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Роль основных факторов риска и эндокринных клеток антрального отдела желудка, продуцирующих мотилин, в возникновении желчнокаменной болезни
Роль основных факторов риска и эндокринных клеток антрального отдела желудка, продуцирующих мотилин, в возникновении желчнокаменной болезни
Свистунов А.А., Осадчук М.А., Миронова Е.Д., Гуляев П.В., Васильева И.Н. Роль основных факторов риска и эндокринных клеток антрального отдела желудка, продуцирующих мотилин, в возникновении желчнокаменной болезни. Терапевтический архив. 2022;94(2):194–199.
DOI: 10.26442/00403660.2022.02.201370
DOI: 10.26442/00403660.2022.02.201370
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Материалы доступны только для специалистов сферы здравоохранения. Авторизуйтесь или зарегистрируйтесь.
Аннотация
Цель. Установить роль основных факторов риска и эндокринных клеток антрального отдела желудка, продуцирующих мотилин (М-клетки), в возникновении желчнокаменной болезни (ЖКБ).
Материалы и методы. В 1-ю группу включены 122 пациента с ЖКБ; 2-ю группу составили 30 здоровых лиц, прошедших диспансеризацию. Группы сопоставимы по полу и возрасту. В работе анализировались анамнестические, биохимические и антропометрические данные. Всем пациентам выполнялась эзофагогастродуоденоскопия с прицельной биопсией слизистой оболочки из антрального отдела желудка. Биоптаты подвергнуты цитологическому и иммуногистохимическому исследованию с целью верификации Helicobacter pylori и оценки количества М-клеток.
Результаты. Пациенты с ЖКБ чаще относились к группе лиц умственного труда, имели низкую физическую активность, оказались привержены нерациональному питанию и чаще указывали на наличие отягощенной наследственности по ЖКБ. У пациентов с ЖКБ отмечались более высокие показатели индекса массы тела, объема талии, уровня общего холестерина (ХС), ХС липопротеидов низкой плотности, триглицеридов, глюкозы, более низкий уровень ХС липопротеидов высокой плотности, чаще верифицировалась инфекция H. pylori и установлена гипоплазия М-клеток в слизистой оболочке желудка по сравнению с представителями 2-й группы.
Заключение. Полученные нами результаты дают основание сделать вывод о том, что определенные внешние факторы, особенности питания, компоненты метаболического синдрома, гипоплазия М-клеток в слизистой оболочке желудка являются важными факторами формирования конкрементов в желчном пузыре.
Ключевые слова: желчнокаменная болезнь, факторы риска, М-клетки, мотилин, Helicobacter pylori
Materials and methods. The first group included 122 patients with cholelithiasis. The second group consisted of 30 healthy individuals who underwent medical examination. The groups were matched for gender and age. The work analyzed anamnestic, biochemical and anthropometric data. All patients underwent esophagogastroduodenoscopy with targeted biopsy of the mucous membrane from the antrum. Biopsies were subjected to cytological and immunohistochemical studies in order to verify Helicobacter pylori and estimate the number of M-cells.
Results. Patients with cholelithiasis more often belonged to the group of people of mental labor, had low physical activity, were committed to inappropriate nutrition and more often indicated the presence of aggravated heredity for cholelithiasis. Patients with gallstone disease had higher body mass index, waist volume, total cholesterol, low-density lipoprotein cholesterol, triglycerides, glucose, lower high-density lipoprotein cholesterol, H. pylori infection was more often verified and M-cell hypoplasia in the mucous membrane was established. stomach in comparison with the representatives of the second group.
Conclusion. Our results suggest that certain external factors, nutritional characteristics of the metabolic syndrome components, hypoplasia of M-cells in the gastric mucosa are important factors in the formation of calculi in the gallbladder.
Keywords: gallstone disease, risk factors, M-cells, motilin, Helicobacter pylori
Материалы и методы. В 1-ю группу включены 122 пациента с ЖКБ; 2-ю группу составили 30 здоровых лиц, прошедших диспансеризацию. Группы сопоставимы по полу и возрасту. В работе анализировались анамнестические, биохимические и антропометрические данные. Всем пациентам выполнялась эзофагогастродуоденоскопия с прицельной биопсией слизистой оболочки из антрального отдела желудка. Биоптаты подвергнуты цитологическому и иммуногистохимическому исследованию с целью верификации Helicobacter pylori и оценки количества М-клеток.
