The binding of bile acids by hydrotalcite and other antacid preparations.
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Biomedical subjects
Publications and source records attributed to G M Murphy.
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Using the immunoelectrophoretic method alpha-1-antitrypsin was detected in all but 6 of 26 samples of duodenal fluid obtained from 16 patients with various gastroenterological problems. The concentrations (mg/100 ml) of alpha-1-antitrypsin in duodenal aspirates from children with liver disease (7.32 plus or minus 6.1) were less than those from children with cystic fibrosis, Shwachman Diamond syndrome, or Hirschsprung's disease (16.7 plus or minus 11.9; p smaller than 0.02). Alpha-1-antitrypsin was detected in all but one of 6 samples of gallbladder bile, the exception being that from a patient with extrahepatic biliary atresia. No significant correlation was found between the alpha-1-antitrypsin concentration in the samples studied and the corresponding total antitrypsin activity.
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Four children with chronic diarrhoea and perianal excoriation after a pull-through operation for Hirschsprung's disease have been shown to have increased but not markedly raised levels of faecal bile acids. Bile acid analysis of the 'bile-rich' duodenal fluid obtained after pancreozymin stimulation in 3 of the patients indicated a marked reduction in the proportion of deoxycholic acid conjugates. These findings are compatible with colonic malabsorption of secondary bile acids in these patients which is related in some way to the pull-through operation, but which is not likely to be the cause of the diarrhoea and the anal excoriation.
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Although, in suitable patients, oral chenodeoxycholic acid (CDCA) dissolves gallstones, the results of recent animal studies suggest that it might be hepatotoxic. Liver function was therefore studied in patients with gallstones before and during treatment with CDCA and liver biopsies were carried out both in patients with cholelithiasis given bile acid therapy and in those who had been given no medical treatment. In 25 patients treated with 0.5-1.5 g CDCA/day (7-20 mg kg body weight(-1) day(-1)) there was no significant change in serum bilirubin, albumin, globulin, transaminase, isocitric dehydrogenase, alkaline phosphatase, and gamma glutamyl transpeptidase levels before and at monthly intervals during six months' treatment. The kinetics of bromsulphthalein (BSP) clearance and its apparent transport maximum were not significantly changed during CDCA therapy. The mean fasting serum bile acid concentrations of 18.0 +/- SEM 1.2 mumoles/litre before and 20.0 +/- 3.5 mumoles/litre during treatment were both significantly greater than control values. Liver histology was not appreciably different in 11 patients treated with CDCA from that in eight patients with untreated cholelithiasis and in three patients who had received CDCA three to four months before biopsy. These results suggest that in doses of 0.5 to 1.5 g/day CDCA is not hepatotoxic in man.
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