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)

Human plasma containing the Australia (hepatitis-associated) antigen was fractionated by the cold ethanol method of Cohn, Strong, Hughes, Mulford, Ashworth, Melin, and Taylor (1946) and small aliquots were examined for the presence of this antigen by immunodiffusion and by electron microscopy. The findings were in general agreement with the postulated risk of transmitting hepatitis by blood derivatives. The Australia (hepatitis-associated) antigen was detected in fibrinogen, thrombin, and antihaemophilic globulin as well as in other fractions. The antigen was not found in gamma globulin (immunoglobulin fraction) nor in albumin.The use of radioiodinated fibrinogen for the diagnosis of deep vein thrombosis is discussed and it is concluded that the use of fibrinogen for diagnostic procedures should be assessed against the possible risk of hepatitis.
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PMID:The Australia (hepatitis-associated) antigen in fibrinogen and other fractions of human plasma. 499 77

When plasma containing a hepatitis-associated antigen (Au/SH) is fractionated, the antigen is localized in fractions III and IV with none in fraction II and only small amounts in fractions I and V. The amount of antigen found in each of these fractions is probably not predictive of clinical infectivity of Cohn ethanol fractions from normnal pooled plasna.
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PMID:Australia antigen: distribution during Cohn ethanol fractionation of human plasma. 544 35

Alcohol induces a variety of changes in the liver: fatty change, hepatitis, fibrosis, and cirrhosis. The histopathological appearances of these conditions are discussed, with special attention to differential diagnosis. Many forms of alcoholic liver disease are associated with Mallory body formation and fibrosis. Mallory bodies are formed, at least in part, from intermediate filaments. Associated changes in intermediate filament organisation in alcoholic liver disease also occur. Their significance in the pathogenesis of hepatocyte death may be related to abnormalities in messenger RNA function. The mechanisms underlying hepatic fibrogenesis are also discussed.
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PMID:Alcohol induced liver disease. 608 22

Alcohol is the most significant liver poison. Its degradation takes above all place by the alcohol dehydrogenase and the microsomal alcohol-oxidizing system. In the first step of degradation acetaldehyde develops which in enrichment evokes immediately toxic defects on the mitochondrias of the cells of the liver parenchyma and thus introduces a vicious circle. Furthermore, an increased affection of pharmacometabolites as a sequel of the alcohol-conditioned enzyme induction may lead to a defect. Alcohol influences intermediary metabolic functions: the gluconeogenesis is inhibited, multi-layer disturbances in the lipid metabolism lead to fatty degeneration of the liver. A hyperuricaemia results from overproduction in the liver as well as from decreased renal excretion. The proline formation is increased. Distinct increase of the gamma-GT-activity is an early and relatively specific indicator of the alcoholic liver defect. Morphologic and clinical manifestations are fatty degeneration of the liver, hepatitis based on fatty degeneration of the liver and cirrhosis. Apart from dose and duration of the alcohol intake additional factors require consideration. The author adopts a definite attitude to etiopathogeneis and therapeutic possibilities.
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PMID:[Alcohol and the liver]. 611 57

Circulating antibodies reacting specifically with hepatocytes isolated from ethanol pretreated rabbits have been demonstrated by two techniques - induced cytotoxicity and immunofluorescence. In the cytotoxicity assay antibodies were found in seven of 19 (39%) of patients with alcoholic fatty liver (with or without fibrosis), six of 13 (46%) of those with alcoholic hepatitis, 15 of 36 (43%) of those with cirrhosis, and seven of 14 patients (50%) of those with hepatitis and cirrhosis. In the immunofluorescence studies, nine of 15 sera induced a granular pattern of fluorescence on the ethanol pretreated hepatocytes; two sera which induced significant cytotoxicity did not induce immunofluorescence. No ethanol related antibodies were found in normal individuals or in patients with other types of acute or chronic liver disease. These results show that antibodies directed against ethanol altered liver cell determinants are present in the serum of 43% of patients with alcoholic liver disease, and suggest a mechanism whereby chronic alcohol consumption may, by inducing antigenic changes in hepatocyte membranes, trigger a cell damaging immune reaction.
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PMID:Antibodies to alcohol altered liver cell determinants in patients with alcoholic liver disease. 619 63

A rapid, microanalytical procedure for the reproducible isolation of RNA from small cultured cell samples and application to dot-blot hybridization is described. The procedure employs guanidine hydrochloride solubilization of whole cells, disruption by syringing, and selective precipitation of RNA with ethanol. The method can be performed in a single tissue culture tube and obviates the need for removal of nuclei or for organic solvent extractions. Recovery of RNA from small cell samples (10(6) cells) is 51%, while 97% of the DNA and 99% of the protein are eliminated by the procedure. Detection of specific RNA by dot-blot hybridization using a labeled probe demonstrates high reproducibility of recovered RNA and lack of "masking" with up to a 10-fold excess of starting cell material. Applicability of the procedure to detection of virus-specific RNA in cells persistently infected with mouse hepatitis virus is described.
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PMID:A reproducible microanalytical method for the detection of specific RNA sequences by dot-blot hybridization. 620 30