Результаты. Пациенты с ЖКБ чаще относились к группе лиц умственного труда, имели низкую физическую активность, оказались привержены нерациональному питанию и чаще указывали на наличие отягощенной наследственности по ЖКБ. У пациентов с ЖКБ отмечались более высокие показатели индекса массы тела, объема талии, уровня общего холестерина (ХС), ХС липопротеидов низкой плотности, триглицеридов, глюкозы, более низкий уровень ХС липопротеидов высокой плотности, чаще верифицировалась инфекция H. pylori и установлена гипоплазия М-клеток в слизистой оболочке желудка по сравнению с представителями 2-й группы.
Заключение. Полученные нами результаты дают основание сделать вывод о том, что определенные внешние факторы, особенности питания, компоненты метаболического синдрома, гипоплазия М-клеток в слизистой оболочке желудка являются важными факторами формирования конкрементов в желчном пузыре.
Ключевые слова: желчнокаменная болезнь, факторы риска, М-клетки, мотилин, Helicobacter pylori
________________________________________________
Materials and methods. The first group included 122 patients with cholelithiasis. The second group consisted of 30 healthy individuals who underwent medical examination. The groups were matched for gender and age. The work analyzed anamnestic, biochemical and anthropometric data. All patients underwent esophagogastroduodenoscopy with targeted biopsy of the mucous membrane from the antrum. Biopsies were subjected to cytological and immunohistochemical studies in order to verify Helicobacter pylori and estimate the number of M-cells.
Results. Patients with cholelithiasis more often belonged to the group of people of mental labor, had low physical activity, were committed to inappropriate nutrition and more often indicated the presence of aggravated heredity for cholelithiasis. Patients with gallstone disease had higher body mass index, waist volume, total cholesterol, low-density lipoprotein cholesterol, triglycerides, glucose, lower high-density lipoprotein cholesterol, H. pylori infection was more often verified and M-cell hypoplasia in the mucous membrane was established. stomach in comparison with the representatives of the second group.
Conclusion. Our results suggest that certain external factors, nutritional characteristics of the metabolic syndrome components, hypoplasia of M-cells in the gastric mucosa are important factors in the formation of calculi in the gallbladder.
Keywords: gallstone disease, risk factors, M-cells, motilin, Helicobacter pylori
Полный текст
Список литературы
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20. Tung TH, Ho HM, Shih HC, et al. A population-based follow-up study on gallstone disease among type 2 diabetics in Kinmen, Taiwan. World J Gastroenterol WJG. 2006;12(28):4536-40. DOI:10.3748/wjg.v12.i28.4536
21. Dixon JB, O’Brien PE. Obesity and the white blood cell count: changes with sustained weight loss. Obes Surg. 2006;16(3):251-7. DOI:10.1381/096089206776116453
22. Chen LY, Qiao QH, Zhang SC, et al. Metabolic syndrome and gallstone disease. World J Gastroenterol. 2012;18(31):4215-20. DOI:10.3748/wjg.v18.i31.4215
23. de Boer SY, Masclee AA, Lamers CB. Effect of hyperglycemia on gastrointestinal and gallbladder motility. Scand J Gastroenterol Suppl. 1992;194:13-8. DOI:10.3109/00365529209096020
24. Biddinger SB, Haas JT, Yu BB, et al. Hepatic insulin resistance directly promotes formation of cholesterol gallstones. Nat Med.2008;14(7):778-82.DOI:10.1038/nm1785
25. Smelt AHM. Triglycerides and gallstone formation. Clin Chim Acta. 2010;411(21-2):1625-31. DOI:10.1016/j.cca.2010.08.003
26. Budzyński J, Kłopocka M. Brain-gut axis in the pathogenesis of Helicobacter pylori infection. World J Gastroenterol WJG. 2014;20(18):5212-25. DOI:10.3748/wjg.v20.i18.5212
27. Murakami K, Fujioka T, Shiota K, et al. Influence of Helicobacter pylori infection and the effects of its eradication on gastric emptying in non-ulcerative dyspepsia. Eur J Gastroenterol Hepatol. 1995;7(1):S93-7.
