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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Numerous studies have revealed the personal risk of contamination of the virus hepatitis B (HBV). Dental surgeons are chiefly concerned about their almost continual contact, professionally, with blood and saliva. The authors report the results of a study done at the Dental Institute of Dakar. This study revealed the importance of AgHBS and its different functions during the period of observation. A particular point of this study is to emphasis subjects of serology, notably AgHBS+ Anti HBC-, which produce an alternative virus. This study, which is being followed up, has already enabled the commencement of disease prevention programmes of hepatitis through the vaccination of some students: protecting both the dental surgeons and their patients.
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PMID:[Hepatitis B at the Dakar Dental School]. 227 Feb 7

B-cell differential factor (BCDF) activities were determined in 58 patients with various types of hepatitis B. In comparison with normal subjects, BCDF activities were significantly increased in patients with FH and CAH (P less than 0.01), markedly decreased in HBsAg carriers (P less than 0.01) and presented no change in patients with CPH and AH. It is interesting that there was a significant positive correlation between BCDF activity and serum titer of anti-HBC or serum globulin levels. No correlation was observed between BCDF activity and serum anti-HBs levels. It is suggested that abnormal BCDF activity might attribute to aberration of immunoregulation of HBV infections.
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PMID:[B-cell differential factor (IL-6) in peripheral mononuclear cells in viral hepatitis B infections]. 280 37

We report the case of a newborn of an HBsAg carrier mother who was infected by vertical transmission and developed a subclinical hepatitis B at four months of age, notwithstanding the passive-active prophylaxis performed right after birth. The mother's HBV marker status was: HBsAg positive, HBeAg positive, anti-HBc IgM positive at low titer, anti-HBc IgG negative, anti-HBs negative, anti-HBe negative. It is assumed that the absence of anti-HBC antibodies might have favoured, perhaps in utero, the HBV infection whose antigenic expression was subsequently delayed by HBIg administered at birth. These findings suggest that the positivity for anti-HBc IgM must be considered an additional marker of maternal infectivity especially in the absence of anti-HBc IgG antibodies.
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PMID:Absence of maternal antibodies to hepatitis B core antigen and HBV vertical transmission: one case of infection notwithstanding passive-active prophylaxis. 340 35

To investigate HBV transmission in families on three islands in Okinawa, Japan, prevalence of HBV markers in two groups of inhabitants was determined. One group consisted of members of families in which there was at least one HBsAg carrier (carrier families); the other group consisted of members of families in which there were no HBsAg carriers (non-carrier families). A total of 3,261 serum samples were collected from subjects on Iriomote Island, Hateruma Island, and Yonaguni Island. These samples were tested for HBsAg by reversed passive hemagglutination (RPHA) and for antibody to hepatitis B core antigen (anti-HBc) by radioimmunoassay. Overall prevalences of HBsAg and anti-HBc were 8.2 and 65.8 per cent respectively. The prevalence of anti-HBC among members of carrier families (80.8%) was significantly higher than that among members of non-carrier families (61.6%) (P less than 0.001). The prevalence of anti-HBc among members of carrier families was higher in all age groups, and was particularly so in children. Within carrier families, the prevalence of anti-HBc was significantly higher in families in which there was at least one HBsAg carrier with HBeAg (94.5%) than in families with no HBeAg-positive carriers (76.1%). This difference was especially marked in young children. These data suggest that in families with HBsAg carrier(s), the risk of transmitting HBV to members, particularly to young children, is higher than in families without carriers, and that the risk is further increased in families with HBeAg-positive carrier(s).
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PMID:Large-scale survey of hepatitis B virus infection in families. 407 45

Primary hepatocellular carcinoma (HCC), is reported in three and probably a fourth member of a New Zealand Chinese family, with a high carrier rate of HBsAg. Hepatitis B virus (HBV) markers and HLA tissue types were analysed in the three generations of the expanded family of 35. Twenty-one of the three generations were positive for one or more serum HBV markers, including six of the 18 children. Intrafamilial spread of HBV was seen in four of the eight families. Tissue types did not correlate with HBV status. The two propositi of the four with HCC studied and four of six siblings were positive for HBsAg: both propositi had identical HLA haplotypes, including Bw46/DRw9. Evidence is as yet insufficient that this haplotype may represent a disease susceptibility gene for HCC. Other family members at risk will be those positive for HBsAg and/or anti HBC, but those with Bw46/DRw9 will be monitored with special interest.
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PMID:Familial hepatocellular carcinoma and hepatitis B antigenemia in a New Zealand Chinese family. 631 59

