Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bile salt pool size and kinetics were evaluated in 8 morbidly obese women before and following jejunoileal bypass. The results indicate that following jejunoileal bypass pool sizes of both chenodeoxycholate and cholate decrease, turnover rates increase, and the rates of bile salt synthesis increase. Influenced by pool size, hepatic synthesis and the degree of malabsorption, the daily bile salt loss may actually decrease in time. Chenodeoxycholate is more efficiently absorbed than cholate in both the preoperative and postoperative states. In spite of greater cholate synthetic capabilities, in this malabsorptive state the chenodeoxycholate pool decreases less than the cholate pool. Although all patients received an identical surgical procedure, the effect on bile salt kinetics and pool sizes varied in these patients. Since some of the postoperative complications may be related to the degree of interference with bile salt metabolism, the individual patient's capacity for increased hepatic synthesis of bile salts and increased reabsorption of bile salts from the remaining small bowel may vary the clinical postoperative course.
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PMID:Bile salt metabolism following jejunoileal bypass for morbid obesity. 83 37

Deficiency of 3 beta-hydroxy-delta 5-C27-steroid dehydrogenase, the second enzyme in the sequence that catalyses the synthesis of bile acids from cholesterol, leads to chronic liver disease in childhood as well as to malabsorption of fat and fat soluble vitamins. A 4 year old boy with this condition has been successfully treated by oral administration of a bile acid--chenodeoxycholic acid. He had been jaundiced since birth, grew poorly because of rickets, and had severe pruritus. Plasma transaminase activities were persistently raised. Chenodeoxycholic acid 125 mg twice daily for two months, and then 125 mg daily, cured his jaundice and pruritus, returned his transaminase activities to normal, and eliminated the need for calcitriol for prevention of rickets. On this treatment he has so far remained well for two years. A diagnosis of 3 beta-hydroxy-delta 5-C27-steroid dehydrogenase deficiency should be considered in any child with unexplained chronic hepatitis or cirrhosis, especially if the liver disease is accompanied by a clinically obvious malabsorption of fat soluble vitamins. A simple colorimetric test of the urine confirms the diagnosis and effective treatment can be started.
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PMID:Treatment of chronic liver disease caused by 3 beta-hydroxy-delta 5-C27-steroid dehydrogenase deficiency with chenodeoxycholic acid. 224 2

Biliary and fecal bile acid composition was studied in 13 patients 3-12 years after a partial ileal bypass operation and in 10 unoperated controls, all with heterozygous familial hypercholesterolemia. Three operated patients were taking cholestyramine. The relative amount of cholic acid in the bile was decreased at the expense of chenodeoxycholic acid in the operated subjects. Chenodeoxycholic acid content of the bile correlated negatively with the fractional cholesterol absorption, suggesting that in compromised absorption chenodeoxycholic acid is absorbed more efficiently than cholic acid. Despite a ninefold increase in total bile acid synthesis the cholic/chenodeoxycholic acid synthesis ratio was not significantly different in the operated and control subjects. However, the lower the chenodeoxycholic acid synthesis the higher was the proportion of deoxycholic acid in the bile and feces, suggesting regulation of chenodeoxycholic acid synthesis by deoxycholic acid. Ileal exclusion had increased the proportion of primary bile acids in the feces from below 10 to over 50%. Despite increased fecal water excretion the concentration of fecal total and dihydroxy bile acids was higher in the operated than in control subjects. However, the fecal concentration of the potentially cancer-promoting bile acids, deoxycholic acid and lithocholic acid, was not increased in the operated subjects. In the operated subjects, fecal water output was positively correlated with total bile acid and chenodeoxycholic acid synthesis. It is concluded that the severe bile acid malabsorption caused by ileal exclusion activates the synthesis of both primary bile acids in similar amount. However, after ileal exclusion the relative amount of cholic acid in the bile is decreased, obviously because loss of ileal absorption predominantly affects the absorption of cholic acid.
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PMID:Fecal and biliary bile acid composition after partial ileal bypass operation. 339 74

The pharmacokinetics of chenodeoxycholic and ursodeoxycholic acids are reviewed in this article. Chenodeoxycholic acid is well absorbed by the intestine, whereas the absorption of ursodeoxycholic acid is incomplete. They are extracted efficiently by the liver, conjugated with glycerine and taurine, secreted in bile, and then undergo enterohepatic circulation with the endogenous bile acids. Therapeutic bile acids are metabolised by intestinal bacteria to lithocholic acid which is mainly excreted with faeces. Since the large majority of bile acid is confined within the enterohepatic circulation (resulting in low serum concentrations) their volume of distribution is relatively high. Despite the high hepatic extraction, the clearance of therapeutic bile acids is relatively low because of the highly efficient enterohepatic recirculation. Elimination of therapeutic bile acids mainly occurs in the faeces either unmodified or after biotransformation. At present the main clinical indication for therapeutic bile acids is ursodeoxycholic acid treatment for chronic cholestatic liver disease. In these patients, ursodeoxycholic acid is efficiently absorbed but its hepatic uptake and biliary secretion are impaired, thus leading to reduced biliary enrichment and high serum concentrations of this exogenous bile acid. In patients with cystic fibrosis-associated liver disease, bile acid malabsorption also occurs, thus indicating the need for higher dosages. The volume of distribution and clearance of ursodeoxycholic acid reduced in the presence of liver disease. Also in this case, elimination mainly occurs with the faeces but, in the presence of severe cholestasis, renal clearance may become relevant. Sulphation or conjugation with glucose and N-acetylglucosamine facilitate urinary excretion.
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PMID:Clinical pharmacokinetics of therapeutic bile acids. 874 34

Bile acids have secretory, motility and antimicrobial effects in the intestine. In patients with bile acid malabsorption the amount of primary bile acids in the colon is increased compared to healthy controls. Deoxycholic acid is affecting the intestinal smooth muscle activity. Chenodeoxycholic acid has the highest potency to affect intestinal secretion. Litocholic acid has little effect in the lumen of intestine compared to both deoxycholic acid and chenodeoxycholic acid. There is no firm evidence that clinically relevant concentrations of bile acids induce colon cancer. Alterations in bile acid metabolism may be involved in the pathophysiology of constipation.
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PMID:Bile acids: short and long term effects in the intestine. 2033 75