28. Cen L, Pan J, Zhou B, et al. Helicobacter pylori infection of the gallbladder and the risk of chronic cholecystitis and cholelithiasis: a systematic review and meta-analysis. Helicobacter. 2018;23(1). DOI:10.1111/hel.12457
29. Apostolov E, Al-Soud WA, Nilsson I, et al. Helicobacter pylori and other Helicobacter species in gallbladder and liver of patients with chronic cholecystitis detected by immunological and molecular methods. Scand J Gastroenterol. 2005;40(1):96-102. DOI:10.1080/00365520410009546
30. Hoffmeister A, Rothenbacher D, Bode G, et al. Current infection with Helicobacter pylori, but not seropositivity to Chlamydia pneumoniae or cytomegalovirus, is associated with an atherogenic, modified lipid profile. Arterioscler Thromb Vasc Biol. 2001;21(3):427-32. DOI:10.1161/01.atv.21.3.427
31. Weber SN, Bopp C, Krawczyk M, Lammert F. Genetics of gallstone disease revisited: updated inventory of human lithogenic genes. Curr Opin Gastroenterol. 2019;35(2):82-7.
DOI:10.1097/MOG.0000000000000511
32. Shabanzadeh DM, Novovic S. Alcohol, smoking and benign hepato-biliary disease. Best Pract Res Clin Gastroenterol. 2017;31(5):519-27. DOI:10.1016/j.bpg.2017.09.005
2. Osadchuk MA, Svistunov AA. Mironova ED, et al. Diseases of biliary tract in the context of association with oncological diseases of the digestive system. Terapevticheskii Arkhiv (Ter. Arkh.). 2019;91(12):98-104 (in Russian). DOI:10.26442/00403660.2019.12.000455
3. Uspenskiy YP, Fominykh YuA, Nadzhafova KN, et al. Pathogenetic aspects of the development of cholelithiasis in patients with metabolic syndrome. Terapevticheskii Arkhiv (Ter. Arkh.). 2021;93(2):209-14 (in Russian). DOI:10.26442/00403660.2021.02.200616
4. Thomas LA, Veysey MJ, Murphy GM, et al. Octreotide induced prolongation of colonic transit increases faecal anaerobic bacteria, bile acid metabolising enzymes, and serum deoxycholic acid in patients with acromegaly. Gut. 2005;54(5):630-5. DOI:10.1136/gut.2003.028431
5. van Erpecum KJ, van Berge Henegouwen GP. Intestinal aspects of cholesterol gallstone formation. Dig Liver Dis Off J Ital Soc Gastroenterol Ital Assoc Study Liver. 2003;35(3):S8-11. DOI:10.1016/s1590-8658(03)00086-0
6. Xie M, Kotecha VR, Andrade JDP, et al. Augmented cholesterol absorption and sarcolemmal sterol enrichment slow small intestinal transit in mice, contributing to cholesterol cholelithogenesis. J Physiol. 2012;590(8):1811-24. DOI:10.1113/jphysiol.2011.224717
7. Zhang ZH, Wu SD, Wang B, et al. Sphincter of Oddi hypomotility and its relationship with duodenal-biliary reflux, plasma motilin and serum gastrin. World J Gastroenterol. 2008;14(25):4077-81. DOI:10.3748/wjg.14.4077
8. Wu Z, Luo H, Liang C. Role and mechanism of motilin in colonic motility disorder. Zhonghua Yi Xue Za Zhi. 2012;92(14):984-8.
9. Lang IM, Sarna SK, Condon RE. Myoelectric and contractile effects of motilin on dog small intestine in vivo. Dig Dis Sci. 1986;31(10):1062-72. DOI:10.1007/BF01300259
10. Apu AS, Mondal A, Kitazawa T, et al. Molecular cloning of motilin and mechanism of motilin-induced gastrointestinal motility in Japanese quail. Gen Comp Endocrinol. 2016;233:53-62. DOI:10.1016/j.ygcen.2016.05.017
11. Kamerling IMC, Van Haarst AD, De Kam ML, et al. Gallbladder volume as a biomarker for the motilin effect in healthy volunteers and patients with functional dyspepsia. Aliment Pharmacol Ther. 2004;19(7):797-804. DOI:10.1111/j.1365-2036.2004.01905.x
12. Vahrushev YaM, Hohlacheva NA. Factors contributing to gallstone formation and their interaction. Terapevticheskii Arkhiv (Ter. Arkh.). 2010;82(1):8-11 (in Russian).
