Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study demonstrates that the fibrinolytic activity is significantly increased and the level of plasminogen antiactivator diminished in the blood of patients with advanced liver cirrhosis and chronic aggressive hepatitis as compared with the values for healthy subjects. Total fibrinogen concentration was similar in patients and controls. However, electrophoresis of plasma with the use of SDS-polyacrylamide gel (3.5%) showed considerable differences in the composition of fibrinogen fractions. Lower molecular weight (LMW and LMW1) clottable protein was significantly (p less than 0.01) increased in the patients. In two out of 22 patients the higher molecular weight (HMW) fraction was virtually absent. In vitro incubation (37 degrees C for 48 hr) of diluted (1:10) plasma from a patient resulted in extensive degradation of a low-solubility fibrinogen fraction (HMW) previously added to the sample. No degradation was observed in any undiluted plasma samples. It is concluded that the increased concentration of lower-molecular-weight forms of clottable protein in the blood of patients with liver disease is probably related to increased in vivo degradation rather than abnormal synthesis. An association rather than a direct correlation with fibrinolytic activity was found.
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PMID:Abnormal fibrinogen heterogeneity and fibrinolytic activity in advanced liver disease. 40 38

Hypertriglyceridaemia occurring in patients with liver disease has been studied by measuring hepatic triglyceride lipase (H-TGL) and plasma lipoprotein lipase (LPL) by selective precipitation of H-TGL with specific antibodies. Lipid analysis, determination of lecithin-cholesterol-acyltransferase (LCAT) activity, and liver function tests were performed in parallel in fifty patients with acute hepatitis, twenty patients with chronic active or persistent hepatitis and fifty with cirrhosis of the liver. Total post-heparin lipolytic activity (PHLA) decreased with the severity of liver dysfunction. This decrease was due to low H-TGL and only to some degree to low LPL activity. With improvement over several weeks of hospitalization, hypertriglyceridaemia disappeared with a concomitant increase of H-TGL and LPL. It is concluded that impaired triglyceride metabolism in liver disease is at least partly caused by diminished plasma hepatic TGL activity.
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PMID:Secondary hypertriglyceridaemia in patients with parenchymal liver disease. 41 76

Twelve patients with liver disease related to methyldopa were seen between 1967 and 1977. Illness occurred within 1--9 weeks of commencement of therapy in 9 patients, the remaining 3 patients having received the drug for 13 months, 15 months and 7 years before experiencing symptoms. Jaundice with tender hepatomegaly, usually preceded by symptoms of malaise, anorexia, nausea and vomiting, and associated with upper abdominal pain, was an invariable finding in all patients. Biochemical liver function tests indicated hepatocellular necrosis and correlated with histopathological evidence of hepatic injury, the spectrum of which ranged from fatty change and focal hepatocellular necrosis to massive hepatic necrosis. Most patients showed moderate to severe acute hepatitis or chronic active hepatitis with associated cholestasis. The drug was withdrawn on presentation to hospital in 11 patients, with rapid clinical improvement in 9. One patient died, having presented in hepatic failure, and another, who had been taking methyldopa for 7 years, showed slower clinical and biochemical resolution over a period of several months. The remaining patient in the series developed fulminant hepatitis when the drug was accidentally recommenced 1 year after a prior episode of methyldopa-induced hepatitis. In this latter patient, and in 2 others, the causal relationship between methyldopa and hepatic dysfunction was proved with the recurrence of hepatitis within 2 weeks of re-exposure to the drug.
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PMID:Patterns of hepatic injury induced by methyldopa. 42 37

The levels of cupriuresis before and after DL-Penicillamine have been investigated in 168 cases. The mean copper excretion before Penicillamine in chronic activ liver disease, chronic persistant hepatitis, cirrhosis and in transitional cases of aggressiv chronic hepatitis and primary biliary cirrhosis ranged from 29 gamma to 48 gamma/24 hr.; however, in some cases the daily copper excretion exceeds 100 gamma, as well in subjects with liver disease as in normals too. After ingesting 900 mg DL-Penicillamine the mean values of cupriuresis ranged from 500 gamma to 600 gamma/24 hr. Abnormal results were found in about 15% of those subjects with liver diseases; in only two of 20 cases with hypercupruria after Penicillamine Wilson's Disease was established.
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PMID:[Spontaneous and DL-penicillamine-induced renal copper excretion in liver diseases (author's transl)]. 43 70

The association of high amplitude echoes returned from the liver and advanced cirrhosis is well recognized. We have become increasingly aware of a bright liver echo pattern in relatively mild cases of cirrhosis and in other chronic liver diseases. The pattern is very characteristic but non-specific in pathological terms. We have undertaken a small pilot study based on the observation of this characteristic ultrasound appearance to assess its clinical significance. Recognition of this pattern has always corresponded with liver disease of one of five types: cirrhosis, fatty infiltration, portal tract fibrosis, severe hepatitis or longstanding congestive cardiac failure. Although the use of ultrasound appears to be sensitive in the detection of generalized liver disease, it is relatively non-specific.
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PMID:Ultrasound in the detection of chronic liver disease (the "bright liver"). 43 96

