Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008370 (cholestasis)
 9,378 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors report two cases of gold-salt-induced cholestasis. They make a review of the thirteen cases previously related in the literature ; the cholestasis was constant, the hepatocytic necrosis was unusual and the gold-salts were difficult to visualize in the liver biopsy and more especially at the ultrastructural level. The immunological mechanism of hypersensibility is well established ; the possibility of an associated hepatotoxicity is debated.
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PMID:[Anatamo-pathologic aspects of gold-salt induced cholestasis. Report of two cases with ultrastructural study (author's transl)]. 627 43

Bile salt sulphation in liver disease was investigated by measuring the bile salt sulphotransferase level in percutaneous liver biopsy specimens from 27 patients. The same magnitude of mean specific enzyme activity was found in patients with cholestatic and non-cholestatic liver disease. No significant difference of the mean bile salt sulphotransferase activity was found when patients with and without reduced liver function as evidence from the intravenous galactose tolerance test were compared. The present results indicate that induction of liver bile salt sulphotransferase does not occur to a significant extend in clinical conditions with cholestasis.
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PMID:Enzymatic sulphation of bile salts in man. Bile salt sulphotransferase activity in percutaneous liver biopsy specimens from patients with liver disease. 629 Nov 35

To evaluate the potential role of taurine deficiency in the pathogenesis of parenteral nutrition-induced cholestasis, 20 premature (less than 34 weeks AGA) infants were randomized to receive parenteral nutrition with and without taurine (10.8 mg/kg/day) during the first 10 days of life. Birth weight, gestational age, and protein and caloric intake were similar in both groups. Plasma taurine levels and hepatic function were assessed before the study began (3 +/- 1 days of age), at 5 +/- 1 days of age, and at 9 +/- 1 days of age. Although plasma taurine levels were significantly greater at 5 +/- 1 and 9 +/- 1 days of age (p = 0.009) in the group receiving supplementation, no differential effect on hepatocellular function could be detected during this short period of time. A decrease in plasma ammonia (p = 0.001), alanine aminotransferase (ALT) (p = 0.036), gamma-glutamyltranspeptidase (GGTP) (p = 0.05), 5'-nucleotidase (5'N) (p = 0.001), and bile salt concentrations was noted in both groups, indicating the rapid maturation of hepatic function even in the presence of parenteral nutrition during the first 10 days of life.
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PMID:Effect of taurine supplementation on hepatic function during short-term parenteral nutrition in the premature infant. 642 96

The investigation was performed in 6 cholecystectomized chronic bile fistula dogs in which, except in complete common bile duct obstruction, the bile was diverted and replaced with a constant taurocholate infusion of 0.3 mumoles per min. per kg. Iodipamide and iodoxamate were i.v. infused at a rate of 6.7 mumoles per minute per kg for 30 minutes. Different degrees of extrahepatic obstruction were simulated by producing different intrabiliary pressure conditions. Progressive hepatic parenchymal disease was induced by oral administration of dimethylnitrosamine. In both conditions basal (precontrast) bile flow, maximum biliary excretion rate and bile concentration of the contrast agents decreased with increasing hepatic dysfunction. This investigation suggests that, regardless of the underlying mechanism, the bile iodine concentration required for radiographic visualization of the biliary system is no longer attained in intravenous cholangiography when the basal bile flow decreases below 2 microliter per min per kg in the presence of a physiologic bile salt plasma pool. In hepatic dysfunction alkaline phosphatase correlated better with the maximum biliary excretion rate and concentration of the contrast agents than SGPT, SGOT, and serum bilirubin and therefore seems to be the best parameter to predict the chance of a successful intravenous cholangiography.
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PMID:Biliary iodipamide and iodoxamate excretion as function of basal bile flow in normal, common bile duct obstructed and liver-damaged dogs. 645 32