13. Shaodong C, Haihong Z, Manting L, Get al. Research of influence and mechanism of combining exercise with diet control on a model of lipid metabolism rat induced by high fat diet. Lipids Health Dis. 2013;12:21. DOI:10.1186/1476-511X-12-21
14. Kay RG, Foreman RE, Roberts GP, et al. Mass spectrometric characterisation of the circulating peptidome following oral glucose ingestion in control and gastrectomised patients. Rapid Commun Mass Spectrom. 2020;34(18):e8849. DOI:10.1002/rcm.8849
15. Hou L, Shu XO, Gao YT, et al. Anthropometric measurements, physical activity, and the risk of symptomatic gallstone disease in Chinese women. Ann Epidemiol. 2009;19(5):344-50. DOI:10.1016/j.annepidem.2008.12.002
16. Kiani Q, Farooqui F, Khan MS, et al. Association of body mass index and diet with symptomatic gall stone disease: a case-control study. Cureus. 2020;12(3):e7188. DOI:10.7759/cureus.7188
17. Ryu S, Chang Y, Kim YS, Kim HJ. Prolonged sitting increases the risk of gallstone disease regardless of physical activity: a cohort study. Scand J Gastroenterol. 2018;53(7):864-9. DOI:10.1080/00365521.2018.1476910
18. Aronov DM, Gulyaeva SF, Shihova EV, Vedernikov VA. Physical exercise in combined outpatient rehabilitation of coronary patients with biliary dysfunction. Terapevticheskii Arkhiv (Ter. Arkh.). 2011;83(1):21-5 (in Russian).
19. Del Pozo R, Mardones L, Villagrán M, et al. Effect of a high-fat diet on cholesterol gallstone formation. Rev Med Chil. 2017;145(9):1099-105.
DOI:10.4067/s0034-98872017000901099
20. Tung TH, Ho HM, Shih HC, et al. A population-based follow-up study on gallstone disease among type 2 diabetics in Kinmen, Taiwan. World J Gastroenterol WJG. 2006;12(28):4536-40. DOI:10.3748/wjg.v12.i28.4536
21. Dixon JB, O’Brien PE. Obesity and the white blood cell count: changes with sustained weight loss. Obes Surg. 2006;16(3):251-7. DOI:10.1381/096089206776116453
22. Chen LY, Qiao QH, Zhang SC, et al. Metabolic syndrome and gallstone disease. World J Gastroenterol. 2012;18(31):4215-20. DOI:10.3748/wjg.v18.i31.4215
23. de Boer SY, Masclee AA, Lamers CB. Effect of hyperglycemia on gastrointestinal and gallbladder motility. Scand J Gastroenterol Suppl. 1992;194:13-8. DOI:10.3109/00365529209096020
24. Biddinger SB, Haas JT, Yu BB, et al. Hepatic insulin resistance directly promotes formation of cholesterol gallstones. Nat Med.2008;14(7):778-82.DOI:10.1038/nm1785
25. Smelt AHM. Triglycerides and gallstone formation. Clin Chim Acta. 2010;411(21-2):1625-31. DOI:10.1016/j.cca.2010.08.003
26. Budzyński J, Kłopocka M. Brain-gut axis in the pathogenesis of Helicobacter pylori infection. World J Gastroenterol WJG. 2014;20(18):5212-25. DOI:10.3748/wjg.v20.i18.5212
27. Murakami K, Fujioka T, Shiota K, et al. Influence of Helicobacter pylori infection and the effects of its eradication on gastric emptying in non-ulcerative dyspepsia. Eur J Gastroenterol Hepatol. 1995;7(1):S93-7.
28. Cen L, Pan J, Zhou B, et al. Helicobacter pylori infection of the gallbladder and the risk of chronic cholecystitis and cholelithiasis: a systematic review and meta-analysis. Helicobacter. 2018;23(1). DOI:10.1111/hel.12457
29. Apostolov E, Al-Soud WA, Nilsson I, et al. Helicobacter pylori and other Helicobacter species in gallbladder and liver of patients with chronic cholecystitis detected by immunological and molecular methods. Scand J Gastroenterol. 2005;40(1):96-102. DOI:10.1080/00365520410009546
30. Hoffmeister A, Rothenbacher D, Bode G, et al. Current infection with Helicobacter pylori, but not seropositivity to Chlamydia pneumoniae or cytomegalovirus, is associated with an atherogenic, modified lipid profile. Arterioscler Thromb Vasc Biol. 2001;21(3):427-32. DOI:10.1161/01.atv.21.3.427
31. Weber SN, Bopp C, Krawczyk M, Lammert F. Genetics of gallstone disease revisited: updated inventory of human lithogenic genes. Curr Opin Gastroenterol. 2019;35(2):82-7.
