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)

A retrospective examination in South-west Scotland of formalin-fixed paraffin-embedded liver tissue by an immunoperoxidase technique revealed hepatitis B surface antigen (HBsAg) in eight out of 81 cases (10%) of primary hepatocellular carcinoma (PHC) and in four out of 82 cases (5%) of cirrhosis. No positive staining was found in 112 controls without overt liver disease matched for age and sex. Unlike most previous studies showing an association between HBsAg and PHC, the present investigation was carried out in an area where HBs antigenaemia is infrequent and PHC is an uncommon tumour. While possibly hepatitis infection is an important cause of PHC, the association between HBsAg and PHC could be due merely to activation by the tumour of latent virus B in a previously infected person.
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PMID:Incidence in South-west Scotland of hepatitis B surface antigen in the liver of patients with hepatocellular carcinoma. 20 8

135 children with hepatitis and 179 patients with hepatomegaly of undetermined etiology were investigated for complement fixing antibodies to cytomegalovirus. 69 patients with hepatitis (51%) and 74 patients with hepatomegaly (41%) had a titer of 1:4 or above as compared with a control group of children without hepatic pathology in whom positive response occurred in only 20 resp. 18%. The mean titer found in the sero-positive patients was also significantly higher than that in the control group. In contrast, the incidence of positive sera in newborns with hyperbilirubinemia of unknown etiology did not differ significantly from that in a healthy control collective. Of 57 patients with liver disease, 20 excreted cytomegalovirus which was isolated 55 times from 103 urine specimens. These patients included 9 with hepatitis and 11 with hepatomegaly. Of 129 children without any indication of liver disease, cytomegalovirus could be demonstrated in only 3. Our results point toward a causal connection between the presence of cytomegalovirus and the development of hepatic disease in childhood.
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PMID:[Hepatic disease in childhood and cytomegalovirus infection (author's transl)]. 20 47

The serologic and tissue markers of hepatitis B virus (HBV) were studied in 50 patients in whom hepatocellular carcinoma (HCC) was confirmed at autopsy. Serologic and tissue markers included serum hepatitis B surface antigen (HBsAg), tissue HBsAg, tissue hepatitis core antigen (HBcAg), and serum antibody to HBcAg (anti-HBc). Twenty-two patients had HCC arising in alcoholic cirrhosis; 2 of the 22 (9.1%) had one or more of the HBV tissue and serologic markers. This infection rate is similar to the rate of 7.9% observed in 63 control alcoholic cirrhotic patients without HCC. In contrast, 15 of 20 (75.0%) patients with HCC in nonalcoholic chronic active liver disease showed evidence of active HBV infection. One of 8 patients with HCC in normal liver had serum HBV markers. This result indicates that there is an extremely high prevalence of HBV infection among HCC patients with nonalcoholic chronic liver disease in the U.S.A. The prevalence of HBV infection in these patients is as high as that observed in Asia and Africa. Thus, it can be concluded that the lower prevalence rate of active HBV infection in HCC patients in the U.S.A. is the result of statistical dilution of HCC-B-viral disease by the large numbers of the alcoholic cirrhotic patients with HCC, and that if chronic active hepatitis type B were as common in the United States as it is in Africa and Asia, the frequency of occurrence of HCC might also be as high.
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PMID:Hepatocellular carcinoma in the U.S.A., etiologic considerations. Localization of hepatitis B antigens. 21 88

The etiology of 72 episodes of liver disease that developed in 62 of 162 renal-transplant recipients was evaluated. Infection with hepatitis B virus was a minor problem, and none of our patients had evidence of infection with hepatitis A. Cytomegalovirus infection was ubiquitous in the population and probably accounted for many episodes of acute liver disease. This agent's role in causing chronic hepatitis is less secure. Infections with other viruses including Epstein-Barr virus, adenovirus, and the herpes viruses were only rarely associated with hepatic disease. Azathioprine was responsible for some episodes of acute cholestasis but could not be incriminated as a direct cause of chronic disease. A cause could be identified for the majority of episodes of acute hepatic dysfunction, but the cause of most of the chronic hepatitis remains undetermined. It is likely that infection with non-A, non-B hepatitis virus accounts for much of this serious, often fatal, complication of renal transplantation.
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PMID:Etiology of liver disease in renal-transplant patients. 22 42

The plasma lecithin: cholesterol acyltransferase was determined in patients with various liver diseases and the relationship between this enzyme activity and the other liver function tests were studied including long term observations. Lecithin: cholesterol acyltransferase activity in fulminant hepatitis and liver cirrhosis showed a significant decrease in comparison with normal volunteers. Although the enzyme activity of hepatoma showed significant decrease, they were ascribed to the influence of concomitant liver cirrhosis. The enzyme activity showed insignificant changes in the acute and chronic hepatitis and alcoholic liver disease. Lecithin: cholesterol acyltransferase activity was correlated with the concentration of cholesterolester rather than with the ratio of esters to cholesterol. In addition, it was well correlated with pseudocholine esterase and serum albumin. The lecithin: cholesterol acyltransferase activity in the cases during follow-up period varied in good parallel with cholesterol-esters concentration and pseudocholine esterase in the cases with acute hepatitis; with serum albumin in the cases with liver cirrhosis. Furthermore, it varied inversely with SGPT in the cases with acute hepatitis. In a case with hepatoma, lecithin: cholesterol acyltransferase activity decreased more sharply than the cholesterolesters concentration and serum albumin immediately before death.
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PMID:Plasma lecithin: cholesterol acyltransferase activity in liver disease. 23 Sep 93