Seventy-eight black patients and white patients with primary hepatocellular carcinoma (PHC), 70 years or younger at diagnosis, and 78 age-, sex-, and race-matched neighborhood controls were interviewed. Information sought included usual dietary and drinking habits, cigarette smoking habits, prior medical conditions including a history of hepatitis, prior exposure to blood products, and occupational history. Cigarette smoking was a risk factor for PHC; the relative risk (RR) for current smokers of more than one pack/day compared to nonsmokers was 2.6. Alcohol consumption was also a significant risk factor for PHC; individuals who drank 80 g or more of ethanol per day had a RR of 4.2 compared to those drinking less than 10 g/day. In addition, a history of hepatitis (RR = 13.0) and a history of blood transfusions (RR = 7.0) were significant risk factors for PHC. Each of these factors remained significant after adjustment was made for the others.
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PMID:Hepatitis, alcohol consumption, cigarette smoking, and hepatocellular carcinoma in Los Angeles. 631 25

We report herein results of comparative study of different methods for determination of M or G classes of antibodies applied to serodiagnosis of type A hepatitis. We have examined retrospectively 259 sera with a technique employing protein A and 2 kits, HAVAB-M (RIA-M) and Hepanostika anti-HAV-IgM (ELISA-M). Some sera were studied after treatment by 2-mercapto-ethanol. We have obtained the same results with RIA-M and ELISA-M: 119 sera contain Ac anti-HAV of M class and 116 of G class, 24 sera non classified with protein A owing to their low level of Ac anti-HAV, are all but one of G class. We have observed 23 discrepancies between protein A or RIA-M and ELISA-M. A first group is constituted by 15 sera obtained during late convalescence and containing rates of Ac anti-HAV-M too low to be determined with protein A or 2-mercapto-ethanol so they are classified G, while RIA-M and ELISA-M, more sensitive, could detect such antibodies. Another group is constituted by 8 sera containing low rates of anti-HAV antibodies so we could not dilute them for reaction, and IgG were not adsorbed entirely on protein A while 2-mercapto-ethanol, RIA-M and ELISA-M led them being classified Ac anti-HAV-G. RIA-M and ELISA-M are useful tools particularly for sera obtained during late convalescence while protein A and 2-mercapto-ethanol are effective for diagnosis during 1 month after acute phase.
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PMID:[Comparative study of various methods for the determination of the IgM or IgG class of antibodies, applied to the diagnosis of hepatitis A]. 634 23

The propensity to develop alcoholic cirrhosis is probably, at least in part, genetically determined. A striking similarity exists histologically between perhexiline and alcohol-related hepatitis and both are potentially precirrhotic lesions. Liver damage due to perhexiline is associated with impaired drug oxidation capacity which is genetically determined and tested by use of debrisoquine. Oxidation phenotyping might be used to predict susceptibility to perhexiline liver damage; it might also predict the potential to develop alcoholic cirrhosis. Oxidation phenotyping was therefore undertaken, using debrisoquine in 100 alcoholic patients, 30 of whom had only fatty liver despite prolonged alcohol abuse, while the remaining 70 had alcoholic hepatitis and/or cirrhosis. One hundred patients with nonalcoholic chronic liver disease served as controls. The number of patients with severely impaired drug oxidation capacity (poor metabolizer phenotype) was similar in the alcoholic group (8%) and the nonalcoholic control group (7%). In particular, the incidence of the poor metabolizer phenotype was similar in alcoholics with severe liver disease (10%) and in those with only fatty change (3%). There appears to be no association between the susceptibility to develop alcoholic cirrhosis and drug oxidizing capacity.
Alcohol Clin Exp Res
PMID:Oxidation phenotyping in alcoholics with liver disease of varying severity. 639 Dec 52

The pharmacokinetics of thiopentone were compared in nine control patients and 10 patients with chronic alcoholism (without signs of cirrhosis or hepatitis) undergoing orthopaedic or abdominal surgery under general anaesthesia. The mean (+/- SD) alcohol intake was 92 +/- 14 litre of ethanol per year in the alcoholic patients and less than 10 litre yr-1 in the controls. Thiopentone plasma concentrations were measured by high pressure liquid chromatography after the administration of a single bolus dose (5-9 mg kg-1). The plasma clearance of thiopentone was significantly increased from 3.7 +/- 0.9 ml min-1 kg-1 in the controls to 5.4 +/- 2.2 ml min-1 kg-1 in the patients with chronic alcoholism. The volume of the central compartment and the total apparent volume of distribution were similar in both groups. The terminal elimination half-life was of 684 +/- 168 min in the alcoholics and did not differ significantly from the value found in the controls (750 +/- 212 min).
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PMID:Thiopentone pharmacokinetics in patients with chronic alcoholism. 649 49


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