DOI:10.1097/MOG.0000000000000511
32. Shabanzadeh DM, Novovic S. Alcohol, smoking and benign hepato-biliary disease. Best Pract Res Clin Gastroenterol. 2017;31(5):519-27. DOI:10.1016/j.bpg.2017.09.005
2. Осадчук М.А., Свистунов А.А., Миронова Е.Д., и др. Болезни билиарного тракта в контексте ассоциации с онкологическими заболеваниями пищеварительной системы. Терапевтический архив. 2019;91(12):98-104 [Osadchuk MA, Svistunov AA. Mironova ED, et al. Diseases of biliary tract in the context of association with oncological diseases of the digestive system. Terapevticheskii Arkhiv (Ter. Arkh.). 2019;91(12):98-104 (in Russian)]. DOI:10.26442/00403660.2019.12.000455
3. Успенский Ю.П., Фоминых Ю.А., Наджафова К.Н., и др. Патогенетические аспекты развития желчнокаменной болезни у пациентов с метаболическим синдромом. Терапевтический архив. 2021;93(2):209-14 [Uspenskiy YP, Fominykh YuA, Nadzhafova KN, et al. Pathogenetic aspects of the development of cholelithiasis in patients with metabolic syndrome. Terapevticheskii Arkhiv (Ter. Arkh.). 2021;93(2):209-14 (in Russian)]. DOI:10.26442/00403660.2021.02.200616
4. Thomas LA, Veysey MJ, Murphy GM, et al. Octreotide induced prolongation of colonic transit increases faecal anaerobic bacteria, bile acid metabolising enzymes, and serum deoxycholic acid in patients with acromegaly. Gut. 2005;54(5):630-5. DOI:10.1136/gut.2003.028431
5. van Erpecum KJ, van Berge Henegouwen GP. Intestinal aspects of cholesterol gallstone formation. Dig Liver Dis Off J Ital Soc Gastroenterol Ital Assoc Study Liver. 2003;35(3):S8-11. DOI:10.1016/s1590-8658(03)00086-0
6. Xie M, Kotecha VR, Andrade JDP, et al. Augmented cholesterol absorption and sarcolemmal sterol enrichment slow small intestinal transit in mice, contributing to cholesterol cholelithogenesis. J Physiol. 2012;590(8):1811-24. DOI:10.1113/jphysiol.2011.224717
7. Zhang ZH, Wu SD, Wang B, et al. Sphincter of Oddi hypomotility and its relationship with duodenal-biliary reflux, plasma motilin and serum gastrin. World J Gastroenterol. 2008;14(25):4077-81. DOI:10.3748/wjg.14.4077
8. Wu Z, Luo H, Liang C. Role and mechanism of motilin in colonic motility disorder. Zhonghua Yi Xue Za Zhi. 2012;92(14):984-8.
9. Lang IM, Sarna SK, Condon RE. Myoelectric and contractile effects of motilin on dog small intestine in vivo. Dig Dis Sci. 1986;31(10):1062-72. DOI:10.1007/BF01300259
10. Apu AS, Mondal A, Kitazawa T, et al. Molecular cloning of motilin and mechanism of motilin-induced gastrointestinal motility in Japanese quail. Gen Comp Endocrinol. 2016;233:53-62. DOI:10.1016/j.ygcen.2016.05.017
11. Kamerling IMC, Van Haarst AD, De Kam ML, et al. Gallbladder volume as a biomarker for the motilin effect in healthy volunteers and patients with functional dyspepsia. Aliment Pharmacol Ther. 2004;19(7):797-804. DOI:10.1111/j.1365-2036.2004.01905.x
12. Вахрушев Я.М., Хохлачева Н.А. Факторы, способствующие образованию желчных камней, и их взаимодействие. Терапевтический архив. 2010;82(1):8-11 [Vahrushev YaM, Hohlacheva NA. Factors contributing to gallstone formation and their interaction. Terapevticheskii Arkhiv (Ter. Arkh.). 2010;82(1):8-11 (in Russian)].
