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

The natural incidence of the etiologically distinct types of viral hepatitis was determined by investigating acute phase sera of symptomatic hepatitis cases occuring in the Hannover area in 1975 for the presence of hepatitis B surface antigen, antibodies to hepatitis A, hepatitis B core and surface antigens, and by measuring the IgM serum levels. Fourteen different seroepidemiologic patterns were recognized. Although there was a high prevalence of hepatitis A antibody in the population, the frequency of hepatitis A was low (n = 56) suggesting that the hepatitis A virus does not play a major role in symptomatic hepatitis in the Hannover area at present. Spread of the hepatitis A virus was mostly associated with person-to-person contact or tourist travel in southern Europe. Hepatitis B was the predominant type of hepatitis (n = 211). Hepatitis non-A, non-B was observed infrequently (n = 62). A high percentage of patients with hepatitis B and hepatitis non-A, non-B reported parenteral exposure to potentially contaminated materials. No other findings, however, suggested an infectious etiology of hepatitis non-A, non-B.
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PMID:The seroepidemiological pattern of acute viral hepatitis. An epidemiological study on viral hepatitis in the Hannover region. 20 14

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

Viral hepatitis is one of the most serious infectious diseases in the United States and is of great concern to the public health agencies, hospitals and research laboratories. Progress in our knowledge of this disease has been based on cooperation between specialists in many diverse scientific disciplines employing sophisticated scientific instruments and technics. Close cooperation between clinical pathologists and clinicians is of great importance in diagnosis. Biologic, immunologic, epidemiologic and morphologic studies have resulted in the demonstration that the disease is the result of infection with at least two different viruses, described as type A and type B hepatitis viruses. The first induces type A hepatitis (infectious or epidemic, or MS-2 strain) of longer incubation period, is transmitted parenterally and apparently by inhalation or ingestion of virus-containing material, by venereal means as well as by other means. Extremely sensitive methods are now available for the detection of hepatitis type B infection, based on the results of biochemical, biophysical and immunoelectronmicroscopic studies that resulted in our knowledge of structure and composition of type B virus, and our knowledge of host immune responses to the various components of this virus. Thus it is now known that two antigen-antibody systems are associated with viral hepatitis type B: hepatitis B surface antigen (HBsAg) and antibody (HBsAb) and hepatitis B core antigen (HBcAg) and antibody to it (HBcAb). The test for antibody to HBcAg appears to be a sensitive indicator of viral replication when only subdetectable amounts of HBsAg are circulated. Since the recent discovery and characterization of type A hepatitis virus, great progress has been made in our understanding of the relationship between type A and type B hepatitis viruses. There is no cross immunity between the two viruses, and as is now suspected, there may be at least another virus, described as type C virus, which may play an etiologic role in viral hepatitis. There is no doubt now that type A and type B hepatitis viruses can be transmitted to monkeys; type A to marmosets and chimpanzees, type B to chimpanzees and rhesus monkeys. The two viruses are serologically and immunologically distinct. This knowledge and the results of biologic experiments have laid a solid foundation of meaningful diagnostic procedures for the two types of viral hepatitis. Advances in biophysical and biochemical procedures of treatment of sera of hepatitis B patients have resulted in availability of viral material, noninfectious but immunogenic, for vaccination of chimpanzees. Protective efficacy trials of the vaccine in chimpanzees have demonstrated the vaccine to be fully protective against high doses of infectious hepatitis B virus...
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PMID:Viral type A and type B hepatitis: morphology, biology, immunology and epidemiology--a review. 21 39

Immunofluorescence studies for hepatitis A virus and hepatitis B surface and core antigen were performed on liver biopsies from 48 patients with acute viral hepatitis. Hepatitis A virus was detected in 11 out of 17 patients with type A hepatitis and was not found in patients with type B or non-A non-B hepatitis. Hepatitis B surface and core antigens were detected in 2, hepatitis B core antigen alone in 1, and hepatitis B surface antigen alone in 4 out of 24 patients with type B hepatitis. Neither hepatitis B surface nor core antigen were found in patients with type A or non-A non-B hepatitis. One patient with both type A and B hepatitis were all negative for hepatitis A virus, and hepatitis B surface and core antigens. Immunofluorescence examination for hepatitis A virus in human liver biopsies appears to be a sensitive and specific technique and might be valuable in the search for possible chronic carriers of hepatitis A virus.
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PMID:Immunofluorescence studies for hepatitis A virus and hepatitis B surface and core antigen in liver biopsies from patients with acute viral hepatitis. 22 38

