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Query: UMLS:C0008370 (cholestasis)
 9,378 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alcohol can induce a wide spectrum of histological changes in the liver. Three morphologic patterns of alcoholic liver injury are now generally accepted, i.e. fatty change, alcoholic hepatitis and alcoholic cirrhosis, but a broad array of lesions has been added to this list in recent years. These damage patterns differ considerably in their significance as to indication and diagnostic power of liver biopsies. Liver biopsy is recommended in patients with clinically suspected alcoholic liver disease for diagnostic and prognostic reasons. Moreover, clinicians want to exclude nonalcoholic liver diseases that might otherwise be missed. Alcoholic hepatitis, which is associated with increased morbidity and mortality, has the highest degree of diagnostic specificity in biopsies, because its features are well-defined and are mimicked by a rather small group of other causes. When associated with perivenular and pericellular fibrosis, it may provide prognostic parameters. In contrast, fatty liver, which may be induced by alcohol as well as other etiologies, usually does not need liver biopsy, with some exceptions. It may lead to cholestasis severe enough to mimic obstructive jaundice, or may result in abnormal imaging studies suggesting metastases. Verification of histological findings may be important when these circumstances arise. Cirrhosis is easily verified in biopsies of appropriate quality; however, advanced cirrhosis is a morphologically nonspecific alteration, because cirrhotic tissue patterns converge irrespective of their cause. Liver biopsy may help to identify nonalcoholic liver disease in patients suspected of harboring alcoholic liver disease. In fact, up to 20% of biopsies may show other, potentially treatable disorders, thus extending the indication for liver biopsy in situations of complex clinical and laboratory patterns.
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PMID:[Liver biopsy in suspected alcoholic liver damage]. 162 Dec 36

In 65 patients (36 men, 29 women; mean age 74 [43-90] years) obstructive jaundice caused by malignant biliary stenosis was treated by endoscopic retrograde insertion of a 10 or 12 F synthetic endoprosthesis. The rate of complications of the endoscopic intervention was 5% (n = 3), 30-day mortality rate was 11% (n = 7) and method-related mortality was 8% (n = 5). Good drainage was achieved in 39 of 41 patients (95%) with the 12 F endoprosthesis, and in 15 of 21 patients with a 10 F one (71%) (P less than 0.001). Renewed jaundice due to prosthesis occlusion occurred in 31 patients an average of 103 (11-350) days after placement. Interval until occlusion correlated with the site of the stenosis and the length of the endoprosthesis. Jaundice recurred earlier in patients with long prostheses and proximal biliary stenosis than in those with a short prosthesis and distal stenosis. In 20 patients with renewed jaundice the endoprosthesis was replaced endoscopically. At that time 13 of the patients had a cholangitis. Occlusion of the new endoprosthesis was more common in patients with cholangitis (9 of 13) than those without (2 of 7; P less than 0.05). These findings indicate that endoscopic biliary tract drainage should be performed with as short a 12 F endoprosthesis as possible. In view of the potential need for early change of endoprosthesis the biochemical parameters of cholestasis should be regularly monitored.
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PMID:[The endoscopic treatment of malignant biliary tract stenoses with endoprostheses]. 173 74

We examined the effect of prolonged bile duct obstruction, and subsequent biliary decompression, on biochemical and metabolic parameters, using a reversible jaundice model in male Fischer 344 rats. The animals were studied after biliary obstruction for varying periods (4 days, one week, and two weeks) and following decompression. They were sacrificed one or two weeks following decompression. All the rats were compared to sham operated, pair-fed, controls. Obstructive jaundice rapidly increased bilirubin, liver enzymes, serum free fatty acid, and triglyceride levels. Glucose levels were significantly decreased in the jaundice rats compared to their pair-fed controls. Only after two weeks of jaundice was significant hypoalbuminemia observed. Following decompression, all biochemical and metabolic values gradually returned to normal levels, except for albumin. Hypoalbuminemia was not reversed within the two-week post-decompression period. The rats jaundiced for two weeks had significantly higher mortality, compared to the other groups. We conclude that prolonged jaundice adversely affects the metabolic capacity of the rats, with albumin concentration being markedly decreased, and that biliary decompression could not reverse completely all the alterations seen with cholestasis, especially following two weeks of bile duct obstruction.
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PMID:Metabolic alterations in obstructive jaundice: effect of duration of jaundice and bile-duct decompression. 177 9

