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)

Drug hepatitis emphasized the importance of a careful history including the question to the use of laxatives in all patients with both acute and chronic hepatitis. From predictable and unpredictable hepatotoxicity we should learn to be alert to the possibility of new and unrecorded hepatic lesions resulting from drugs and other chemical or environmental toxins.
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PMID:Acute structural hepatic alteration due to poisons. 30 72

A study was performed on a family of 7 followed up over a 4-year period in which an outbreak of B-antigen-positive hepatitis occurred. Of the 5 male members who acquired HBsAg, 1 became a chronic asymptomatic carrier and 4 had episodes of acute icteric hepatitis during a 15-month period with development of histologically documented chronic hepatitis with persistent HBs antigenaemia in all. Of the 2 female members, 1 had an attack of acute HBsAg-positive hepatitis but recovered normally and cleared HBsAg from her serum, while the other was found to have anti-HBs with no evidence of liver disease. Serological and immunological studies carried out in all members of this family suggested that a sex-linked defect of T cell function itself could explain the differing host immune response to HBV infection in genetically related subjects.
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PMID:Clustering of HBsAg in a family. 30 17

Lymphocytes forming E-rosettes with sheep erythrocytes which do not disintegrate at 37 degrees C have been demonstrated in increased numbers in peripheral blood of patients with acute type B hepatitis (6--20% of lymphocytes) and with HBsAg negative active chronic hepatitis (9--28% of lymphocytes). They were not increased in patients with HBsAg positive active chronic hepatitis. Such lymphocytes were adherent to nylon wool and a large proportion of them had FcIgG receptors (21--69%). These are properties of a subpopulation of T lymphocytes having suppressor function.
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PMID:Lymphocytes forming stable E-rosettes in acute and chronic hepatitis. 31 86

E and EAC rosette-forming cells in the peripheral blood and in the liver of subjects with acute and chronic hepatitis were studied. We found a highly significant reduction (P less than 0.01) of E rosette percentage in the lymphocytes isolated from the liver patients with chronic persistent, and chronic active, hepatitis. EAC rosette-forming cells were significantly increased in the liver of patients with chronic active hepatis (P less than 0.01). In this condition lymphocytes with Fc receptor were also found.
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PMID:T and B lymphocytes in the liver and peripheral blood of subjects with acute and chronic hepatitis. 31 35

Serial determinations of titers of binding antibodies to single stranded DNA were performed over a period of three years in 43 type B hepatitis patients with persisting HBsAg who had either developed chronic hepatitis or were asymptomatic carriers. Patients with histopathological diagnosis of chronic active or chronic persistent hepatitis, with or without clinical symptoms, showed high titers of anti-DNA throughout the course of the disease, whereas in most of these patients the serum alanine transaminase and bilirubin levels fluctuated widely and were often normal; in such cases the elevation of anti-DNA was frequently the only positive sign present. On the other hand anti-DNA titers were within the normal range in chronic asymptomatic HBsAg carriers who showed no histopathological or biochemical changes. Anti-DNA determinations are proposed as a reliable diagnostic aid to supplement current procedures for assessment of the disease status during the course of chronic hepatitis B virus infections.
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PMID:Antibodies to single stranded DNA: a diagnostic aid in chronic hepatitis B virus infections. 31 70

Frozen, unfixed sections of human liver biopsies from patients with acute, subchronic, and chronic hepatitis or fibrotic liver disease were studied in indirect immunofluorescence with specific antisera to type I and type III procollagen. In early stages of both hepatitis and fibrotic liver disease, intralobular type III collagen synthesis is increased. Maximum values are reached years after the onset of disease. Intralobular procollagen I content is not increased in the acute stage, but rises only later. An increase of procollagen I seems to herald irreversible liver changes. This approach allows for exact localization and semiquantitative analysis of the synthesis of type I and type III collagen, and adds a new parameter to the diagnostic approaches in liver diseases.
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PMID:The diagnostic application of specific antiprocollagen sera. II. Analysis of liver biopsies. 34 27

The classification of chronic hepatitis introduced in 1968 is still current, but has been modified. The concept of bridging hepatic necrosis has been incorporated, and is recognised as an important feature of both acute and chronic aggressive (active) hepatitis (CAH). In the pathogenesis of the latter, piecemeal necrosis is, however, thought to be the more important factor. The histological picture of CAH varies widely. Several causes of CAH have been identified, including hepatitis B virus. Recognition of surface and core components of the virus in tissue sections has facilitated study of the relationship between host response and pathological lesion in chronic hepatitis. CAH and primary biliary cirrhosis share histological features, and a mixed form has been postulated. Staining for copper sometimes helps to distinguish the two lesions. A third histological category, chronic lobular hepatitis, comprises patients with histological lesions like those of acute hepatitis, but with a chronic or recurrent course.
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PMID:Liver biopsy in chronic hepatitis: 1968-78. 35 68

The classification, clinical course, etiology and treatment of chronic hepatitis are discussed. The clinical manifestations of chronic hepatitis are of limited diagnostic use. Diagnosis must be made by liver biopsy. The disease is classified as chronic persistent or chronic active hepatitis. The prognosis for chronic persistent hepatitis is excellent, and no treatment is required. Chronic active hepatitis may progress to cirrhosis and is associated with a poor prognosis if untreated. Recognized causes of chronic active hepatitis are hepatitis-B virus infection, post-transfusion hepatitis not associated with hepatitis-B virus, and certain drugs. For drug-induced hepatitis, discontinuation of the medication is indicated. For other types of chronic active hepatitis the recommended treatment is prednisone 10 mg and azathioprine 50 mg daily.
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PMID:Drug therapy reviews: chronic hepatitis. 35 29

In a study of apparently normal, healthy Korean Army recruits performed in 1962, we found that 42 of 1,906 screened subjects had elevations of their serum glutamic pyruvate transaminase. Liver biopsies were obtained from 32 of these subjects and 9 of these had a "novel" antigen present, which reacted specifically with a convalescent serum from a case of serum hepatitis. We have recently tested frozen serum obtained from 8/9 of these cases and found that all 8 had HBsAg in their serum which, in some cases, persisted for at least three months. We reviewed the histological specimens from the original 32 cases using newly defined criteria: 18 were diagnosed as chronic active hepatitis and the 8 HbsAg positive cases with the "novel" antigen were in this group. In four of these cases the lesion appeared to progress to cirrhosis during a 3--4 month follow-up period. Since none of the cases had a prior history of hepatitis and no symptoms developed during the follow-up period, our findings emphasize the significance of chronic hepatitis B virus carrier state in the etiology of cryptogenic cirrhosis.
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PMID:The etiology of chronic active hepatitis in Korea. 37 25

The favorable effect of glucocorticoids on the development of the chronic active hepatitis is statistically proved on the basis of the amelioration of the survival rate in controlled studies. The so-called lupoid hepatitis is significantly better influenced than the HBs-Ag positive chronic hepatitis. By additional therapy with azathioprine it is possible to reduce the dose of glucocorticoids. Therefore it is better to combine glucocorticoids and azathioprine in some cases, especially in those with a high dosed glucocorticoid therapy. Further prospective studies are necessary to check more precisely the therapeutic effect of the different remedies. The effect of D-penicillamine is vague. A treatment with chloroquine is indicated in cases with contraindications again glucocorticoids and azathioprine.
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PMID:[Therapy of chronic hepatitis (author's transl)]. 37 53


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