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A paucity of liver disease in C anadian I nuit with chronic hepatitis B virus, subgenotype B 6 infection
Author(s) -
Minuk G. Y.,
MacRury S.,
Uhanova J.,
Caouette S.,
Coleman N.,
Cummings K.,
Larke B.,
Vardy L.,
Triet Huyn C.,
Osiowy C.
Publication year - 2013
Publication title -
journal of viral hepatitis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 100
eISSN - 1365-2893
pISSN - 1352-0504
DOI - 10.1111/jvh.12121
Subject(s) - hepatitis b virus , medicine , serology , viral load , genotype , hepatitis b , liver disease , hbsag , virus , chronic liver disease , immunology , gastroenterology , virology , biology , antibody , gene , biochemistry , cirrhosis
Summary Clinical observations suggest that chronic hepatitis B virus ( HBV ) infections in the Canadian Inuit are less often associated with serious adverse outcomes than has been described in other HBV ‐infected patient populations. The aim of this study was to document the clinical and biochemical features, liver‐related morbidity and all‐cause mortality in Canadian Inuit with chronic HBV infections. Administrative databases were reviewed for individuals identified as hepatitis B surface antigen ( HB sAg) positive during a 1983–85 seroepidemiological survey of viral hepatitis in B affin I sland, C anada. An equal number of age‐ and gender‐matched HB s A g‐negative individuals from the same communities served as controls. Baseline HBV viral loads, genotypes and specific mutations were compared in HB s A g‐positive survivors and nonsurvivors. A subset of surviving HB sAg‐positive carriers were reassessed 25–30 years following their initial diagnosis for evidence of advanced liver disease and changes to their serological/virological findings. One hundred and forty four HB s A g‐positive individuals were identified. All were C anadian I nuit. The mean age at diagnosis was 38 ± 17 years and 69 (61%) were male. Median follow‐up was 23 years (range: 2–28 years). Viral quantitation from stored sera could be performed in 70 infected individuals. The median viral load was 4.3 log 10 IU/ml (range: 2.3–8.8 log 10 IU/ml), and all were genotype B , subgenotype B 6. Liver biochemistry, morbidity and all‐cause mortality rates were similar in HB s A g‐positive carriers and controls. Following multivariate analyses, only age at diagnosis predicted mortality in HB sAg carriers. In a subset of 30 HB sAg‐positive survivors who underwent follow‐up assessments, clinical, biochemical and radiological examinations of the liver were essentially normal. 23/30 (77%) remained HB sAg positive and 17/19 (90%) HBV ‐ DNA positive. The genotype and prevalence of genomic mutations in this cohort remained largely unchanged, but quantifiable viral loads were significantly lower ( P < 0.003). The results of this study suggest that chronic HBV infections in the C anadian Inuit are infrequently associated with serious adverse outcomes. Whether this finding reflects unique features of the host, presence or absence of external factors that influence the course of HBV and/or intrinsic properties of the HBV B 6 subgenotype remains to be determined.