The results of clinical (200 patients) and experimental (30 dogs) studies reported by the authors show that lipid peroxidation in obstructive jaundice plays an essential role in hepatic functional and morphological abnormalities. Current examination methods were used which confirmed the well-known pathophysiological abnormalities in the body of patients with obstructive jaundice leading to marked hypoxia of hepatocytes and proved that lipid peroxidation is significantly intensified in a liver affected by subhepatic cholestasis. The authors suggest their own conception of the pathophysiological and biochemical shifts in the organism of a patient with obstructive jaundice which are capable of causing stimulation of lipid peroxidation and accumulation of highly toxic products of this process in the body. A scheme of prevention and treatment of hepatic insufficiency is suggested for practical surgery by antioxidants of direct and mediated action which were selected from a series of drugs currently in use.
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PMID:[Clinical-experimental bases of the use of antioxidants in the treatment of mechanical jaundice]. 177 48

The source of activation of T lymphocytes in primary biliary cirrhosis (PBC) is undefined. Hence, T-cell-mediated reactivity against a biliary tract antigenic protein from human bile was studied. The bile protein was fractionated by 30-50% saturated ammonium sulphate and gel-chromatography, and analysed by SDS-PAGE and Western immunoblotting using rabbit antisera to the bile protein. The antisera reacted specifically with human bile duct epithelium. Western blotting of bile proteins showed two major bands, the B1 and B2 antigens. B1 stained for sialoglycoprotein but not lipid, but B2 was negative for both. Cell-mediated reactivity was tested by proliferation of peripheral lymphocytes against B1. Taking the upper limit of the normal range for stimulation indices (S.I.) as less than 1.89 (= mean + 2 SD), a mitogenic response was detected in 14 of 16 patients with PBC (S.I.: 11.7 to 2.3), and in 4 of 15 patients with chronic active hepatitis, but in none of 12 patients with drug-induced intrahepatic cholestasis or obstructive jaundice. The B2 protein was non-stimulatory. Lymphocyte proliferation to B1 in PBC was confined to T cell fractions of peripheral blood leucocytes. There was no cross-antigenicity between B1 and the M2 antigens, according to Western blotting using the rabbit antisera and PBC sera with anti-M2 reactivity. Thus, the B1 biliary protein is a possible source of T cell activation in PBC and hence could be an immunological co-factor in the pathogenesis of this disease.
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PMID:A biliary protein identified by immunoblotting stimulates proliferation of peripheral blood T lymphocytes in primary biliary cirrhosis. 177 11

The morphological and functional alterations of hepatocytes were investigated on autopsy cases of human obstructive jaundice and experimentally common bile duct ligated rats. The livers were morphologically observed by light and electron microscopes, and in order to make clear the mechanism of bile flow, horse radish peroxidase (HRP) was injected in male Wistar rats from the inferior mesenteric vein and administered in retrograde from the common bile duct. In the extrahepatic bile duct obstruction, bile canaliculi were dilated and canalicular microvilli were decreased in number and showed bleb formation, and pericanalicular filamentous structure formed thick network. Injected HRP as a tracer was not presented in the laminar and intercellular space of hepatocytes, and administered HRP in retrograde was presented in the intercellular space through tight junction from bile canaliculi and presented pericanalicular cytoplasmic vesicles. These results suggest that extrahepatic bile duct obstruction induces morphological change in pericanalicular regions and the functional abnormality in the membrane structure of hepatocytes may be persistent cholestasis.
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PMID:[Mechanism of retardation of obstructive jaundice: pathological investigation of alteration in bile flow]. 188 72

