Posttransfusion Fulminant Hepatitis B Associated with Precore-Defective HBV Mutants

Kojima, M.; Shimizu, M.; Tsuchimochi, T.; Koyasu, M.; Tanaka, S.; Iizuka, H.; Tanaka, T.; Okamoto, H. (f); Tsuda, F.; Miyakawa, Y.; Mayumi, M.

doi:10.1159/000461244

Cited by 22 publications

(27 citation statements)

References 18 publications

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“…Elsewhere, donations are tested for antibodies to hepatitis B core antigen,8 which can detect infectious donors undetectable by tests for hepatitis B surface antigen 9. In the United States, testing for antibody to hepatitis B core antigen may prevent 33% to 50% of cases of hepatitis B potentially transmissible from donors who test negative for hepatitis B surface antigen 10.…”

Section: Discussionmentioning

confidence: 99%

Prospective investigation of transfusion transmitted infection in recipients of over 20 000 units of blood

Regan¹

2000

BMJ

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Objectives To follow up recipients of 20 000 units of blood to identify any transmissions of infections through blood transfusion. Design Follow up study of recipients of transfusion. Setting 22 hospitals in north London. Participant Adult patients who had recently been transfused. Main outcome measures Patients had further blood samples taken at 9 months that were tested for markers of hepatitis B and C and HIV and human T cell leukaemia/lymphoma virus type I or II (HTLV) infections. Recent infections were distinguished from pre-existing infections by comparison with blood samples taken before transfusion. Results 9220 patients were recruited, and 5579 recipients of 21 923 units of blood were followed up. No transfusion transmitted infections were identified. The incidence of transfusion transmitted infections was 0 in 21 043 units (95% confidence interval for risk 0 to 1 in 5706 recipients) for hepatitis B; 0 in 21 800 units (0 to 1 in 5911 recipients) for hepatitis C; 0 in 21 923 units (0 to 1 in 5944 recipients) for HIV; and 0 in 21 902 units (0 to 1 in 5939 recipients) for human T cell leukaemia/lymphoma virus. Three patients acquired hepatitis B during or after hospital admission but not through transfusion; 176 (3%) had pre-existing hepatitis B infection. Sixteen (0.29%) patients had hepatitis C, and five (0.09%) had human T cell leukaemia/lymphoma virus. Conclusions The current risk of transfusion transmitted infections in the United Kingdom is very small, though hospital acquired infections may arise from sources other than transfusion. A considerable proportion of patients have pre-existing infections.

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Section: Discussionmentioning

confidence: 99%

Prospective investigation of transfusion transmitted infection in recipients of over 20 000 units of blood

Regan¹

2000

BMJ

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“…Therefore, the presence of core promotor and precore mutations in the transmitted virus may have effects on the HBV DNA and HBsAg expression in the recipient and be associated with a higher risk of an occult (HBsAg‐negative) course or fulminant hepatitis 19‐21 in the acute stage. Infection with these mutations, however, is not predictive for an occult course in the acute phase, because we saw three donors infected with mutant virus (Donors 7, 11, and 13) that developed detectable HBsAg for an estimated period of 28 to 40 days.…”

Section: Discussionmentioning

confidence: 99%

Lengths of hepatitis B viremia and antigenemia in blood donors: preliminary evidence of occult (hepatitis B surface antigen–negative) infection in the acute stage

Yoshikawa

Gotanda²,

Minegishi³

et al. 2007

Transfusion

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“…16 17 There have been a few reports that have described a relationship between precore mutations and fulminant hepatitis (FH). [18][19][20][21][22][23] Similarly, Sato et al reported the presence of an A to T mutation at nt 1762 and a G to A mutation at nt 1764 in the core promoter region (T1762 and A1764) in Japanese patients with FH who did not manifest precore stop codon mutations. 24 However, a study of patients from the USA and Europe failed to reveal such an association.…”

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confidence: 99%

Distribution of hepatitis B viral genotypes and mutations in the core promoter and precore regions in acute forms of liver disease in patients from Chiba, Japan

Imamura

Yokosuka²,

Kurihara³

et al. 2003

Gut

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Background: Although it has been reported that different hepatitis B virus (HBV) genotypes induce different clinical characteristics in patients with chronic liver diseases (CLD), there have been few reports that have detailed the distribution of HBV genotypes in acute forms of liver disease. Methods: HBV genotypes were determined in 61 patients who had acute forms of liver disease (45 had acute self limited hepatitis (AH) and 16 had fulminant hepatitis (FH)) and in 531 patients with CLD, including 19 patients with severe acute exacerbation of CLD. We also analysed the enhancer II, core promoter, and precore region sequences for the presence of mutations. Results: Expression of genotype B in patients with acute forms of liver disease was significantly greater than in those with CLD (39.3% v 11.7%, respectively; p,0.001). Furthermore, expression of genotype B was significantly greater in patients with FH than in those with AH (62.5% v 31.1%, respectively; p = 0.027). The precore mutation A1896 and the core promoter mutation at nt 1753 and 1754 were found more frequently in FH than in AH, and genotype B was predominant in FH regardless of the presence of these mutations. Conclusions: HBV genotype B was found more frequently in patients with acute forms of liver disease than in patients with CLD, and more frequently in patients with FH than in those with AH. These results suggest that this HBV genotype may induce more severe liver damage than other viral genotypes, at least in patients from Chiba, Japan.

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Posttransfusion Fulminant Hepatitis B Associated with Precore-Defective HBV Mutants

Cited by 22 publications

References 18 publications

Prospective investigation of transfusion transmitted infection in recipients of over 20 000 units of blood

Prospective investigation of transfusion transmitted infection in recipients of over 20 000 units of blood

Lengths of hepatitis B viremia and antigenemia in blood donors: preliminary evidence of occult (hepatitis B surface antigen–negative) infection in the acute stage

Distribution of hepatitis B viral genotypes and mutations in the core promoter and precore regions in acute forms of liver disease in patients from Chiba, Japan

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