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 methods to detect antimitochondrial antibodies (AMAs), which are characteristically positive in primary biliary cirrhosis (PBC), have some problems in technical difficulty, sensitivity and specificity. Based on the finding that one of the major antigens corresponding to AMAs was the E2 component of pyruvate dehydrogenase complex (PDH), a very simple enzyme-linked immunosorbent assay (ELISA) to detect anti-PDH antibody (anti-PDH) has been developed in this study. Among 68 patients with PBC, IgG class anti-PDH and IgM class anti-PDH were detected in 64 patients (94.1%) and in 55 patients (80.8%), respectively, while only three cases (4.4%) were both negative. Mean optical densities (O.D.) of sera from patients with PBC were 0.536 +/- 0.386 (mean +/- SD) in IgG class and 0.308 +/- 0.342 in IgM class. No positive cases were detected in the following patients by this ELISA: 20 patients with acute viral hepatitis, 24 with chronic persistent hepatitis, 32 with chronic active hepatitis, 19 with liver cirrhosis, 19 with hepatocellular carcinoma, 19 with acute intrahepatic cholestasis, 10 with autoimmune hepatitis, and six with systemic lupus erythematosus. Among nine AMAs negative cases with PBC by conventional indirect immunofluorescence (IF) assay, seven cases were found to be positive by this ELISA. The inter-assay coefficient of the variation of this method ranged from 4.9% to 5.8% and the intra-assay coefficient of variation from 3.8% to 5.1%. Therefore, this ELISA is useful for diagnosis of PBC.
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PMID:Detection of anti-pyruvate dehydrogenase complex antibody in primary biliary cirrhosis by an enzyme-linked immunosorbent assay. 221 Feb 21

A 41 year old woman developed chronic active hepatitis with prominent cholestasis. She was treated with prednisolone over 3 years with symptomatic benefit and improvement in serum biochemistry. However, various steroid-related side effects were encountered and steatorrhoea eventually occurred with very troublesome nocturnal diarrhoea. Therapy with ursodeoxycholic acid 750 mg daily was started. Serum alanine aminotransferase and gamma-glutamyl transferase normalized for the first time since her illness began. Steatorrhoea was abolished. There was good control of symptoms as prednisolone therapy was gradually reduced. However, when prednisolone was completely withdrawn there was a prompt biochemical deterioration. Addition of low-dose azathioprine has maintained normal blood tests over 24 months without return of the original symptoms. There are no side effects of ursodeoxycholic acid in subjects without gallstones and this agent may be effective treatment for cholestatic liver disease.
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PMID:Ursodeoxycholic acid therapy in chronic active hepatitis. 223 18

Ultrasonography (US) and computed tomography (CT) were performed on respectively 67 and 42 (altogether 72) patients, for the assessment of intrahepatic cholestasis. The diagnostic ability to differentiate between malignant (17 patients) and benign (55 patients) liver disease was analyzed. Coarse echogenicity of the liver led to inconclusive results in differentiating between cirrhosis (2 out of 29 patients) and malignant infiltration (4 out of 15 patients) by US. Other benign liver diseases in 23 patients, including acute hepatitis, chronic active hepatitis, fatty liver, and liver congestion, were correctly interpreted as benign. CT correctly disclosed malignant liver disease in all cases. A false positive diagnosis of malignancy was encountered in 4 (out of 17) patients with decompensated hepatic cirrhosis because of non-homogeneous expansive areas on CT in 3 cases. The true cause was in 2 patients non-uniform fatty infiltration, and in one patient with acute hepatitis A, small hypodense lesions. Among cholestatic patients, decompensated cirrhosis and malignant liver infiltration could not always be differentiated on US or CT.
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PMID:Ultrasonography and computed tomography in diffuse liver disease with cholestasis. 226 Dec 94

Copper granules in hepatocytes were examined by the p-dimethylaminobenzylidene rhodanine method in 965 liver biopsy specimens obtained from patients with various liver abnormalities other than Wilson's disease and biliary diseases. The granules were found in chronic active hepatitis (incidence of positive cases: 17.2%) and alcoholic fibrosis (22%) with lobular disarray and fibrosis, nonbiliary liver cirrhosis (28%), and drug-induced cholestasis (15%). Copper granules were present in the periportal or periseptal hepatocytes where the granules were mainly found in the perinuclear cytoplasm. These intracellular and intralobular distribution patterns of copper granules resembled those of primary biliary cirrhosis. These data suggest that hepatic fibrosis and lobular disarray with fibrosis in these chronic liver disease may lead to distortion or interruption of small biliary branches followed by disturbance of bile flow and deposition of copper granules. Copper stain seems to provide a valuable information for assessment of progression of these chronic liver diseases. Impaired biliary excretion seems important in deposition of copper granules in drug-induced cholestasis.
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PMID:Survey of copper granules in liver biopsy specimens from various liver abnormalities other than Wilson's disease and biliary diseases. 246 23