Colchicine, a drug which interferes with microtubular function, has no effect on the secretion of taurodehydrocholate into bile; it is therefore suggested that bile salts are unlikely to be packaged in vesicles during cellular transit from sinusoidal to canalicular membranes. Colchicine greatly reduces the secretion of phospholipid and cholesterol into bile; it is suggested that this is due to an interruption in the supply of vesicles bringing lipids to repair the canalicular membrane during bile salt output. In the absence of the protective effect of a continuous supply of repair vesicles, micelleforming bile salts damage the canalicular membrane; the increased concentration of plasma membrane enzymes in bile and the increased aspartate aminotransferase activity in plasma and bile are evidence of this damage. Damage to the canalicular membrane may also be an explanation for the reduction in taurocholate transport and the taurocholate-induced cholestasis which are seen with colchicine-treated livers. Such membrane damage is not observed in colchicine-treated livers during the secretion of the non-micelle forming bile salt, taurodehydrocholate.
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PMID:The effects of colchicine on secretion into bile of bile salts, phospholipids, cholesterol and plasma membrane enzymes: bile salts are secreted unaccompanied by phospholipids and cholesterol. 646 98

Hepatobiliary imaging with 99mTc-p-isopropyl-iminodiacetic acid (PIPIDA) and other acetanilidoiminodiacetic acid derivatives is a frequently used clinical tool in evaluating patients with jaundice. However, there has been little objective assessment of the effects of cholestasis on hepatic transport of acetanilioiminodiacetic acid derivatives. In our studies, transport of 99mTc-PIPIDA by isolated rat hepatocytes obtained from animals with extrahepatic obstruction secondary to bile duct ligation or intrahepatic cholestasis induced by ethinyl estradiol therapy was determined. Uptake constants for 99mTc-PIPIDA by hepatocytes isolated from livers of animals with ligated bile ducts were significantly decreased compared with uptake by liver cells from sham-operated controls (0.0030 +/- 0.0003 vs. 0.0089 +/- 0.0010 femtomole X 10(6) cells-1 X min-1 X pmol/L-1; p less than 0.001). Hepatocytes isolated from livers of animals given ethinyl estradiol also demonstrated significantly reduced 99mTc-PIPIDA uptake compared with controls given propylene glycol (0.0034 +/- 0.0002 vs. 0.0060 +/- 0.0004 fmol X 10(6) cells-1 X min-1 X pmol/L-1; p less than 0.001). Fractional rates of efflux of the study compound from hepatocytes preincubated with 99mTc-PIPIDA were significantly decreased in experiments using ethinyl estradiol (p less than 0.005) but did not differ significantly from controls in studies of bile duct ligation. 99mTc-PIPIDA uptake was significantly decreased in the presence of high bile salt concentrations (100 to 200 mumol/L), but unconjugated bilirubin concentrations as high as 200 mumol/L (approximately 12 mg/dl) had no effect on hepatocyte uptake of the ligand. The finding that cholestasis significantly impairs hepatocyte uptake of 99mTc-PIPIDA provides a possible explanation for the clinical observation that a patent biliary tree and normal serum bilirubin level are not always sufficient to ensure normal hepatobiliary imaging. These data also suggest that elevation of bile acid levels during cholestasis may either contribute to impaired uptake of hepatobiliary imaging agents or serve as a marker of cholestasis-induced abnormalities in the liver functions responsible for hepatic transport of these compounds.
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PMID:Effect of cholestasis on hepatic transport of 99mtechnetium p-isopropyl-iminodiacetic acid. 648 Dec 15

The authors report the case of a 51-year-old woman who developed cholestatic and cytolytic hepatitis after an overdose of sodium aurothiopropanol sulfonate 1.1 g, namely 300 mg gold metal. Liver biopsy demonstrated cholestasis, centrolobular steatosis and portal fibrosis. Electron microscopy showed abundant lipo-pigments in the hepatic and cellular cells, as well as myelinic bodies. Gold analysis by atomic absorption spectroscopy showed a level of 22.76 micrograms per ml in the plasma and a level of 2.16 micrograms per g in the liver. Chelating agents increased the urinary gold excretion, but were without effect on the course of hepatitis. Dimercaptopropanol seemed to favor the occurrence of other gold salt side-effects and penicillamine increased the hepatic cytolysis. The patient recovered without sequelae.
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PMID:[Hepatitis secondary to a gold salt overdose]. 648 87