13. Shaodong C, Haihong Z, Manting L, Get al. Research of influence and mechanism of combining exercise with diet control on a model of lipid metabolism rat induced by high fat diet. Lipids Health Dis. 2013;12:21. DOI:10.1186/1476-511X-12-21
14. Kay RG, Foreman RE, Roberts GP, et al. Mass spectrometric characterisation of the circulating peptidome following oral glucose ingestion in control and gastrectomised patients. Rapid Commun Mass Spectrom. 2020;34(18):e8849. DOI:10.1002/rcm.8849
15. Hou L, Shu XO, Gao YT, et al. Anthropometric measurements, physical activity, and the risk of symptomatic gallstone disease in Chinese women. Ann Epidemiol. 2009;19(5):344-50. DOI:10.1016/j.annepidem.2008.12.002
16. Kiani Q, Farooqui F, Khan MS, et al. Association of body mass index and diet with symptomatic gall stone disease: a case-control study. Cureus. 2020;12(3):e7188. DOI:10.7759/cureus.7188
17. Ryu S, Chang Y, Kim YS, Kim HJ. Prolonged sitting increases the risk of gallstone disease regardless of physical activity: a cohort study. Scand J Gastroenterol. 2018;53(7):864-9. DOI:10.1080/00365521.2018.1476910
18. Аронов Д.М., Гуляева С.Ф., Шихова Е.В., Ведерников В.А. Физические тренировки в комплексной амбулаторно-поликлинической реабилитации больных ишемической болезнью сердца, ассоциированной с дисфункцией билиарного тракта. Терапевтический архив. 2011;83(1):21-5 [Aronov DM, Gulyaeva SF, Shihova EV, Vedernikov VA. Physical exercise in combined outpatient rehabilitation of coronary patients with biliary dysfunction. Terapevticheskii Arkhiv (Ter. Arkh.). 2011;83(1):21-5 (in Russian)].
19. Del Pozo R, Mardones L, Villagrán M, et al. Effect of a high-fat diet on cholesterol gallstone formation. Rev Med Chil. 2017;145(9):1099-105.
DOI:10.4067/s0034-98872017000901099
20. Tung TH, Ho HM, Shih HC, et al. A population-based follow-up study on gallstone disease among type 2 diabetics in Kinmen, Taiwan. World J Gastroenterol WJG. 2006;12(28):4536-40. DOI:10.3748/wjg.v12.i28.4536
21. Dixon JB, O’Brien PE. Obesity and the white blood cell count: changes with sustained weight loss. Obes Surg. 2006;16(3):251-7. DOI:10.1381/096089206776116453
22. Chen LY, Qiao QH, Zhang SC, et al. Metabolic syndrome and gallstone disease. World J Gastroenterol. 2012;18(31):4215-20. DOI:10.3748/wjg.v18.i31.4215
23. de Boer SY, Masclee AA, Lamers CB. Effect of hyperglycemia on gastrointestinal and gallbladder motility. Scand J Gastroenterol Suppl. 1992;194:13-8. DOI:10.3109/00365529209096020
24. Biddinger SB, Haas JT, Yu BB, et al. Hepatic insulin resistance directly promotes formation of cholesterol gallstones. Nat Med.2008;14(7):778-82.DOI:10.1038/nm1785
25. Smelt AHM. Triglycerides and gallstone formation. Clin Chim Acta. 2010;411(21-2):1625-31. DOI:10.1016/j.cca.2010.08.003
26. Budzyński J, Kłopocka M. Brain-gut axis in the pathogenesis of Helicobacter pylori infection. World J Gastroenterol WJG. 2014;20(18):5212-25. DOI:10.3748/wjg.v20.i18.5212
27. Murakami K, Fujioka T, Shiota K, et al. Influence of Helicobacter pylori infection and the effects of its eradication on gastric emptying in non-ulcerative dyspepsia. Eur J Gastroenterol Hepatol. 1995;7(1):S93-7.
28. Cen L, Pan J, Zhou B, et al. Helicobacter pylori infection of the gallbladder and the risk of chronic cholecystitis and cholelithiasis: a systematic review and meta-analysis. Helicobacter. 2018;23(1). DOI:10.1111/hel.12457
29. Apostolov E, Al-Soud WA, Nilsson I, et al. Helicobacter pylori and other Helicobacter species in gallbladder and liver of patients with chronic cholecystitis detected by immunological and molecular methods. Scand J Gastroenterol. 2005;40(1):96-102. DOI:10.1080/00365520410009546
30. Hoffmeister A, Rothenbacher D, Bode G, et al. Current infection with Helicobacter pylori, but not seropositivity to Chlamydia pneumoniae or cytomegalovirus, is associated with an atherogenic, modified lipid profile. Arterioscler Thromb Vasc Biol. 2001;21(3):427-32. DOI:10.1161/01.atv.21.3.427
31. Weber SN, Bopp C, Krawczyk M, Lammert F. Genetics of gallstone disease revisited: updated inventory of human lithogenic genes. Curr Opin Gastroenterol. 2019;35(2):82-7.