Cholestatic and hepatitic liver cell rosettes, gland-like formations found respectively in chronic cholestasis and in chronic active hepatitis, represent structural modifications of liver cell plates in response to injury. Differences in cytokeratin expression, ultrastructure and three-dimensional (3-D) configuration have been investigated. Cholestatic rosettes are considered to be a form of biliary metaplasia of hepatocytes, linking with newly-formed bile ductules in adjacent septa and probably providing some protection from injury caused by abnormal bile constituents. Hepatitis rosettes, by contrast, are a form of liver cell regeneration developing in isolated surviving hepatocytes or small groups of hepatocytes within areas of collapse.
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PMID:Liver cell rosettes: structural differences in cholestasis and hepatitis. 246 88

A retrospective study over 26 female patients with chronic active hepatitis was made. The mean age was 39 years old, the mean length of illness of 8 months; 5 patients had positive markers for hepatitis B. Patients were selected with the grade of histological activity: 8 patients had a mild form from disease (2A) and 16 with a severe one (2B). The predominant group was 2B. Severe inflammatory infiltration was the hallmark and multilobular necrosis, bridging, eosinophils and hyperplasia of Kupffer cells were found only in this group. Clinical features range from hepatic manifestations to systemic ones. Chronic active hepatitis may present with cholestasis, but the latter is not always related with the grade of activity. Group 2B had elevated aminotransferases and a low concentration for protrombine.
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PMID:[Chronic active hepatitis: the clinical, biochemical and histopathological correlations]. 249 Sep 74

The clinical, biochemical, histopathological and immunological features of 30 cases of clometacin-induced hepatitis are described. The age range of the patients was 32-84 years with a notable female predominance of 29:1. The hepatitis was highly cytolytic with high values of transaminases but with little or no cholestasis. Gammaglobulins were higher than 18 g/l in 73% of the cases. 25 liver biopsies were performed and showed acute hepatitis with a predominant centrilobular necrosis in 17; chronic aggressive hepatitis was noted in 8 cases but 1 showed concomitant cirrhotic changes. Anti-tissue antibodies were looked for in all cases. Anti-smooth muscle antibodies of anti-actin cable type (titre 1/80 to 1/2, 560) were detected in 19 cases, anti-nucleus antibodies in 16 cases which were associated to the former in 14 cases. The above findings show that clometacin produces a hepatitis syndrome quite akin to autoimmune chronic active hepatitis (lupoid hepatitis) and to the hepatopathy induced by oxyphenisatin.
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PMID:Characteristics of clometacin-induced hepatitis with special reference to the presence of anti-actin cable antibodies. 249 6

A retrospective study over 26 female patients with chronic active hepatitis was made. The mean age was 39 years old, the mean length of illness of 8 months; 5 patients had positive markers for hepatitis B. Patients were selected with the grade of histological activity: 8 patients had a mild form from disease (2A) and 16 with a severe one (2B). The predominant group was 2B. Severe inflammatory infiltration was the hallmark and multiobulillar necrosis, bridging, eosinophils and hiperplasia of kuppfer cells were found only in this group. Clinical features range from hepatic manifestations to systemic ones. Chronic active hepatitis may present with cholestasis, but the latter is not always related with the grade of activity. Group 2B had elevated aminotransferases and a low concentration for protrobine.
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PMID:[Chronic active hepatitis: clinical, biochemical, and histopathologic correlation]. 249

The morphology of the microvasculature in the small portal tracts was examined in normal livers, idiopathic portal hypertension (IPH) and other hepatic diseases. The microvasculature examined was arbitrary divided into two groups: that near the limiting plate and that within portal tracts, particularly around bile ducts. Based on comparisons of histology, immunohistochemistry and vascular casts, it is suggested that the former corresponded to inlet venules and the latter to distributing portal veins and peribiliary capillary plexus. Both of these microvasculatures were positive for Ulex europaeus lectin I, and (infrequently and weakly) for factor VIII-related antigen. Morphometry disclosed that inlet venules were reduced in number in IPH compared with normal livers and that distributing portal veins, peribiliary capillary plexus and inlet venules were increased in extrahepatic portal obstruction, chronic active hepatitis and extrahepatic obstructive cholestasis. We believe that the change in the microvasculature reflects abnormal microcirculation in the small portal tracts, and that the reduction of inlet venules plays an important role in the development of portal hypertension in IPH.
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PMID:Microvasculature in the small portal tracts in idiopathic portal hypertension. A morphological comparison with other hepatic diseases. 249 79

Over the last few years, ultrasound became important in characterization of space -occupying solid lesions of the liver. Recently, Canadian authors using this method, described a 23% incidence of intrahepatic or subcapsular hematoma after liver biopsy. We prospectively evaluated the incidence of this complication after liver biopsy under laparoscopic guidance in 8 cirrhotic patients, 7 with steatosis, 7 chronic active hepatitis and 4 with intrahepatic cholestasis. Biopsy was performed under general anesthesia provided that prothrombin activity was over 50%, serum fibrinogen was over 100% and platelets over 50.000/mm3. In none of 26 consecutive patients, was an intrahepatic or subcapsular hematoma observed.
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PMID:[Intrahepatic and subcapsular hematoma of the liver after hepatic biopsy under laparoscopy. Contribution of ultrasonography]. 253 99


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