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Controlled Attenuation Parameter but Not
PNPLA3 Polymorphism Is the Independent
Factor of Abnormal ALT after Well Viral
Suppression in Chronic Hepatitis B Infection
Patients
Hung-Chih Chiu, Ting-Tsung Chang, Yen-Cheng Chiu, I-Chih
Wu and Pin-Nan Cheng, Division of Gastroenterology and
Hepatology, Department of Internal Medicine, National Cheng
Kung University Hospital, College of Medicine, National
Cheng Kung University, Tainan, Taiwan
Background: Treatment of chronic hepatitis B (CHB) by
nucleoside or nucleotide analogues (NUC) can achieve the
goal of viral suppression. However, a substantial proportion of
patients with well viral suppression after taking NUC could still
exhibit abnormal liver enzyme. The impacts of nonalcoholic
fatty liver disease (NAFLD) or Patatin-like phospholipase
domain-containing 3 (PNPLA3) polymorphism on CHB
patients are still in debates. Therefore, the study aimed to
evaluate if anthropometric, metabolic factors and PNPLA3
polymorphism are predictors of abnormal ALT after well
viral suppression in CHB patients. Methods: Total 177 CHB
patients taking NUC with well viral suppression were enrolled.
Well viral suppression was defined as undetectable HBV DNA
or <12 IU/mL for three consecutive sessions with at least three
months apart. Liver stiffness measurement and controlled
attenuation parameter (CAP) by transient elastography
were measured. Glucose and lipid profile, anthropometric
data, PNAPLA3 polymorphism were tested. Medical history
of diabetes mellitus, hypertension, or dyslipidemia were
recorded. Results: Abnormal ALT was presented in 18.1%
(32/177) of patients. Comparison of patients with normal ALT
and abnormal ALT, the latter exhibited prominent features
of metabolic syndrome including significantly higher BMI
and waist circumference, higher triglyceride and lower HDL,
and more patients with hypertension and dyslipidemia. By
transient elastrography, higher rate of significant fibrosis
(LSM≥7.2)(34.4% vs. 12.4%, p=0.006), cirrhosis (LSM≥11.0)
(31.3% vs. 4.1%, p<0.001), steatosis (CAP≥250)(90.6% vs.
41.4%, p<0.001) and severe steatosis (CAP≥327)(31.3% vs
6.2%, p<0.001) in abnormal ALT patients. The distribution of
PNPLA3 polymorphism was not different between two groups.
In multivariate analysis, CAP was the only independent
factor of abnormal ALT (odds ratio: 1.017 [1.006-1.029]).
Conclusion: Steatosis identified by CAP is associated with
abnormal ALT after well viral suppression by NUC. PNPLA3
polymorphism is not an independent factor of abnormal ALT.
However, the long term impacts of abnormal ALT, steatosis,
and PNPLA3 polymorphism on clinical outcomes might need
further longitudinal studies.作者: StephenW 时间: 2018-10-19 13:58