DOI:10.1097/MOG.0000000000000511
32. Shabanzadeh DM, Novovic S. Alcohol, smoking and benign hepato-biliary disease. Best Pract Res Clin Gastroenterol. 2017;31(5):519-27. DOI:10.1016/j.bpg.2017.09.005
________________________________________________
2. Osadchuk MA, Svistunov AA. Mironova ED, et al. Diseases of biliary tract in the context of association with oncological diseases of the digestive system. Terapevticheskii Arkhiv (Ter. Arkh.). 2019;91(12):98-104 (in Russian). DOI:10.26442/00403660.2019.12.000455
3. Uspenskiy YP, Fominykh YuA, Nadzhafova KN, et al. Pathogenetic aspects of the development of cholelithiasis in patients with metabolic syndrome. Terapevticheskii Arkhiv (Ter. Arkh.). 2021;93(2):209-14 (in Russian). DOI:10.26442/00403660.2021.02.200616
4. Thomas LA, Veysey MJ, Murphy GM, et al. Octreotide induced prolongation of colonic transit increases faecal anaerobic bacteria, bile acid metabolising enzymes, and serum deoxycholic acid in patients with acromegaly. Gut. 2005;54(5):630-5. DOI:10.1136/gut.2003.028431
5. van Erpecum KJ, van Berge Henegouwen GP. Intestinal aspects of cholesterol gallstone formation. Dig Liver Dis Off J Ital Soc Gastroenterol Ital Assoc Study Liver. 2003;35(3):S8-11. DOI:10.1016/s1590-8658(03)00086-0
6. Xie M, Kotecha VR, Andrade JDP, et al. Augmented cholesterol absorption and sarcolemmal sterol enrichment slow small intestinal transit in mice, contributing to cholesterol cholelithogenesis. J Physiol. 2012;590(8):1811-24. DOI:10.1113/jphysiol.2011.224717
7. Zhang ZH, Wu SD, Wang B, et al. Sphincter of Oddi hypomotility and its relationship with duodenal-biliary reflux, plasma motilin and serum gastrin. World J Gastroenterol. 2008;14(25):4077-81. DOI:10.3748/wjg.14.4077
8. Wu Z, Luo H, Liang C. Role and mechanism of motilin in colonic motility disorder. Zhonghua Yi Xue Za Zhi. 2012;92(14):984-8.
9. Lang IM, Sarna SK, Condon RE. Myoelectric and contractile effects of motilin on dog small intestine in vivo. Dig Dis Sci. 1986;31(10):1062-72. DOI:10.1007/BF01300259
10. Apu AS, Mondal A, Kitazawa T, et al. Molecular cloning of motilin and mechanism of motilin-induced gastrointestinal motility in Japanese quail. Gen Comp Endocrinol. 2016;233:53-62. DOI:10.1016/j.ygcen.2016.05.017
11. Kamerling IMC, Van Haarst AD, De Kam ML, et al. Gallbladder volume as a biomarker for the motilin effect in healthy volunteers and patients with functional dyspepsia. Aliment Pharmacol Ther. 2004;19(7):797-804. DOI:10.1111/j.1365-2036.2004.01905.x
12. Vahrushev YaM, Hohlacheva NA. Factors contributing to gallstone formation and their interaction. Terapevticheskii Arkhiv (Ter. Arkh.). 2010;82(1):8-11 (in Russian).
13. Shaodong C, Haihong Z, Manting L, Get al. Research of influence and mechanism of combining exercise with diet control on a model of lipid metabolism rat induced by high fat diet. Lipids Health Dis. 2013;12:21. DOI:10.1186/1476-511X-12-21
14. Kay RG, Foreman RE, Roberts GP, et al. Mass spectrometric characterisation of the circulating peptidome following oral glucose ingestion in control and gastrectomised patients. Rapid Commun Mass Spectrom. 2020;34(18):e8849. DOI:10.1002/rcm.8849
15. Hou L, Shu XO, Gao YT, et al. Anthropometric measurements, physical activity, and the risk of symptomatic gallstone disease in Chinese women. Ann Epidemiol. 2009;19(5):344-50. DOI:10.1016/j.annepidem.2008.12.002
16. Kiani Q, Farooqui F, Khan MS, et al. Association of body mass index and diet with symptomatic gall stone disease: a case-control study. Cureus. 2020;12(3):e7188. DOI:10.7759/cureus.7188
17. Ryu S, Chang Y, Kim YS, Kim HJ. Prolonged sitting increases the risk of gallstone disease regardless of physical activity: a cohort study. Scand J Gastroenterol. 2018;53(7):864-9. DOI:10.1080/00365521.2018.1476910
18. Aronov DM, Gulyaeva SF, Shihova EV, Vedernikov VA. Physical exercise in combined outpatient rehabilitation of coronary patients with biliary dysfunction. Terapevticheskii Arkhiv (Ter. Arkh.). 2011;83(1):21-5 (in Russian).
