Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study has been undertaken to determine the incidence of serum markers of hepatitis B virus (HBV) infection in British caucasian patients with biopsy-proven alcoholic liver disease (n = 56), HBsAg negative chronic active liver disease (CALD) (n = 47) and primary liver cell cancer (PLCC) (n = 27), compared to a hospital control population without liver disease (n = 112). No increased incidence of any serum marker of HBV infection was found in alcoholic liver disease or in 'lupoid' CALD (antinuclear factor positive 1:40 and/or smooth muscle antibody positive greater than 1:40). In contrast, the incidence of antibody to HB surface and core antigens was significantly increased (p less than 0.05) in patients with cryptogenic CALD. The incidence of hepatitis B surface antigen and antibodies to HB core and 'e' antigens was significantly increased (p less than 0.005) in PLCC.
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PMID:Incidence of hepatitis B virus infection in alcoholic liver disease, HBsAg negative chronic active liver disease and primary liver cell cancer in Britain. 687 51

Inhibition assay of 125I-C1q binding to IgG-p-azobenzamidoethyl Sepharose 6B (IgG-Sepharose) by immune complexes was developed for the detection of circulating soluble immune complexes in the liver disease and was compared with polyclonal rheumatoid factor (pRF) binding inhibition assay and with C1q binding assay. The C1q inhibition assay was proved to be very sensitive, reproducible and rapid. Sucrose density gradient ultracentrifugal analysis showed that the assay could detect aggregates of human IgG (AHGG) larger than 19s. C1q inhibition activity (C1qIA) correlated with severity of the liver disease, defined by histological criteria. The highest C1qIA was observed in sera of patients with primary biliary cirrhosis, followed by liver cirrhosis, fulminant hepatitis, chronic aggressive hepatitis (2B), lupoid hepatitis and hepatocellular carcinoma in the order. There were correlations of C1qIA with serum gamma-globulin levels, sero-positivity for rheumatoid factor and hepatitis B surface antigen, and significant correlations existed also among pRFIA, C1qIA and C1qBA. Ultracentrifugal analysis of sera from patients with the liver disease showed that ClqIA demonstrated two sizes of immune complexes, 7s and larger than 19s, while complexes larger than 8s were seen in pRFIA.
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PMID:Studies on circulating soluble immune complexes of the liver disease. 6. Comparative studies of 125I-pRF inhibition assay, 125I-Clq inhibition assay and 125I-Clq binding assay. 697 71

A long-term follow-up of at least 10 years or until death of 44 patients taking part in a controlled prospective trial of prednisolone therapy in hepatitis B antigen negative chronic active hepatitis (lupoid hepatitis) has been performed at the Royal Free Hospital, London. Patients presenting between 1963 and 1967 were randomly allocated into control and treatment groups. Ten year life table survival curves showed a significantly improved survival in the treatment group where 63% of patients were alive at 10 years compared with only 27% in the control group (log rank test, P = 0.03). The median survival in the treatment group was 12.2 years compared with 3.3 years in the control group. The mean duration of treatment was 4.5 years. Age, presence of antinuclear factor, cirrhosis, or level of serum transaminases at presentation did not appear to affect survival. Male patients if untreated had a poorer prognosis than females (P = 0.02). The natural history of chronic active hepatitis appeared from clinical, biochemical, and histological findings to be from an active hepatitis or cirrhosis to inactive macronodular cirrhosis. Prednisolone therapy significantly improved survival by reducing mortality in the early active phase of the disease.
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PMID:Late results of the Royal Free Hospital prospective controlled trial of prednisolone therapy in hepatitis B surface antigen negative chronic active hepatitis. 698 4

Chronic persistent and chronic active hepatitis are defined and described as diseases of multiple aetiologies. The two major varieties, e g chronic active hepatitis, 'lupoid' and secondary to hepatitis B infection are described and contrasted.
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PMID:Chronic hepatitis. 742 27

A 66-year-old woman was diagnosed as having lupoid hepatitis due to the presence of hypergammaglobulinemia, lupus erythematosus cells, and positivity for antinuclear, anti-DNA, and anti-smooth muscle antibodies. None of the serum hepatitis B markers were positive. Symptomatic relief was obtained by prednisolone administration. Five years after the diagnosis of lupoid hepatitis, hepatocellular carcinoma (HCC) was detected by ultrasonography and computed tomography, after which hepatectomy was performed. Although transcatheter arterial embolization was done on two occasions and repeat hepatectomy was performed twice for recurrent HCC, her liver function remained good with the prednisolone treatment. Antibody for hepatitis C virus has been negative since our first check in 1992. As of this writing, the patient has been alive and well 6 years and 2 months after the first hepatectomy. There have been no previous reports of 6-year survival after hepatectomy for HCC associated with lupoid hepatitis.
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PMID:Hepatocellular carcinoma associated with lupoid hepatitis: a review of Japanese reports. 855 6

Determination of 2- and 16alpha-hydroxylation of estradiol in patients with a variety of liver disorders using a dynamic method of quantitating the extent of hydroxylation revealed specific and characteristic differences in the metabolic response. Patients with acute or silent variants of hepatitis B had estrogen metabolite patterns that were indistinguishable from those found in the control subjects. Female patients with autoimmune hepatitis (formerly known as lupoid hepatitis), however, showed a moderate significant decrease (P < 0.01) in 2-hydroxylation as compared with normal controls (mean 16.3 +/- 1.9 vs. 33.9 +/- 2.5), with no significant change in 16alpha-hydroxylation. Male and female subjects with chronic alcoholic cirrhosis were almost devoid of 2-hydroxylation (mean 2.9 +/- 0.5, P < 0.01), but did show a significant increase in 16alpha-hydroxylation (P < 0.01). The results, therefore, show that the alterations in patterns of biological oxidation are highly specific and do not reflect a general inability to metabolize estrogens in the cirrhotic patient. However, the results also suggest the possibility that a substantial fraction of 16alpha-hydroxylation may occur elsewhere in the body at sites other than in the liver, explaining why this biotransformation pathway is elevated, while the reaction at C-2 is almost absent in the alcoholic cirrhotic subjects.
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PMID:Clues to understanding the oxidation of estradiol in humans: effects of acute infectious hepatitis, autoimmune hepatitis, and chronic liver disease. 1925 Feb 11


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