serotonin adipinate at a dose of 0.05 mg/kg and 0.1 mg/ kg causes stimulatory and inhibitory gastric reactions; at a dose of 0.15 mg/kg — only stimulatory ones. Colon appeared to have only stimulatory reactions. It was also found that intravenous injection of Serotonin adipinate does not intensify stomach and colon contraction. Conclusion. Organs’ stimulatory reactions occur due to activation of muscle 5HT-receptors, inhibitory ones — due to activation of presynaptic 5HT-receptors, locating on organ’s adrenergic terminals, and ejection of inhibitory transmitter noradrenaline by them. When using Serotonin adipinate in experiment and in clinical practice, it is necessary to take into account that the organs’ eff ect from serotonin administration into body may be dual: inhibitory at low doses and stimulatory at higher ones.

      1. Davis R., Pattison J., Th ompson J. et al. 5-hydroxytryptamine (5-HT) reduces total peripheral resistance during chronic infusion: direct arterial mesenteric relaxation is not involved. BMC Pharmacol. 2012; V 12: 4.
      2. Arreola-Ramírez J., Vargas D., Manjarrez-Gutiérrez G. et al. Modifi cations of plasma 5-HT concentrations during the allergic bronchoconstriction in guinea pigs. Exp. Lung. Res. 2013; 39 (7): 269–274.
      3. Veasey S. Serotonin agonists and antagonists in obstructive sleep apnea: therapeutic potential. Amer. J. Respir. Med. 2003; 2(1): 21–29.
      4. Tamura T., Sano I., Satoh M. et al. Pharmacological characterization of 5-hydroxytryptamine-induced motor activity (in vitro) in the guinea pig gastric antrum and corpus. Europ. J. Pharmacol. 1996; 308 (3): 315–324.
      5. Овсянников В. И., Березина Т. П. Механизмы влияния серотонина на моторную активность двенадцатиперстной, тощей и подвздошной кишки у бодрствующих кроликов. Рос. физиол. журн. им. И. М. Сеченова 2002; № 8: 1017–1027.
      6. Ovsiannikov V. I., Berezina T. P. Mechanism of the serotonin eff ect on motility of the duodenum, ileum, and jejunum in awake rabbits. Russian journal of physiology. 2002, no.8, pp.1017-1027
      7. van Lelyveld N., Ter Linde J., Schipper M. et al. Serotonergic signalling in the stomach and duodenum of patients with gastroparesis. Neurogastroenterol. Motil. 2008; 20 (5): 448–455.
      8. Sia T., Whiting M., Kyloh M. 5-HT3 and 5-HT4 antagonists inhibit peristaltic contractions in guinea-pig distal colon by mechanisms independent of endogenous 5-HT. Front. Neurosci. 2013; 7: 136.
      9. Song J., Yin J., Chen J. Acute and chronic eff ects of desvenlafaxine on gastrointestinal transit and motility in dogs. Neurogastroenterol. Motil. 2013; 25 (10): 824.
      10. Lee J., Sung K., Lee O. et al. Th e eff ects of 5-HT4 receptor agonist, mosapride citrate, on visceral hypersensitivity in a rat model. Dig. Dis. Sci. 2012; 57 (6): 1517–1524.
      11. Sinenchenko G. I., Verbitskiy V. G., Kolunov A. V. Endolymphatic infusion of serotonin adipinate in the treatment of postoperative intestinal paresis. MIA Medical Bulletin. 2006; no 2, pp. 21–23.
      12. Kale-Pradhan Pramodini B., Wilhelm Sheila M. Tegaserod for constipation-predominant irritable bowel syndrome. Pharmacotherapy. 2007; 27 (2): 267–277.
      13. MacLean M.R., Dempsie Y. Serotonin and pulmonary hypertension – from bench to bedside. Curr. Opin. Pharmacol. 2009; 9 (3): 281–286.
      14. McKenzie C., Alapati V. R., MacDonald A. et al. Mechanisms involved in the regulation of bovine pulmonary vascular tone by the 5HT1B-receptor. Brit. J. Pharmacol 2010; 159 (1): 188–200.
      15. Purohit A., Herrick-Davis K., Teitler M. Creation, expression, and characterization of a constitutively active mutant of the human serotonin 5-HT6-receptor. Synapse. 2003; 47(3): 218–224.
      16. Th umshirn M., Fraehauf H., Stutz B. et al. Clinical trial: Eff ects of tegaserod on gastric motor and sensory function in patients with functional dyspepsia. Alim. Pharmacol. Th er. 2007; 26 (10): 1399–1407.

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    Smirnov V. M., Sveshnikov D. S., Kuchuk A. V., Trubetskaya L. V., Mongush M. I., Ignatova E. D. The mechanism of multidirectional eff ects of serotonin on the motility of the stomach and colon. Experimental and Clinical Gastroenterology. 2018;159(11): 88–92. (In Russ.) DOI: 10.31146/1682-8658-ecg159-11-88-92
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    1. E. A. Vagner Perm State Medical University, 614990, Perm, Russia

    Abstract:Иван Михайлович Сеченов родился 1 (13) августа 1829 года в селе Теплый Стан Курмыжского уезда Симбирской губернии (ныне – село Сеченово Нижегородской области) в семье помещика-дворянина среднего достатка, отставного секунд-майора Преображенского гвардейского полка Михаила Алексеевича Сеченова. Выйдя в отставку, его отец поселился в своем родовом поместье Теплый Стан. Вопреки традиции, он выбрал себе в жены не соседскую помещичью дочку, а свою крепостную крестьянку Анисью Григорьевну – нежную, кроткую и умную девушку, которой он предоставил вольную и сочетался церковным браком, создав многочисленную, дружную и счастливую семью, в которой было восемь детей – 5 мальчиков и 3 девочки, младшим из которых был сын Иван. Отец помог жене получить начальное образование в близлежащем монастыре. и т.д.

      1. Сеченов И. М. Избранные произведения. – М., 1953. Sechenov I. M. Selected works. Moscow, 1953.
      2. Kachanov V. M. I. M. Sechenov. – Preface to the book. “Selected Works.” Moscow, 1953, pp. 3–30.
      3. Sukhomlinov K. Ivan Mikhailovich Sechenov / In the book: “Doctors who changed the world.” Moscow, 2014, pp. 198–207.
      4. Sechenov I. M. Refl exes of the brain (1863). – In the book: Collected Works. Moscow, 1908, pp. 31–118.
      5. Shoyfet M. S. Sechenov / In the book: “One Hundred Great Doctors.” Moscow, 2011, pp. 307–316.
      6. Sechenov I. M. Elements of thought. – Bulletin of Europe, 1878.

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    Zimmerman Ya. S. Ivan Mikhailovich Sechenov — the Great Russian Physiologist: life path and scientifi c achievements. Experimental and Clinical Gastroenterology. 2018;159(11): 99–102. (In Russ.) DOI: 10.31146/1682-8658-ecg-159-11-99-102
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