AASLD2018[420]受控衰减参数但不是 PNPLA3多态性是独立的 病毒感

StephenW

420
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.

StephenW

20
受控衰减参数但不是
PNPLA3多态性是独立的
病毒感染后ALT异常的因素
抑制慢性乙型肝炎感染
患者
Hung-Chih Chiu，Ting-Tsung Chang，Yen-Cheng Chiu，I-Chih
Wu和Pin-Nan Cheng，消化内科和
国家内科，肝内科
国立医学院，大学医院
台湾台南成功大学
背景：慢性乙型肝炎（CHB）的治疗
核苷或核苷酸类似物（NUC）可以实现
病毒抑制的目标。但是，相当大的比例
服用NUC后病毒抑制良好的患者仍可
表现出异常的肝酶。非酒精饮料的影响
脂肪肝病（NAFLD）或Patatin样磷脂酶
CHB上含有结构域3（PNPLA3）多态性
患者仍在辩论中。因此，该研究旨在
评估人体测量，代谢因素和PNPLA3
多态性是良好的ALT异常的预测因子
CHB患者的病毒抑制。方法：总共177 CHB
招募服用具有良好病毒抑制的NUC的患者。
病毒抑制很好被定义为不可检测的HBV DNA
连续三次，至少三次，或<12 IU / mL
几个月。肝硬度测量和控制
瞬态弹性成像的衰减参数（CAP）
被测量了。葡萄糖和脂质谱，人体测量
数据，PNAPLA3多态性进行了测试。病史
糖尿病，高血压或血脂异常
记录。结果：ALT异常率为18.1％
（32/177）患者。 ALT正常患者的比较
和ALT异常，后者表现出突出的特征
代谢综合征包括明显更高的BMI
腰围，甘油三酯较高，HDL较低，
更多患有高血压和血脂异常的患者。通过
瞬时弹性成像，显着纤维化率较高
（LSM≥7.2）（34.4％vs。12.4％，p = 0.006），肝硬化（LSM≥11.0）
（31.3％vs。4.1％，p <0.001），脂肪变性（CAP≥250）（90.6％vs.
41.4％，p <0.001）和严重脂肪变性（CAP≥327）（31.3％vs
异常ALT患者为6.2％，p <0.001）。的分布
PNPLA3多态性在两组之间没有差异。
在多变量分析中，CAP是唯一的独立分析
ALT异常因素（优势比：1.017 [1.006-1.029]）。
结论：CAP鉴定的脂肪变性与其有关
NUC病毒抑制后ALT异常。 PNPLA3
多态性不是ALT异常的独立因素。
然而，ALT异常，脂肪变性的长期影响，
和PNPLA3多态性可能需要临床结果
进一步的纵向研究