In a cross-sectional survey of hepatitis B immune status, 458 consecutive children below the age of 12 years were studied. 37.3% of these children were positive for one of three markers, HBSAg, anti-HBS or anti-HBC. 15.5% were positive for two and 1.3% were positive for all three. 10.9% were positive for HBSAg, 27.8% for anti-HBC and 19.6% for anti-HB2. The males showed a higher HBSAg carrier rate than the females, 13.5% and 6.8% respectively. This difference was significant (p less than 0.05). This study confirmed that the Singaporeans were exposed to hepatitis B virus infection from very early in life and in order to prevent the infection, immunisation should be considered in early childhood.
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PMID:The immune status of Singapore children to hepatitis B virus. 660 43

1. Use of multiple serological markers was of value to determine different hepatitis B profiles in dialysis patients. 2. HBSAg and anti-HBS alone are insufficient to eliminate the risk of hepatitis B virus infection. Anti-HBC was detected as the only marker in 3.5% of the patients, and these patients should be considered potentially infectious. 3. The incidence of hepatitis B was higher in "in-center" hemodialysis patients (81%) compared to home hemodialysis patients (38.4%), and CAPD patients (23.2%). 4. Most of the patients (39.4%) demonstrated that they already had hepatitis B virus infection and had developed persisting immunity. 5. Eighteen patients (10.5%) should be regarded as highly infectious according to their profile (Pattern III). 6. Two patients had an unusual pattern that showed persistent co-existence of HBSAG+ and anti-HBS+, plus HBeAg+ and anti-HBc+. This pattern was due to reinfection with a different subtype of hepatitis B virus.
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PMID:Multiple hepatitis B virus markers in dialysis patients. 716 53

We evaluated the presence of human immunodeficiency virus (HIV), hepatitis B virus (HBV), hepatitis C virus (HCV), and rapid plasma reagin (RPR) among patients admitted to our trauma unit from April 15 to June 30, 1993. Of 984 patients tested, we found 255 (26%) had evidence of exposure to one or more of these agents: HIV, 4%; HBV, 20%; HCV, 14%; and RPR, 1%. Thirty-eight percent of patients had more than one positive serology, 75% of the HIV patients, 49% of the HBV patients, and 66% of the HCV patients. There was no difference between penetrating and nonpenetrating trauma with respect to any of the viruses. The risk factors for HIV-positive patients were non-White race, positive drug screen, positive alcohol screen, and city resident. Risk factors for HBV patients were non-White race, positive drug screen, and city resident. Risk factors for HBC patients were male sex, non-White race, positive alcohol screen, positive drug screen, and city resident. The risk of blood-borne infections in this group of patients is substantial.
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PMID:Seroprevalence of human immunodeficiency virus, hepatitis B virus, hepatitis C virus, and rapid plasma reagin in a trauma population. 747 20

To estimate the prevalence of antibodies to the hepatitis C virus ((HCV) and hepatitis virus (HBV) and the presence of infection, 101 patients receiving renal replacement therapy and 75 staff members caring for them were tested. Evaluation included detailed history, screening for anti-HCV antibody, HBV markers and liver enzymes 38% of patients were anti-HCV positives and 15 (40%) of these had antibodies to the hepatitis B core antigen indicating previous hepatitis B infection. Positive markers indicating HBV infection only, accounted for another 18% of patients. All staff members were anti-HCV negative, although 34 (45%) were anti-HBc positive. Age, sex and history of blood transfusions did not influence the prevalence of anti-HCV and anti-HBC in patients. There was, however, a significant difference in the prevalence of anti-HCV and anti-HBc positivity between polytransfused and occasionally transfused patients (p < 0.05). During a 24-months follow-up a decline was observed in HBs antigen carriers from 20% to 10% and in HBc antibody carriers from 47% to 33%. At the same time, regardless of accurate preventive measures, an increase in incidence of anti-HCV seropositivity from 30% to 38% was detected.
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PMID:Hepatitis C and hepatitis B virus infection in hemodialysis patients and staff: a two year follow-up. 751 83

Chronic liver inflammation and hepatic regeneration by infection with hepatitis B (HBV) or C virus (HBC) seem to be important risk factors for hepatocellular carcinoma (HCC). Regarding the hepatocarcinogenesis of HBV DNA integration, it has been variously hypothesized that mechanisms such as the alteration of host chromosomal DNA and transcriptional trans-acting activity of the X gene are activated. On the other hand, integration of HCV virus into chromosomal DNA has not been reported. It is suggested that HCV could replicate more efficiently in noncancerous than in cancerous tissues. Therefore, it might affect some oncogenes or cause an inactivation of tumor suppressor genes in the early stage of HCC. Genetic alterations such as a point mutation and loss of heterozygosity are considered to be late events occurring after tumorigenesis. Regeneration of liver cells through chronic hepatitis increases the incidence of genetic alterations in hepatic cells and/or HCCs in both HBV- and HCV-infected patients.
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PMID:Pathogenesis of hepatocellular carcinoma: a review from the viewpoint of molecular analysis. 872 3


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