Family member of 13 patients with hepatitis B surface antigen (HBsAg) positive primary hepatocellular carcinoma (PHC) were tested for the presence of hepatitis B virus-associated antigens and antibodies. Of the 122 members examined, circulating HGsAg was detected in 47 (39%), antibody to HBsAg (anti-HBs) was found in 37 (30%), and antibody to hepatitis B core antigen (anti-HBc) alone was present in 13 (11%). The relatives with the highest frequency of HBsAg positivity were the offspring of the propositus, followed by the nieces and nephews and the grandchildren. Anti-HBs and anti-HBc were detected most often in the spouses and non-blood relatives. Evidence for past and present hepatitis B virus (HBV) infection was more frequently found in the Asian family members when compared to the non-Asians. The e antigen (HBeAg) was present in 38% of the HBsAg positive individuals, including four with PHC; antibody to HBcAg (anti-HBe) was rarely detected. These results indicate that clustering of HBV infection was commonly present in family members of patients with PHC. The HBsAg positive individuals may be major contributors to the endemic pool of the virus, and may themselves be potential cases of chronic active type B hepatitis, cirrhosis, and PHC.
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PMID:Evidence for clustering of hepatitis B virus infection in families of patients with primary hepatocellular carcinoma. 22 43

Hepatitis B associated antigen (HB-Ag) may be observed in the serum in subjects either apparently healthy or exhibiting a number of disease symptoms. Its incidence among the Geneva voluntary blood donors is 0.48% with 54% exhibiting the surface antigen ad and 34% ay. While the HB-Ag positive blood donors appeared clinically healthy, minor pathology was found in the majority of them (thrombocytopenia, histological evidence of inflammatory foci, of persistent hepatitis and of chronic aggressive hepatitis). In 82 patients suffering from hepatitis B the same ad-ay type distribution of the HB-Ag has been found. In 11 out of 31 patients increased Clq binding suggests the presence of circulating complexes. Diminutions in the level of complement components also indicates participation of complement in the formation of immunocomplexes. In 2 out of 3 patients with Hb-Ag positive polyarteritis nodosa, the Clq binding test was also positive. The pathophysiologic implications of hepatitis B infection are discussed in connection with the authors and other findings. It appears that the main defense mechanism leading to elimination of the viruses within the hepatocytes lies in cell mediated immunity. Hepatitis would then represent the side reaction of this defense mechanism. Antibodies are probably useful in preventing the virus from entering the cell, but also in the course of the cell mediated defense mechanism (elimination of viral material liberated during the T-cell hepatocellular interaction). Immune complexes may be operative in certain extrahepatic manifestations such as arthralgia. Polyarteritis nodosa may result from local antibody interaction with antigen fixed within arterial walls.
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PMID:[Physiopathology of hepatitis B virus infection]. 24 Jan 99

Antibody to hepatitis B surface antigen was detected by radioimmunoprecipitation in 74 (5-5%) of 1336 staff members in a large general hospital in Edinburgh, in 14 (2-9%) of 480 volunteer blood donors in the area, and in 12 (6-1%) of 197 pregnant women attending for the first time at the ante-natal clinic in the hospital. Rates of antibody prevalence rose with age in the sample of hospital staff and in that of the blood donors, particularly among males. On the other hand, in the ante-natal patients antibody prevalence declined with age. The rates in hospital staff were higher than those in blood donors of comparable age and sex, and high titres of antibody were more common in the staff group. However, no association was found between antibody prevalence and a history of clinical hepatitis, blood transfusion, or recognized contact with cases of hepatitis. Staff who had previously worked in an infectious disease hospital did not show increased antibody prevalence, indicating that simple isolation measures have been adequate to minimize exposure to hepatitis B. No particular prevalence of infection was seen in physicians and surgeons, in the nursing staff, or in workers in clinical diagnostic laboratories, hospital administration or other areas. One group clearly showing increased antibody prevalence was staff currently working, or who had worked, in the Haemodialysis Unit; this correlated with the outbreak of dialysis-associated hepatitis in 1969--70. However, no evidence suggested that significant dissemination of infection had occurred to other defined groups of hospital staff. Elevated rates were also observed in a small sample of kitchen and portering staff, and in obstetric medical and nursing staff; the latter observation indicate a need for further investigation to identify unsuspected exposure to hepatitis B virus.
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PMID:Prevalence of antibody to hepatitits B surface antigen among staff in an Edinburgh hospital. 26 99

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


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