Терапевтический архив (Feb 2008)
Cholagenic diarrhea
Abstract
Aim. To characterize cholagenic diarrhea as a nosological entity with its specific features of etiology, pathogenesis, clinical picture and treatment. Material and methods. A total of 167 patients with chronic diarrhea (CD) participated in the trial. Of them, 25 patients have undergone resection of the small intestine, 98 - cholecystectomy for cholelithiasis, 44 had concurrent hypokinesia of the gall bladder caused by celiac disease (n = 30) or biliary dyskinesia (n = 14). The examination included estimation of cholic acid in the duodenal content (40% glucose solution or cholecystokinin were used as stimulators); 24-h fecal mass; fecal mass for 24 hours, fat, potassium and sodium content in the feces; electromotor activity (EM A) of the gall bladder, small intestine and colon. Results. Duodenal intubation with 40% glucose in patients with extensive resection of the small intestine detected a fall in cholic acid content in vesical bile to 408 ± 58.39 mg compared to normal (910 ± 97.29 mg%). In intravenous administration of cholecystokinin cholic acid concentration rose insignificantly (547.0 ± 94.7 mg%) and was accompanied with bile loss with feces, polyfecalia, steatorrhea and high sodium concentration in feces. In celiac disease patients bile with high cholic acid concentration was secreted only in administration of cholecystokinin (1673 ± 175.9 mg/%, normal 1701 ± 140.6 mg/%). In patients after cholecystectomy colon EMA was primarily slow-wave and middle-amplitude, typical for hypermotor dyskinesia. Conclusion. CD develops after extensive resection and in inflammatory ileac diseases, suppression of contractile function of the gall bladder and after cholecystectomy. CD after cholecystectomy can be considered as a variant of postcholecystectomy syndrome. The treatment of CD should include drugs binding excessive bile acids in the colon, in hypokinesia of the gall bladder the treatment should include stimulators of its contractile function.
