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)

gamma-Glutamyl transpeptidase (GGTP) is a sensitive but nonspecific index hepatobiliary disease. In infectious mononucleosis (IM) or the mononucleosis-like disease attributable to cytomegalovirus (cytomegalovirus-induced IM), GGTP reverted to normal later than aspartate aminotransferase and alkaline phosphatase. In three cases elevated serum GGTP activity persisted for up to 24 months -- raising the question of persistent 'post-IM' hepatitis. Such prolonged GGTP activity was unusual in other late IM specimens. Possible, but unlikely, causes for such persistent GGTP activity are an unusual degree of hepatic damage during acute IM, excessive induction of microsomal enzyme system activity by drugs, or unusual Epstein-Barr virus carrier state activation that might contribute to ongoing hepatic structural damage. Other markers of chronic hepatocellular disease including aspartate aminotrasferase, alkaline phosphatase, and bilirubin were normal in late specimens from these 3 patients. The cause of their persistent elevated GGTP activities remains unknown.
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PMID:Late persistence of serum gamma-glutamyl transpeptidase activity after mononucleosis. Report of 3 cases. 1 21

Drugs and other chemicals are usually metabolized in the liver in the drug-metabolizing enzyme system. The metabolites sometimes bind with cellular macromolecules and injure the cell directly or serve as new antigens to create immunologic injury in a delayed fashion. The immediate or toxic injury is dose-dependent, predictable and zonal in the liver lobule, usually in the central region. Carbon tetrachloride intoxication and acetaminophen overdose are examples of injury resulting from microsomal metabolism. Other injuries related to microsomal metabolism are those produced by vinyl chloride in polymerization plant workers and by methotrexate in psoriatics or leukemic children. Most adverse drug reactions affecting the liver and producing jaundice are unpredictable, delayed in onset, and only hypothetically related to microsomal metabolism in some instances. The two main types are cholestasis and viral-hepatitis-like. The former may be in a pure form, in which case it may be partly dose-dependent, or in a form mixed with hepatitis. Many drugs produce cholestasis in a small percentage of persons, and because the reaction is benign, albeit prolonged at times, such drugs continue to be used. The viral-hepatitis-like reaction involves few drugs and affects few persons, but can be fatal. The recognition that chronic hepatitis can be caused by drugs such as oxyphenisatin, alpha-methyldopa, and isoniazid has added a new dimension to the clinical problem of adverse drug reactions, which may extend to widely used and commonly available agents like aspirin.
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PMID:Hepatic drug metabolism and adverse hepatic drug reactions. 17 22

While chickens infected with duck hepatitis virus showed no signs of clinical illness, their levels of hepatic cytochrome P-450 in response to phenobarbital induction and their microsomal aryl hydrocarbon hydroxylase activities in response to 3-methylcholanthrene induction were each found to correlate with the titer of virus recovered from the livers. These clear correlations indicate that avian hepatic drug metabolism is significantly modified during viral infection.
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PMID:Correlation of induced drug metabolism with titer of duck hepatitis virus in chickens. 19 18

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

Different methods of performing the (14C) aminopyrine breath test have been assessed. A tracer dose of 2 muCi without a loading dose and with a single breath collection at two hours was the method selected, since it gave the best discrimination between patients with hepatocellular diseases and normal subjects (5.2 +/- 0.2%, mean +/- SEM). Reduced values occurred in patients with chronic active hepatitis (with and without cirrhosis) (1.5 +/- 0.2%), alcoholic cirrhosis (1.7 +/- 0.4%) and hepatitis (2.5 +/- 0.3%), and late primary biliary cirrhosis suggesting defective microsomal function with respect to demethylation. Normal results were common in early primary biliary cirrhosis. Two weeks of prednisolone therapy caused some improvement in the breath test in nine of 10 patients with chronic active hepatitis. It is concluded that the (14C) aminopyrine breath test is a simple test for detecting hepatocellular dysfunction, but has no obvious diagnostic advantage over the determination of serum aspartate transaminase and two hour post-prandial bile-acids.
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PMID:Assessment of the (14C) aminopyrine breath test in liver disease. 62 4

