Functional condition of the stomach,pancreas, liver, ulcer and gall-bladder in celiac disease


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Aim. To study condition of the stomach, gall-bladder, pancreas, liver in celiac disease (CD) and contribution of their dysfunction to clinical presentation of CD symptoms.
Material and methods. A total of 215 CD patients entered the study (191 females and 24 males) aged under 20 years (n = 100), 20 to 50 (n = 74) and over 50 years (n = 41). The control group consisted of 25 healthy volunteers. Acid-forming function of the stomach, blood serum gastrin level were studied. Bile for biochemical test was obtained at duodenal intubation using 40 ml of 40% glucose solution or 25% magnesium solution as food stimulators, and intravenous injection of cholecystokininpancreosimin. Cholic acid was assayed in bile portions B and C. Two-channel probe was used to obtain duodenal content before meal and after intravenous injection of pancreosimin for tripsin, amylase and lipase assay. Clinical and biochemical blood tests were made as well as puncture biopsy of the liver with histological study of biopsy material.
Results. CD patients were found to have high basal and stimulated acid-forming function, high gastrin concentration in the blood. The morphological examination detected lymphocytic gastritis. There were an inert type of pancreatic enzyme secretion, gall-bladder hypokinesia or atony. Gall-bladder contracted only after intravenous injection of cholecystokinin. Changes in the liver were characterized by hypertransaminasemia, steatohepatitis.
Conclusion. Changes in the stomach in patients with new-onset CD promote formation of ulcer. Decline in excretory pancreatic function, slow enzyme secretion, marked hypokinesia of the gall-bladder, hyperenzymemia and steatohepatitis as manifestations of hepatic pathology result in dramatic disorder of digestion and absorption of food substances.

About the authors

Larisa Matisovna Krums

Email: gastroenter@rambler.ru

E A Sabel'nikova

Asfol'd Ivanovich Parfenov

L M Krums

Central Research Institute of Gastroenterology, Moscow

Central Research Institute of Gastroenterology, Moscow

E A Sabelnikova

Central Research Institute of Gastroenterology, Moscow

Central Research Institute of Gastroenterology, Moscow

A I Parfenov

Central Research Institute of Gastroenterology, Moscow

Central Research Institute of Gastroenterology, Moscow

References

  1. Гальперин Ю. М., Лазарев П. И. Пищеварение и гомеостаз. М.: Наука; 1986.
  2. Уголев А. М. Мембранное пищеварение. Л.: Наука; 1985.
  3. Аруин Л. И., Парфенов Д. А. Функционально-морфологические изменения желудка при заболеваниях тонкой кишки. Рос. журн. гастроэнтерол., гепатол. 1994; 3 (1): 63-67.
  4. Castiella A., Arambtrri I., Fernandez J. et al. Coeliac disease presented as duodenal ulcer and stenosis. Rev. Esp. Enferm. Dig. 2007; 99 (12): 736-737.
  5. Schweider C. D., Murray J. A. Postbulbar duodenal ulceration and stenosis associated with celiac disease. Abdom. Imag. 1998; 23 (4): 347-349.
  6. Аруин Л. И., Капуллер Л. Л., Исаков В. А. Морфологическая диагностика болезней желудка и кишечника. М.: Триада Х; 1998.
  7. Логинов А. С., Крумс Л. М., Парфенов А. И., Бычков Ю. П. Роль нарушения секреции панкреатических ферментов, желчи и бактериального обсеменения тонкой кишки в патогенезе диареи у больных целиакией. Клин. мед. 1989; 11: 81-85.
  8. Frimen H. J. Pancreatic endocrine and exocrine changes in celiac disease. Wld J. Gastroenterol. 2007; 13 (47): 6344-6346.
  9. Carroci A., Lacono G., Monalto G. et al. Exocrine pancreatic function in children with celiac disease before and after gluten free diet. Gut 1991; 32 (7): 796-799.
  10. Сабельникова Е. А., Парфенов А. И., Царегородцева Т. М. и др. Изменения печени при глютеновой энтеропатии. Тер. арх. 2003; 2: 31-35.
  11. Сабельникова Е. А., Топорков А. С., Шепелева С. Д. Изменения печени у больных с синдромом нарушенного всасывания. Рос. гастроэнтерол. журн. 2000; 4: 145.
  12. Парфенов А. И., Сабельникова Е. А., Крумс Л. М. и др. Клинико-морфологические изменения печени у больных целиакией. В кн.: Материалы 3-го Российского научного форума "Санкт-Петербург 2001". Гастробюллетень 2001; 2-3: 64.
  13. Hofman P. G., Rosenbusch S. P., Hector V. P., Gansen J. B. Effect of predigest fat stimulation of plasma cholecystokinin and gall bladder motility in coeliac disease. Gut 1995; 36 (1): 172.
  14. Brown A. M., Bradshaw M. J., Richardson R. J. et al. Pathogenesis of impaired gall bladder contraction of celiac disease Gut 1987; 28 (11): 1426-1432.
  15. Nousiq-Arvanitakis S., Fotoulaki M., Tendzidon K. et al. Subclinical exocrine pancreatic dysfunction from decreased cholecystokinin secretion in the presence in intestinal villous atrophy. J. Pediar. Gastroenterol. Nutr. 2006; 43 (3): 307-312.
  16. Крумс Л. М., Иосава Л. И. Биохимическое исследование желчи у больных с патологией тонкой кишки. Сов. мед. 1981; 2: 21-25.
  17. Weizman Z., Hamilton J. R., Kopelman H. P. et al. Treatment failure in celiac disease due to coexistence of exocrine pancreatic insufficiency. Pediatrics 1987; 1 (8): 924-926.
  18. Khan T., Khalid N., Mitton G., Sally G. Congenital pancreas insufficiency and coeliac disease. J. Pediatr. Gasroenterol. Nutr. 1999; 28 (1): 97-98.
  19. Freeman H. J. Hepatobiliary and pancreatic disorders in coeliac disease. Wld J Gastroenterol. 2006; 12 (10): 1503-1508.

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