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)

Delayed cutaneous hypersensitivity response using DNCB was studied in 51 apparently healthy Pakistanis and 60 patents with acute and chronic liver diseases. A Positive response was observed in all the healthy subjects, 22 out of 29 cases with acute viral hepatitis, 8 out of 22 patients with post-necrotic cirrhosis, one out of three cases of liver cancer and all the cases of alcoholic cirrhosis. It was postulated that hyperactive cell mediated immune response and a heavy exposure to hepatitis virus may be resonsible for the observed pattern of liver disease in Pakistan.
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PMID:DNCB sensitivity in healthy Pakistani subjects and patients with liver disease. 65 81

A clinical, biochemical, and pathological study was performed in 38 chronic HBsAg carriers. The study group is a part of 393 carriers found among 117 705 voluntary blood donors at the National Blood Bank, Hospital del Salvador, Santiago, Chile. None of the 38 carriers had a past history of illicit drug abuse, hepatitis, or work involving a high risk of hepatitis B virus infection. Ten individuals had a normal liver biopsy, 17 reactive non-specific hepatitis, one fatty changes, four chr onic persistent hepatitis, one aggressive hepatitis, two post-necrotic cirrhosis, and three alcoholic cirrhosis. There was not a close correlation between liver function test and liver histology. The most significant laboratory finding was the postivity of alpha fetoprotein in two cases. During the follow-up the two alpha fetoprotein patients presented a hepatocarcinoma 12 and 14 months after admission to the study.
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PMID:Clinical and pathological study of asymptomatic HBsAg carriers in Chile. 68 May 91

With an immunofluorescence technique using rabbit hepatocytes isolated by a non-enzymatic method an autoantibody directed against liver-cell-membrance was identified. Sera from 361 patients with various liver diseases and 274 patients with primary non-hepatic diseases-many associated with non-organ-specific auto-antibodies-were examined. The antibody (LMA) was found in 27 out of 72 patients with hepatitis-B-surgace antigen (HBsAg)-negative chronic active hepatitis and in 17 out of 28 patients with HBsAg-negative non-alcoholic cirrhosis. Only two patients had LMA and HBsAg, and both had chronic active hepatitis. One patient with extrhepatic disease was found to have LMA, and this patient had biochemical evidence of liver disease. Hence there is a close correlation between the presence of LMA and HBsAg-negative chronic inflammatory liver diseases and its detection may help in diagnosis.
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PMID:Liver-cell-membrane autoantibody specific for inflammatory liver diseases. 83 76

The serum immunoglobulin (Ig) G, A, and M levels were investigated with respect to their differential diagnostic significance, pathogenesis and estimation of prognosis of different forms of liver disease. The sera of 204 patients with acute hepatitis, fatty liver I and II, and cirrhosis, and of 110 healthy adutls were quantitatively determined for immunoglobulins. 1. IgG- and IgA-concentrations higher than 2000 mg% and 330 mg%, respectively, indicate chronic aggressive hepatitis or cirrhosis, and exclude all other groups. 2. A clear correlation between HBsAG (Australia Antigen) and immunoglobulin content could not be demonstrated in any group; 3. A significantly elevated level of IgA was observed in alcoholic cirrhosis when compared to non-alcoholic cirrhosis. No such differences were found inhe other groups. 4. Acute and chronic persistent hepatitis show a similar increase of immunoglobulins. Thus persistent high levels of Ig following acute hepatitis indicate the development into a chronic hepatitis. 5. A relative increase of IgA rather than IgG corresponds to the degree of inflammatory activity of a liver process.
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PMID:[Quantitative serum immunoglobulin determination: differential diagnostic significance for liver disease (author's transl)s]. 84 Jan 24

The mechanism responsible for making the differences between plasma and serum complement (CH50) was studied on eight patients with hepatitis-B(s) antigen negative alcoholic liver cirrhosis. CH50 and C4 activities of the sera of all patients were equal to those of the corresponding EDTA-plasma, when sera wre separated after clotting the blood at 37 degrees C. CH50 and C4 activities of the sera, prepared at 21 degrees C or 4 degrees C, from four of eight patients were very low. When serum from one of these four patients was added to normal human serum, C4 activity of the serum mixture markedly decreased at 4 degrees C but not at 37 degrees C. The inactivation of C4 was prevented by adding EDTA or heparin to the serum mixture. These results indicated that very low complement in the sera, prepared at 21 degrees C or 4 degrees C, of the four cases were due to the cold activation of the classical complement pathway.
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PMID:The cold activation of the classical complement pathway: The cause of the differences between plasma and serum complement in liver cirrhosis. 84 48