2260 patients with gastroenterologic diseases were examined by ultrasound tomography (sector echotomograph). In 47 (2.8%) of the patients echographic signs of extrahepatic cholestasis were found: dilated ductus choledochus (65.9%), dilated ductus hepaticus (34%), dilated intrahepatic biliary ducts (34%), echographic data for stones in the biliary ducts (54.5%), dilated ductus pancreaticus (18.1%), focal changes in pancreas and liver (13.6%), hydrops of the gall bladder (6.8%). The patients were classified in two groups: in the first group the ultrasound tomography succeeded in proving the cause of the cholestasis (75%) while in the second group the cause of the cholestasis remained unproved (25%), which required other additional examination such as endoscopic retrograde cholangiopancreatography (ERCP) and computed tomography. In two patients the cause of cholestasis was determined intra operationem. The site of the obstruction was determined by the ultrasound examination in all patients. The importance of the ultrasound examination of the biliary ducts and its advantages as a nonaggressive screening method for diagnosis of diseases with obstructive jaundice is pointed out.
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PMID:[The potentials of echotomography in the diagnosis of diseases of the liver, biliary tract and pancreas in the presence of the extrahepatic cholestasis syndrome]. 189 90

Obstructive jaundice causes depression of immune system function but it is unclear at present how rapidly immune function recovers after relief of biliary obstruction. To address this issue, we studied 218 Sprague-Dawley rats with common bile duct obstruction. Mononuclear phagocyte function, cell mediated immune function, portal-systemic shunt fraction, liver function tests, and liver histology were evaluated in normal (sham) rats, obstructed rats, and at weekly intervals after relief of biliary obstruction. Hepatic uptake of radiolabelled bacteria was 82 per cent in sham rats and 66 per cent in rats 21 days after CBD obstruction (P less than 0.05). Phagocytic activity returned to normal within 7 days after choledochoduodenostomy. Cell mediated immunity, measured by skin graft rejection, was significantly prolonged in the obstructed group (P less than 0.05) but had returned to normal 7 days after biliary diversion. Return of hepatocellular function, as measured by liver function tests, paralleled recovery of immune function. This study demonstrates prompt recovery of the immune system after internal biliary drainage for obstructive jaundice. This finding is in contrast to previous studies that demonstrated persistent immune suppression months after biliary diversion. These data may have implications concerning the usefulness of internal biliary drainage before surgery in patients with obstructive jaundice.
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PMID:Effects of relief of biliary obstruction on mononuclear phagocyte system function and cell mediated immunity. 181 Feb 99

Although the development of endoscopic methods of treatment for biliary obstruction has proceeded rapidly in recent years, endoscopic retrograde cholangiopancreatographic (ERCP) services are patchily distributed. A recent survey by the British Society of Gastroenterology has shown that almost half the district general hospitals questioned did not have a sphincterotomy service available locally. To assess the level of provision required, two investigations have been undertaken. Firstly, an epidemiological study of bile duct obstruction has been carried out in the South Western Region. Secondly, the actual surgical and endoscopic workload in treating obstructive jaundice has been analysed in two health districts. Using present incidence and treatment rates at least 50 ERCPs per 100,000 of the population per year are estimated to be required in the future. Surgical treatment rates can be expected to fall as the number of therapeutic ERCPs increases. The implications of this estimate in equipment and staffing terms are discussed.
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PMID:Future needs for ERCP: incidence of conditions leading to bile duct obstruction and requirements for diagnostic and therapeutic biliary procedures. 208 60

Two siblings (a 2-year-old female and 11-month-old male) with similar onset of obstructive jaundice and clinical manifestations from early infancy are described. The jaundice fluctuated but never completely disappeared. Abnormal amounts of cholate, chenodeoxycholate and ursodeoxycholate were found in serum bile acid fractions. Pruritus, hyperbilirubinemia of predominantly the conjugated fraction and bilirubinuria were increased by repeated respiratory infections. Ultrasonography showed several highly echogenic shadows in the gallbladder in both cases, and gallstones were found at surgery. Operative cholangiography showed an anomalous arrangement of pancreaticobiliary ductal system in both cases. The pedigree showed five relatives (including the father) on the paternal side had liver disease, and an autosomal recessive inheritance was suggested. The association of familial intrahepatic cholestasis with a large amount of serum bile acids (which seem to be due to abnormal bile acid metabolism), cholelithiasis and anomalous arrangement of the pancreaticobiliary ductal system is proposed as a new hepatobiliary syndrome.
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PMID:Intrahepatic cholestasis with gallstones in two siblings: a new hepatobiliary syndrome in association with anomalous arrangement of pancreaticobiliary ducts. 209 62


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