A new FAO report on how to estimate the energy and protein requirements of individuals is imminent and has direct application to the management of obese patients. Energy needs, although variable form individual to individual, are reasonably stable unless gross overfeeding or prolonged semi-starvation occurs; unconscious appetite control is surprisingly important. No longer will energy needs be expressed per kg body weight, a reference point difficult to apply to obese subjects anyway. There are now equations for estimating basal metabolic rate (BMR) these can be appled to obese subjects to give BMR in MJ per day; for kcal from kJ divide by 4.184. The equations apply to all races although north Europeans and Americans tend to have high values and Indians low. An obese patient has a higher BMR than a normal person of the same height. Lean body mass is increased in obesity so some long term loss is inevitable with slimming and accounts for the persistent fall in BMR on weight loss. Energy and protein needs are just the beginning of dietary management. Obese patients are prone to cardiovascular and gall bladder disease. A low fat diet is important and a polyunsaturated: saturated ratio (P:S) of 0.5 to 1.0 is appropriate: higher ratios will exacerbate cholestasis in the biliary tract which can be precipitated by weight loss. New evidence suggests that cereal fibre intake is important for preventing secondary bile salt recycling from the colon with its effect on biliary cholesterol saturation. Therefore long term high cereal (not bran) fibre intakes are as important in obese patients as is a low fat diet. High carbohydrate diets produce a slightly higher metabolism rate than iso-energetic diets. Low sugar diets lead to slightly lower energy intakes. Trace element deficient diets can lead to obesity so the obese patient and his family should be advised and shown how to permanently adjust to a 'prudent' diet. The short term approach to management is usually a waste of time.
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PMID:Dietary aspects of obesity. 651 54

Bile salt sulphation in primary biliary cirrhosis was studied by measurements of the liver bile salt sulphotransferase levels in 16 patients. Although the enzyme activity varied among the patients it did not correlate with the severity of cholestasis. Furthermore, the mean bile salt sulphotransferase magnitude in patients with primary biliary cirrhosis did not differ significantly from corresponding enzyme activity in patients with non-cholestatic, alcohol induced liver disease. The present data indicates that chronic cholestasis, as evidenced in patients with primary biliary cirrhosis, does not lead to increased levels of liver bile salt sulphotransferase. It is suggested that mechanisms other than enzymic induction are responsible for the increased bile salt sulphate synthesis as observed in primary biliary cirrhosis.
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PMID:Bile salt sulphation in man. Liver bile salt sulphotransferase activity in patients with primary biliary cirrhosis. 657 90

Several studies reported that ursodeoxycholate (but not its conjugates), when administered intravenously, increased the biliary bicarbonate concentration in the rat (1-3). At the same time, a complete dissociation between bile flow and the bile salt excretion rate was produced in the second hr of infusion (2). In order to examine whether this property was due to the 7 beta-hydroxy group in its molecular structure, the choleretic property of ursocholate (3 alpha, 7 beta, 12 alpha-trihydroxy-5 beta-cholanoic acid) was investigated in male Wistar rats. Immediately after the start of iv infusion of ursocholate at a rate of 1.2 mumole/min/100 g b. wt., both the bile flow and bile salt excretion rate began to increase. However, unlike with ursodeoxycholate, the bile salt excretion rate continued to be high in the second and third hr of infusion, while the bile flow rate gradually increased. Furthermore, the bicarbonate concentration in the bile fell slightly 10 min after the start of ursocholate infusion. Although the concentration tended to return to the baseline value before the bile salt infusion in the later period of observation, no significant increase in bicarbonate concentration was observed during the whole observation period. These properties were quite similar to those of cholate rather than those of ursodeoxycholate. However, a cholate infusion at the same rate of 1.2 mumole/min/100 g b.wt. caused a cholestasis as early as 20 to 30 min after the start of an infusion. These results suggest that the previously reported properties of ursodeoxycholate (that it causes a complete dissociation between the bile flow and bile salt excretion rate in the second hr and that it increases the biliary bicarbonate concentration) were not due to the 7 beta-hydroxy group in its steroidal structure, and that the choleretic property of ursocholate is similar to its 7 alpha-hydroxy epimer, cholate. However, the much lower cytotoxicity of ursocholate compared to cholate appears to be due to the 7 beta-hydroxy group that ursocholate has.
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PMID:The bile flow and biliary excretion of ursocholate in the rat. 664 5


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