Needle-hepatic biopsy of 48 chronic alcoholic patients was investigated by the aid of electron microscopy. On the base of clinical and histological features five stages of the hepatic lesion could be distinguished: 1. fatty liver, 2. fatty liver with increasing activity of the mesenchymal cells, 3. acute alcoholic hepatitis ,4. chronic alcoholic hepatitis, 5. alcoholic cirrhosis. Changes of the liver cell organella and mesenchymal cells in different stages were compared. It was observed, that the damage to the hepatocytes--exept acute alcoholic hepatitis--was not parallel to the severity of the clinical picture. On the other hand proliferation of mesenchymal cells their secretory activity and fibrogenesis seem to go parallely with the progression of the hepatic lesion. Authors assume, that between alcoholic hepatitis and alcoholic cirrhosis there exists an intermedier form of the disease i.e. the chronic agressive alcoholic hepatitis ,which morphologically is similar to the chronic agressive hepatitis. This form of the hepatic lesion can be characterized not by the severity of the lesion of hepatocytes, but the by enormous proliferation of mesenchymal cells and by lymphocytic infiltration.
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PMID:[Electron microscopic study of alcoholic liver damage, with special reference to changes in the mesenchymal liver cells]. 85 35

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

Serial measurements of complement components were performed in fifty-nine patients with acute, uncomplicated hepatitis and twelve with alcoholic cirrhosis. Thirty-one of the former group had detectable hepatitis B antigen. Abnormal complement profiles were observed in nine patients with hepatitis B and seven with antigen-negative hepatitis. Low levels of C4, C3 and factor B were common in the subjects with cirrhosis and confined to those cases with severe reduction in serum albumin and/or prothrombin index. By contrast, the complement changes in the patients with hepatitis occurred without significant alteration in these parameters; certain subjects also had reduction in C1q and C5 and a significant number had C3d detectable in fresh plasma. The pattern of abnormality suggests predominant involvement of the classical pathway and it is concluded that this results, at least in part, from an immune process evident only in the early clinical phase of hepatitis. Such gross changes in complement are likely to reflect immune-complex activity and it is proposed that these complexes may be important in the clearance of virus material. The data supports a previous suggestion that recovery from acute hepatitis is primarily dependent on host immune competence rather than viral cytotoxicity or generation of immune complexes.
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PMID:Acute hepatitis: significance of changes in complement components. 89 Oct 25

Lymphocytes from thirty-four untreated patients with various liver diseases were stimulated in a lymphocyte transformation test with liver-specific protein (LSP). Eight of ten patients with chronic active or persistent hepatitis, two of five patients with non-alcoholic cirrhosis and six of nineteen patients with acute hepatitis showed a positive in vitro reactivity to LSP. In a control group of twelve persons without evidence of liver disease, eleven gave a negative response to LSP stimulation, whereas one person showed a positive response. Among fourteen patients with chronic hepatitis or non-alcoholic cirrhosis treated with prednisone at the time of the investigation, only one showed reactivity to LSP stimulation. Three patients in this group had previously had a positive reaction before prednisone was given. There was no statistically significant correlation between the reactivity to LSP stimulation and the presence or absence of hepatitis-associated antigen (HBAg) in serum, or with the biochemical liver parameters. The response to in vitro stimulation with phytohaemagglutinin (PHA) was found to be significantly lower as compared with the control group in eleven patients with alcoholic liver disease and in the patients with acute hepatitis who had HBAg in serum. This decrease in reactivity could apparently not be ascribed to immuno-suppressive factors in the patients' sera.
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PMID:Lymphocyte transformation test with liver-specific protein and phytohaemagglutinin in patients with liver disease. 94 67

A sensitive radioimmunoassay for cholylglycine, chenodeoxycholylglycine, deoxycholylglycine, and sulfolithocholylglycine was established using antibodies obtained from rabbits injected with albumin conjugates of these bile acids. Glycine-conjugated bile acid levels were measured in sera from 25 control subjects and 110 patients who had hepatic disease (alcoholic cirrhosis, hepatitis, cholestasis, and hepatic malignancy). Sulfolithocholylglycine was elevated in the sera of all 110 patients with hepatic disease. Cholylglucine was within normal range in only three. Chenodeoxycholylglycine was elevated in most sera of patients who had hepatitis, cholestasis, or hepatic malignancy. It was normal in most sera of patients who had alcoholic cirrhosis, suggesting that chenodeoxycholic acid may be subject to further biotransformations in these patients. Deoxycholylglycine was elevated in a minority of patients, none of whom had cholestasis. The data suggest that serum bile acids, particularly sulfolithocholylglycine, are a highly sensitive index for hepatic dysfunction.
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PMID:Levels of immunoreactive glycine-conjugated bile acids in health and hepatobiliary disease. 98 91


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