The authors report the cases of 3 patients who died from fulminant hepatitis after receiving iproclozide, a hydrazine-containing monoamine oxidase inhibitor. Fulminant hepatitis in these patients resembled that reported in patients receiving other hydrazine-containing monoamine oxidase inhibitors: (1) the 3 patients were women; (2) the monoamine oxidase inhibitor has been ingested for 1 month or more; (3) the main clinical manifestations were jaundice and disorders of consciousness; (4) hypersensitivity manifestations were absent; (5) the predominant liver lesion was necrosis; (6) all 3 patients died. In our 3 patients, jaundice occurred 7 to 10 days after the adjunction to iproclozide of a microsomal enzyme inducer. These observations suggest that concomitant administration of iproclozide and of microsomal enzyme inducers may produce fulminant hepatitis in man. It is speculated that iproclozide could be, like iproniazid, transformed into a hepatotoxic metabolite, the production of which would be increased by microsomal enzyme induction.
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PMID:Iproclozide fulminant hepatitis. Possible role of enzyme induction. 68 May 6

1. Mitochondria and microsomal fractions have been isolated from liver biopsies from patients with alcoholic cirrhosis, cryptogenic cirrhosis or chronic aggressive hepatitis. 2. Cirrhotic livers yieled fewer mitochondria than normal liver. 3. The most significant change was a decrease in mitochondrial respiratory control. Cirrhotic microsomal fractions had a 50% diminution in cytochrome b5 and cytochrome P-450 content. 4. The two patients with chronic aggressive hepatitis showed similar mitochondrial and microsomal changes.
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PMID:Mitochondrial functions and content of microsomal and mitochondrial cytochromes in human cirrhosis. 88 31

Electron microscopic findings made on microsomal fractions of rat liver after treatment with microsomal antibodies obtained from the blood of patients diagnosed as having chronic aggressive hepatitis and liver cirrhosis and after incubation with peroxidase-labelled antihuman IgG are described and presented in this paper. Interpretation of these findings as the substrate of an antibody reaction directed against membranes of the endoplasmic reticulum of hepatocytes is discussed.
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PMID:The immunoelectron-microscopical demonstration of antibodies against endoplasmic reticulum (microsomes) in chronic aggressive hepatitis and liver cirrhosis. 88 90

The urinary excretion of D-glucaric acid and the plasma clearance of antipyrine were estimated during the acute phase of viral hepatitis and again during recovery. The plasma clearance of antipyrine was impaired during the acute stage of hepatitis, while the urinary excretion of D-glucaric acid was paradoxically high. Both parameters returned to normal during recovery. These findings suggest that the use of urinary D-glucaric acid excretion as an index of microsomal enzyme induction is unreliable when there is liver injury.
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PMID:Paradoxical urinary excretion of D-glucaric acid in acute viral hepatitis. 95 55

The specific activity of coumarin-7-hydroxylase was measured in liver microsomes from normal subjects and patients with liver disease. Liver specimens were obtained by needle biopsy and the microsomal fraction was separated by differential centrifugation. Its freedom from mitochondria was demonstrated by the absence of succinic dehydrogenase, a marker enzyme for mitochondria. Liver from healthy subjects showed variation in the specific activity of coumarin-7-hydroxylase from 0.16 to 0.65 nmol-mg-1-min-1, which is probably due to genetic factors. Patients with cirrhosis of the liver, chronic fatty hepatitis (chronic alcoholic hepatitis) and chronic active hepatitis showed a significantly lower mean hydroxylase activity. There was no significant difference in the mean level of hydroxylase between patients with subacute viral hepatitis or chronic persistent hepatitis and the normal controls.
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PMID:Coumarin-7-hydroxylase activity in microsomes from needle biopsies of normal and diseased human liver. 96 89


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