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 behaviour of gamma-glutamyl transpeptidase was compared with other serum enzyme activities and functional parameters in a carefully selected and relatively extensive series of patients with liver disease, including alcoholics, in an investigation of the underlying pathogenesis and its clinical expression. Reference. to the literature and to personal data showed that increased gamma-glutamyl transpeptidase levels could be attributed to enzyme induction (caused by drugs or alcohol), liver damage in the broad sense, and intra- or extrahepatic cholestasis. These causes were individually predominant, or nearly so, on occasions, though their concomitance was more common. High levels, however, were not pathognomonic for a given disease. In alcoholism, they were highly indicative, especially if accompanied by GLD changes. They were a virtually constant, early, and typical finding in intra- and extra-hepatic cholestasis, and tended to persist for a time after the resolution of icterus. Lastly, they were an aid in the early diagnosis of aggressive hepatitis and liver cancer.
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PMID:[Critical observations on changes in gamma-glutamyl-transpepdidase in hepatopathies]. 0 98

Serum gamma-glutamyl transpeptidase (gamma-GT) level was estimated in 132 patients with different liver diseases (chronic persistent and chronic active hepatitis, postnecrotic cirrhosis, chronic alcholic hepatitis and alcoholic cirrhosis, cholestasis syndrome, fatty liver, Gilbert disease) and malignancies with and without liver involvement. The gamma-GT levels were compared with the values for serum bilirubin, transaminases (GOT, GPT) and alkaline phosphatase in the same patients. gamma-GT values were normal in chronic persistent hepatitis and increased in chronic active hepatitis. Very high activities were measured in chronic alcoholic cirrhosis in contrast to postnecrotic cirrhosis. gamma-GT proved to be more sensitive than alkaline phosphate as an index of cholestasis and liver involvement in malignancies. It is suggested that gamma-GT activity offers valuable aid in differential diagnostics of liver-diseases. gamma-GT being an inducible enzyme, its activity may be raised by enzyme inducing drugs also in subjects without liver disease.
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PMID:Serum gamma-glutamyl transpeptidase: its clinical significance. 2 44

The interpretation of the morphological features of alcoholic hepatitis is discussed in terms of a comparison with the results of an ultrastructural and histoenzymological study of the liver biopsies of nine patients. In these patients liver biopsies were performed in the initial stage of the illness and fifteen days after five were re-biopsied, when the clinical and biological signs were improved. The correlations between morphological and biological data were good, especially for the levels of serological and histoenzymological alkaline phosphatase and gamma-glutamyltranspeptidase evaluations. However, when histological appearances had returned to normal, after two weeks of abstinence from alcohol several histological and ultrastructural features of the initial hepatitis persisted. The presence of evolving cirrhosis was a contributing factor to the severity of the changes seen. Morphologically, apart from the changes due to chronic alcoholic intoxication (steatosis, mitochondrial alteration), the hepatitic lesions comprise Mallory's bodies, cytoplasmic oedema and mitochondrial swelling. Cholestasis was invariably present. Histo-enzymologically there was a reduction in ATPase activity suggesting a metabolic failure in the energy producing pathways. In addition, in the periphery of lobules an active cirrhotic process was present, with tubular de-differentiation of hepatocytes and an increase in gamma-glutamyltranspeptidase on the cytoplasmic membrane. Because of the absence of any topographical relationship between hepatitis and cirrhosis, the presence of lymphocytes in the neighbourhood of the ductules suggested an indirect relationship between both processes, perhaps an autoimmune response initiated by Mallory's bodies.
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PMID:[The hepatocyte in acute alcoholic hepatitis. Histoenzymological and ultrastructural analysis (author's transl)]. 3 Oct 27

The GGTP is an enzyme localized, in the liver cell, inside microsome. At beginning the use of the GGTP was introduced for the diagnosis of chronic hepatitis; after it was noted as this was steady increased in the cholestasis and in the alcoholism. We have, hence, wanted to experiment if the changing of the level of the GGTP allowed to us a diagnosis of chronic alcoholic hepatitis. Our research is based on seventy-five patients with several liver diseases. It has been noted as the highest levels of the GGTP have appeared in cases of chronic alcoholic hepatitis with signs, histologicals and biochemicals, o cholestasis. In fact we have, on overage, levels of 955 mU/ml in the chronic alcoholic hepatitis with signs of cholestasis and of 135 mU/ml in that without it. In conclusion the GGTP is a good index for the diagnosis of chronic alcoholic cholestatic hepatitis.
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PMID:[The gamma-glutamyl transpeptidase (GGTP) as an index for the diagnosis of chronic alcoholic cholestatic hepatitis (author's transl)]. 3 45

10 of a series of 108 patients with alcoholic liver disease presented with cholestasis associated with non-cirrhotic alcoholic liver disease and without evidence of extrahepatic biliary obstruction. In 7 patients liver histology and the associated conditions presenting as cholestasis were heterogeneous. However, in 3 patients who had been drinking excessively before cholestatic jaundice developed, cholestasis was a major feature of liver histology. The term acute alcoholic cholestasis is suggested for this apparently distinct syndrome of cholestatic jaundice in the absence of hepatitis.
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PMID:Cholestasis in acute alcoholic liver disease. 7 24

