Performance Evaluation of Four Dominant Anti-Hepatitis B Core Antigen (HBcAb) Kits in Japan for Preventing de novo Hepatitis B Virus (HBV) Infection

Background. Changes of hepatitis B core antigen antibody (anti-HBc) in liver pathological involvement in patients with chronic hepatitis B virus (HBV) infection have not been investigated in detail. This study aimed to explore evolving patterns of anti-HBc following liver pathological states and to investigate validities of anti-HBc for predicting liver pathological states. Methods. 254 HBeAg-positive and 237 HBeAg-negative patients with chronic HBV infection were enrolled. Liver pathological diagnoses referred to Scheuer standard, and anti-HBc was measured using chemiluminescence microparticle immunoassay. Results. Anti-HBc was significantly positively correlated with pathological grades and stages in both HBeAg-positive (rs = 0.312, P<0.0001, and rs = 0.268, P<0.0001) and HBeAg-negative (rs = 0.270, P<0.0001, and rs = 0.147, P=0.0237) patients. The medians of anti-HBc in pathological grades of G1, G2, and G3 and stages of S1, S2, S3, and S4 in HBeAg-positive patients were all significantly lower than those in HBeAg-negative patients (all P<0.005). The areas under receiver-operating characteristic curves (95% confidence interval) of anti-HBc for predicting pathological grades ≥G2 and ≥G3, and stages ≥S2 and =S4 in HBeAg-positive patients were 0.683 (0.622–0.740) and 0.662 (0.601–0.720), and 0.627 (0.564–0.687) and 0.683 (0.622–0.740), respectively, and in HBeAg-negative patients were 0.681 (0.618–0.740) and 0.702 (0.639–0.760), and 0.569 (0.503–0.633) and 0.630 (0.565–0.691), respectively. Conclusion. Following hepatic aggravation of necroinflammation and progression of fibrosis, anti-HBc increases gradually in HBeAg-positive patients and continues to increase gradually in HBeAg-negative patients, which is a useful but unsatisfactory marker for monitoring pathological states.

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Determination of hepatitis B virus DNA incidence, viral load, and mutations in blood donors with HBsAg and anti-HBs-negative serology and antibodies to hepatitis B core antigen

European Journal of Internal Medicine ◽

10.1016/j.ejim.2007.07.001 ◽

2007 ◽

Vol 18 (8) ◽

pp. 571-575 ◽

Cited By ~ 12

Author(s):

Duygu Findik ◽

Ugur Arslan ◽

Mahmut Baykan

Keyword(s):

Viral Load ◽

Hepatitis B Virus ◽

Hepatitis B ◽

Blood Donors ◽

Core Antigen ◽

Hepatitis B Virus Dna ◽

B Virus ◽

Hepatitis B Core Antigen

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Severe de novo Hepatitis B Recovered from Late-Onset Liver Insufficiency with Prolonged Ascites and Hypoalbuminemia due to Hepatitis B Virus Genotype Bj with Precore Mutation

Case Reports in Gastroenterology ◽

10.1159/000450543 ◽

2016 ◽

Vol 10 (3) ◽

pp. 553-559 ◽

Cited By ~ 1

Author(s):

Akira Sato ◽

Toshiya Ishii ◽

Fumiaki Sano ◽

Takayuki Yamada ◽

Hideaki Takahashi ◽

...

Keyword(s):

Hepatitis B Virus ◽

Hepatitis B ◽

De Novo ◽

Liver Volume ◽

B Cell Lymphoma ◽

Hbv Dna ◽

Hepatocellular Damage ◽

Precore Mutation ◽

B Virus ◽

De Novo Hepatitis B

De novo hepatitis B is associated with a high risk of hepatic failure often resulting in fatal fulminant hepatitis even when nucleotide analogues are administered. A 77-year-old female developed de novo hepatitis B after R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone) treatment for diffuse large B-cell lymphoma. Hepatitis B virus (HBV) isolated from the patient was of genotype Bj, with a precore mutation (G1896A) exhibiting an extremely high viral load at the onset of hepatitis. She showed markedly high levels of transaminase with mild jaundice on admission and rapid decrease of prothrombin activity after admission. Although acute liver failure was averted by the administration of entecavir and corticosteroid pulse therapy, liver volume decreased to 860 ml, and marked hypoalbuminemia accompanying massive ascites occurred 2 months after the onset of hepatitis and persisted for 3 months with high levels of HBV DNA and mild abnormal alanine aminotransferase levels. Frequent infusions of albumin solution, nutrition support, and alleviation therapy showed limited effect. However, overall improvement along with HBV DNA reduction was observed after increasing the dose of entecavir and completion of prednisolone that was administered with a minimum dose for adrenal insufficiency. An immediate and sufficient suppression of virus replication with potent antiviral therapy is critical, particularly in patients infected with HBV precore mutation (G1896A) and/or Bj genotype, which may have a high viral replication and direct hepatocellular damage.

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