The HBeAg was detected in 5 of 24 patients with acute type B hepatitis (20.8%), 33 of 95 with chronic hepatitis (34.7%), 6 of 33 with liver cirrhosis (18.2%), and 3 of 39 with hepatocellular carcinoma (7.7%). On the other hand, anti-HBe was found in 4.2% of acute hepatitis, 18.9% of chronic hepatitis, 9.1% of liver cirrhosis, and 12.8% of hepatocellular carcinoma. We found that an early detection of HBeAg in patients with acute hepatitis is of no prognostic value, but its persistence may provide the earliest evidence of potential chronicity. In chronic liver diseases, HBeAg-positive cases showed remarkable fluctuations of serum transaminase levels, severe histological changes and poor responses to treatment. Many of the HBeAg-positive patients lost their initial positivity of HBeAg within six months or one year and in some cases serocoverted to anti-HBe after acute exacerbation. Follow-up study more than several years revealed that the presence of anti-HBe reflect an inactive stage and a more favorable outcome, whereas persistence of HBeAg may provide an active and continuing hepatocellular damage. From these results, we believed that serial measurements of HBeAg/anti-HBe system are useful prognostic marker in patients with HBsAg-positive liver disease.
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PMID:Incidence and clinical significance of HBe antigen and antibody in HBsAg-positive various liver diseases. 23 Sep 94

In this descriptive epidemiologic study, prevalence rates of hepatitis B surface antigen (HBsAg) and its antibody (anti-HBs) among fourth-year dental students and second-year dental hygiene students were found to be comparable to those of a control population and a local age-adjusted blood donor group. This observation contrasts with the rates reported for practicing dentists, especially oral surgeons, and indicates that the increased risk experienced by dentists after dental school may be attributable to potentially greater exposure to the hepatitis B virus resulting from an expanded patient load. No significant correlation was found between a positive serologic response and several potential risk factors: previous liver disease, prior contact with hepatitis patients, parenteral injections, facial hair, and punctures sustained during dental procedures. In contrast, prevalence of HBsAg and anti-HBs was increased significantly among black students.
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PMID:Hepatitis B prevalence within a dental student population. 26 21

The relationship of chronic hepatitis B and/or liver dysfunction to treatment in 113 hemophiliacs was evaluated by the enzyme tests, SGOT and SGPT, and by the presence of circulating hepatis B surface antigen (HbsAg) or antibody (anti-Hbs). The hemophiliacs were divided into three groups according to treatment pattern. Individuals who had received multiple doses of plasma fractions, derived from four or more commercial lots were placed in tgroup I "large Exposure". Group II "Small Exposure" had been treated with fractions from three or fewer lots and Group III "Cryo" had never received commercial fractions, but had been treated with cryoprecipitate. Abnormal liver function tests (LFT's) were found in 87% of Group I and 76% of Group II, but in only 16% of the "Cryo" group. Differences in LFT's were not great between treated VIII and IX deficient patients. All patients treated with 100,000 units or more showed either persistent or intermittent abnormalities. In the high exposure group, this history of past, overt hepatitis had no influence on observed LFT's. The sera of all patients in the high exposure and all, except one, in the low exposure groups were positive for HbsAg or anti-Hbs by RIA. Splenomegaly was found in 13% of fraction-treated patients. We conclude that there is biochemical evidence of liver disease following large exposure to commercial VIII or IX fractions, which should temper the physician's decision to start treatment with these fractions. On the other hand, evidence that their continued use produces mounting liver dysfunction is insufficient to withdraw this very effective and life-changing treatment from these individuals.
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PMID:Chronic hepatitis in hemophilia. 26 94

Fractionation technology has made Factor IX concentrates available. In addition to a very high incidence of hepatitis, thrombosis is being recognized as a consequence of their use. Contradictory reports exist in the literature as to the incidence of thrombotic events. A recent study of thrombohemorrhagic phenomena after infusion with Factor IX concentrates in patients with congenital Factor IX deficiency (hemophilia B) or liver disease, revealed an incidence of twenty episodes in 188 cases (11%). It is imperative to delineate the thrombogenic factors and find methods for their removal to insure the safety of Factor IX products.
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PMID:Factor IX and thrombosis. 26 96

Total lymphocyte counts, B-, T-, C'3 receptor-bearing lymphocytes, and K-cell activity were studied in peripheral blood in patients with Crohn's disease and inflammatory liver disease. Patients with active untreated Crohn's disease and acute virus B hepatitis exhibited a markedly increased K-cell activity measured in a plaque assay when compared with normal controls (P less than 0.01). Patients with immunosuppressive treated Crohn's disease, HBsAg-positive chronic active hepatitis, and cirrhosis of the liver showed only a slight increase of K-cell activity (P less than 0.01). In the postacute phase of hepatitis (four to 12 weeks from onset) K-cell activity fell to normal levels. The number of B-lymphocytes showed a relative and absolute decrease in all groups of patients. With the exception of patients with acute HBsAg-positive hepatitis and the post-acute phase of hepatitis all the other groups showed statistically decreased absolute numbers for C'3 receptor-bearing lymphocytes. The significant decrease in K-cell activity and the number of T-lymphocytes in Crohn's disease treated with immunosuppressive drugs was interpreted as an effect of azathioprine and prednisone on these lymphocyte subpopulations.
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PMID:K-lymphocytes (killer-cells) in Crohn's disease and acute virus B-hepatitis. 30 25


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