A 59-year-old woman was admitted to the hospital for evaluation of her hypertension. She was treated with hydralazine; two days later a severe acute hepatitis supervened. On discontinuation of the agent, the liver damage disappeared, relapsed during inadvertent rechallenge, and healed following permanent withdrawal from the drug. Histologic study of the liver showed severe acute hepatitis with bridging necrosis (so-called subacute hepatitis). Six months after discontinuation of hydralazine, a second liver biopsy specimen showed a complete remission of the disease. This hydralazine-induced hepatitis appears to be fully reversible and to differ both on clinical and histological grounds from two previous reports documenting a granulomatous liver disease.
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PMID:Acute hepatitis with bridging necrosis due to hydralazine intake. Report of a case. 44 77

The course and possible risks of pregnancy in 7 women between the ages of 20 and 30 yr with chronic-persistent hepatitis (CPH) were evaluated. Ten pregnancies occurred in these women during the follow-up period which ranged from 3 to 8 yr. Four of the fetuses were aborted electively for nonmedical reasons. The other six pregnancies resulted in normal spontaneous vaginal deliveries at term. Each of the women experienced uneventful pre- and postnatal courses, and the neonates were all healthy and developmentally normal at birth. There was no biochemical or clinical evidence to suggest worsening liver disease during pregnancy. Normal menstrual patterns when not pregnant and normal biphasic basal body temperature patterns in 4 women suggested that ovulation and fertility were not impaired significantly. Pregnancy in women with CPH appears safe to both mother and fetus alike. This finding contrasts with the morbidity and mortality some authors have found to be associated with cirrhosis and with portal hypertension. We speculate that our findings may be relevant to women with other portal lesions resembling CPH such as resolving acute hepatitis and chronic active hepatitis in sustained remission.
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PMID:Chronic-persistent hepatitis and pregnancy. 45 47

Six cases of an association of liver disease with a cryoglobulinaemia syndrome are described. An account of their clinical, body fluid and anatomopathological pictures is followed by a discussion of their possible causes in the light of the relevant literature. It is felt that no assessment can be made of the primary nature of either disease in associations of this kind. In addition to cases in which prior liver disease or exposure to hepatitis virus can be shown, in fact, there are other situations in which liver disease was present before the manifestation of cryoglobulinaemia. Repeated antigen stimulus triggers the antibody response leading to the formation of cryoprecipitating complexes. In most cases, the nature of such antigen is not known, since HB virus or any other virus, bacterial product, or cell catabolism product either eliminated in insufficient quantities, or produced in abnormal quantities, may be responsible.
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PMID:[Cryoglobulinemia syndrome and liver diseases. Case reports]. 46 Jun 49

Human hepatic bile contains a glycoprotein (biliary glycoprotein I, BGP I) which cross-reacts with the carcinoembryonic antigen (CEA). A radioimmunoassay for BGP I was developed. The interference of CEA or 'non-specific cross-reacting antigen' (NCA) in the assay was small. The serum levels of BGP I were determined in healthy subjects, in patients with hepato-biliary diseases and in patients with various infectious or inflammatory disorders. Healthy individuals, including pregnant women, had a serum BGP I concentration of about 0.5-1 mg/l. Diseases of the liver or biliary tract (e.g. hepatitis A or B, cytomegalovirus hepatitis, obstructive jaundice or primary biliary cirrhosis) were associated with elevated serum levels of BGP I, as opposed to infectious diseases not affecting the liver mostly showing values within the normal range. Raised levels of serum BGP I activity may reflect biliary obstruction as a result of interference with normal BGP I secretion to the bile.
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PMID:Elevated serum levels of a biliary glycoprotein (BGP I) in patients with liver or biliary tract disease. 47 33

The concentration of cytochrome P-450 and activities of the microsomal enzymes aryl hydrocarbon hydroxylase and ethylmorphine demethylase were measured in hepatic tissue obtained at biopsy from 69 patients. Antipyrine half-life (AP t1/2) was measured simultaneously as an in vivo marker of drug metabolism. Values for each index of the drug-metabolizing system varied greatly, but the mean values in groups of patients with mild hepatitis or inactive cirrhosis did not differ significantly from those of controls. Hepatic cytochrome P-450 content and aryl hydrocarbon hydroxylase activity were lower in patients with severe hepatitis or active cirrhosis than in controls, but ethylmorphine demethylase activity was unchanged in the patients. Drug ingestion was associated with enhancement of drug-metabolizing enzymes in all patients but those with severe liver disease; ethylmorphine demethylase activity was enhanced proportionately more than aryl hydrocarbon hydroxylase activity or cytochrome P-450 concentration. The observation that aryl hydrocarbon hydroxylase and ethylmorphine demethylase activities are influenced to a different extent by liver disease and also by drug ingestion indicates functional heterogeneity of the hepatic microsomal drug-metabolizing system in man. Correlations between t1/2 and hepatic drug oxidases were weak, even when allowance was made for variation in liver size. Thus, the rate of drug metabolism in vivo assessed by measuring AP t1/2 does not appear to be closely related to the activity of some hepatic drug-metabolizing enzymes.
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PMID:Drug metabolism in liver disease: activity of hepatic microsomal metabolizing enzymes. 48 96


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