19. Del Pozo R, Mardones L, Villagrán M, et al. Effect of a high-fat diet on cholesterol gallstone formation. Rev Med Chil. 2017;145(9):1099-105.
DOI:10.4067/s0034-98872017000901099
20. Tung TH, Ho HM, Shih HC, et al. A population-based follow-up study on gallstone disease among type 2 diabetics in Kinmen, Taiwan. World J Gastroenterol WJG. 2006;12(28):4536-40. DOI:10.3748/wjg.v12.i28.4536
21. Dixon JB, O’Brien PE. Obesity and the white blood cell count: changes with sustained weight loss. Obes Surg. 2006;16(3):251-7. DOI:10.1381/096089206776116453
22. Chen LY, Qiao QH, Zhang SC, et al. Metabolic syndrome and gallstone disease. World J Gastroenterol. 2012;18(31):4215-20. DOI:10.3748/wjg.v18.i31.4215
23. de Boer SY, Masclee AA, Lamers CB. Effect of hyperglycemia on gastrointestinal and gallbladder motility. Scand J Gastroenterol Suppl. 1992;194:13-8. DOI:10.3109/00365529209096020
24. Biddinger SB, Haas JT, Yu BB, et al. Hepatic insulin resistance directly promotes formation of cholesterol gallstones. Nat Med.2008;14(7):778-82.DOI:10.1038/nm1785
25. Smelt AHM. Triglycerides and gallstone formation. Clin Chim Acta. 2010;411(21-2):1625-31. DOI:10.1016/j.cca.2010.08.003
26. Budzyński J, Kłopocka M. Brain-gut axis in the pathogenesis of Helicobacter pylori infection. World J Gastroenterol WJG. 2014;20(18):5212-25. DOI:10.3748/wjg.v20.i18.5212
27. Murakami K, Fujioka T, Shiota K, et al. Influence of Helicobacter pylori infection and the effects of its eradication on gastric emptying in non-ulcerative dyspepsia. Eur J Gastroenterol Hepatol. 1995;7(1):S93-7.
28. Cen L, Pan J, Zhou B, et al. Helicobacter pylori infection of the gallbladder and the risk of chronic cholecystitis and cholelithiasis: a systematic review and meta-analysis. Helicobacter. 2018;23(1). DOI:10.1111/hel.12457
29. Apostolov E, Al-Soud WA, Nilsson I, et al. Helicobacter pylori and other Helicobacter species in gallbladder and liver of patients with chronic cholecystitis detected by immunological and molecular methods. Scand J Gastroenterol. 2005;40(1):96-102. DOI:10.1080/00365520410009546
30. Hoffmeister A, Rothenbacher D, Bode G, et al. Current infection with Helicobacter pylori, but not seropositivity to Chlamydia pneumoniae or cytomegalovirus, is associated with an atherogenic, modified lipid profile. Arterioscler Thromb Vasc Biol. 2001;21(3):427-32. DOI:10.1161/01.atv.21.3.427
31. Weber SN, Bopp C, Krawczyk M, Lammert F. Genetics of gallstone disease revisited: updated inventory of human lithogenic genes. Curr Opin Gastroenterol. 2019;35(2):82-7.
DOI:10.1097/MOG.0000000000000511
32. Shabanzadeh DM, Novovic S. Alcohol, smoking and benign hepato-biliary disease. Best Pract Res Clin Gastroenterol. 2017;31(5):519-27. DOI:10.1016/j.bpg.2017.09.005
Авторы
А.А. Свистунов, М.А. Осадчук*, Е.Д. Миронова, П.В. Гуляев, И.Н. Васильева
ФГАОУ ВО «Первый Московский государственный медицинский университет им. И.М. Сеченова» Минздрава России (Сеченовский Университет), Москва, Россия
*osadchuk.mikhail@yandex.ru
Sechenov First Moscow State Medical University (Sechenov University), Moscow, Russia
*osadchuk.mikhail@yandex.ru
ФГАОУ ВО «Первый Московский государственный медицинский университет им. И.М. Сеченова» Минздрава России (Сеченовский Университет), Москва, Россия
*osadchuk.mikhail@yandex.ru
________________________________________________
Sechenov First Moscow State Medical University (Sechenov University), Moscow, Russia
*osadchuk.mikhail@yandex.ru
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