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Alanine aminotransferase is more sensitive to the decrease in hepatitis B virus‐ DNA load than other liver markers in chronic hepatitis B patients
Author(s) -
Wang HuaBin,
Wang QiongYu,
Yuan Qing,
Shan XiaoYun,
Fu GuanHua
Publication year - 2017
Publication title -
journal of clinical laboratory analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 50
eISSN - 1098-2825
pISSN - 0887-8013
DOI - 10.1002/jcla.22141
Subject(s) - hepatitis b virus , medicine , hepatitis b , alanine aminotransferase , gastroenterology , chronic hepatitis , alanine transaminase , immunology , hepatitis , dna , virus , virology , biology , genetics
Background A direct correlation between hepatitis B virus DNA ( HBV ‐ DNA ) and liver markers has not been identified in chronic hepatitis B ( CHB ) patients. However, the effect of HBV ‐ DNA changes on liver markers remains unclear. We explored the association between decreased HBV ‐ DNA and liver makers in CHB patients. Methods Chronic hepatitis B patients who visited Jinhua Central Hospital twice were selected for analysis. Finally, 171 participants with a 1‐log reduction in HBV ‐ DNA between the two visits were enrolled as the case group, and 158 participants with no significant changes in HBV ‐ DNA were enrolled as the control group. Results There was no significant correlation between HBV ‐ DNA and liver markers ( P> .05). However, in longitudinal analysis, alanine aminotransferase ( ALT ), aspartate aminotransferase ( AST ), and gamma‐glutamyl transpeptidase ( GGT ) were significantly different between the two tests ( P <.05) in the case group. Conversely, there was no significant difference in the control group. When HBV ‐ DNA decreased >26 times, ALT was reduced by half or more. A similar trend was observed with a decrease of >63 times for AST and a decrease of >76 times for GGT . Conclusions A large change in HBV ‐ DNA can lead to a significant variation in liver markers. In particular, ALT was more sensitive than other liver markers to a reduction in HBV ‐ DNA .

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