A histopathological study was carried out on 27 patients with chronic inflammatory liver disease and clinical and/or biochemical evidence of cholestasis who had either mitochondrial antibodies against mitochondrial antigen fractions of 1.19 density ("PBC antigen"; 14 cases) or of 1.13 density ("CAH-PBC mixed-type antigen"; 13 cases). For comparison, the liver biopsies of 17 patients with chronic-aggressive hepatitis (CAH) and antinuclear and/or anti-smooth muscle antibodies but without cholestasis and mitochondrial antibodies, were evaluated. The 14 patients with mitochondrial antibodies against the PBC antigen showed the typical histological features of primary biliary cirrhosis (PBC). The 13 patients with mitochondrial antibodies against the CAH-PBC mixed-type antigen had heterogenous liver alterations. In 11 cases highly active CAH and/or active postnecrotic cirrhosis (AC) were found both with augmented ductular proliferation. Some of these cases showed distinct criteria of PBC as early bile duct lesions or absence of regular bile ducts. The liver histology of one case corresponded to classical PBC; another case to chronic persistent hepatitis. The CAH-patients without cholestasis and mitochondrial antibodies only occasionally showed bile duct proliferation. In conclusion, a high correlation was found between mitochondrial antibodies against the CAH-PBC mixed-type antigen and highly active CAH or early AC with augmented ductular proliferation. This represents an overlapping of CAH and PBC. In contrast, the cases with antibodies reacting to the PBC antigen showed the slowly progressive liver changes of typical PBC.
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PMID:Histopathological features in mixed types of chronic aggressive hepatitis and primary biliary cirrhosis. Correlations of liver histology with mitochondrial antibodies of different specificity. 13 50

Quantitative determination of the abnormal plasma lipoprotein of cholestasis LP-X has been performed in 81 LP-X positive patients with different liver disorders. Great variations in the plasma concentration of LP-X were demonstrated both in the 45 patients with intrahepatic cholestasis (acute hepatitis, toxic hepatitis, primary biliary cirrhosis and cholangitis) and in the 36 patients with extrahepatic cholestasis (extrahepatic biliary obstruction by tumours and choledocholithiasis). The plasma concentratkons of LP-X in the patients with extrahepatic cholestasis (median 158 mg/100 ml) were significantly (psmaller than 0.001) higher than in the patients with intraphepatic cholestasis (median 25 mg/100 ml) was exceeded by 42% of the patients with extrahepatic biliary obstruction, and 33% of the patients with extrahepatic biliary obstruction, had LP-X LEVELS ABOVE 400 MG/100ML. The plasma concentration of LP-X was significantly correlated to the plasma activity of alkaline phosphatases and serum bilirubin, but seemed to be superior to these two parameters in the differentiation between intrahepatic and extrahepatic cholestasis. Plasma levels of LP-X above 400 mg/100 ml are highly indicative of extrahepatic biliary obstruction.
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PMID:Quantitative determination of the abnormal lipoprotein of cholestasis, LP-X, in liver disease. 16 86

The authors report 3 cases and report the diagnostic usefulness of two signs of minor cholestasis described by one of them in 1966. A relative increase, in the absence of obvious virus hepatitis or cirrhosis, of the serum bilirubin, cholesterol, lipids and alkaline phosphatase, together with B.S.P. excretion. suggest minor cholestasis. The sign of "metacritical aggravation" when there is some suspicion of minor cholestasis, the supervision of the course of the disease, or a retrospective inquiry, permit, in the presence of minor symptoms, such as, pain, fever, jaundice, or pruritus, one to make the diagnosis of minor cholestasis. The latter is due either to the presence of small gall stones in the common bile duct, or to inflammation of the ampulla of Vater, or sphincter of Oddi, a Vaterian ampulloma, pancreatitis, or following damage to the common bile duct. In practice, liver biopsy confirms the diagnosis, and intravenous cholangiography, by the perfusion method, is usually able to demonstrate obstruction of the common bile duct.
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PMID:[Relative increase and metacritic aggravation in the diagnosis of anicteric cholestasis]. 16 83

A female patient developed a recurrent hepatitis-like liver damage after ingestion of a laxative containing 4,4'-(2-quinolyl-methylene)-diphenol-hydrochloride. After cessation of the drug the clinical picture improved. The hyperbilirubinemia decreased and the definitely elevated GOT, GPT, alkaline phosphatase and gamma-GTP became normal. Histologically hepato-cellular damage was seen with intra-hepatic cholestasis. As a cause for these symptoms, resembling those after taking oxyphenisatin-containing preparations, immunological procedures were thought responsible, such as "unpredictable hepatic drug reactions".
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PMID:[Liver damage caused by laxatives. A contribution to the hepatotoxicity of 4,4'-(2-quinolylmethylene)-diphenol-hydrochloride]. 16 54

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


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