AASLD2016[1854]非酒精性脂肪性肝病对肝脏的影响 纤维化在慢性

StephenW

1854
The effects of non-alcoholic fatty liver disease on liver
fibrosis in chronic hepatitis B patients on nucleoside
analogue therapy: results from a matched-case control
study.
Rex W. Hui, Wai-Kay Seto, Sze Hang Kevin Liu, Ka-Shing Cheung,
Lung-Yi Mak, James Fung, Danny Wong, Ching-Lung Lai, Man-
Fung Yuen; Medicine, The University of Hong Kong, Queen Mary
Hospital, Hong Kong, Hong Kong
Background The potential synergistic effect of non-alcoholic
fatty liver disease (NAFLD) and chronic hepatitis B (CHB) on
hepatic fibrosis has not been well-investigated. Liver stiffness
(LS) and controlled attenuation parameter (CAP) are non-invasive
methods to quantify hepatic fibrosis and steatosis
respectively. This study aims to use LS and CAP to determine
the effect of NAFLD on fibrosis in CHB patients on long-term
nucleoside analogue (NA) therapy. Methods From December
2014 onwards, we recruited CHB patients on NA therapy and
without concomitant hepatitis C or alcoholic liver disease. Liver
biochemistry, serum hepatitis B virus (HBV) DNA and metabolic
parameters were measured. Recruited patients underwent LS
and CAP measurements using transient elastography (Fibroscan,
Echosens, Paris). Significant fibrosis was defined using the
European Association for the Study of the Liver guidelines (≥9
kPa for patients with normal alanine aminotransferase). Metabolic
syndrome was defined using the International Diabetes
Federation criteria. CHB patients with significant fibrosis and
without significant fibrosis (controls) were matched according
to age, sex, NA type and duration of treatment in a 1:3 ratio.
Results 568 CHB patients (mean age 57.3 years, 73.2% male,
90.5% hepatitis B e-antigen negative) were recruited, with 142
fibrosis patients and 426 controls. Median duration of NA
therapy was 76.7 months (range 6-213 months). There was
no difference in the proportion of patients with undetectable
HBV DNA between fibrosis patients and controls (92.3% vs
92.5%, p=0.938). Patients with significant fibrosis, when compared
to controls, had significantly higher CAP (255 dB/m vs
240 dB/m, p=0.009), HbA1c (6.0% vs 5.7%, p<0.001) and
body-mass index (BMI) (25.0 kg/m2 vs 23.8 kg/m2, p=0.001)
and significantly lower platelet count (135 vs 192 x 109/L,
p<0.001). Patients with significant fibrosis were also more
likely to have metabolic syndrome, central obesity and raised
fasting glucose when compared with controls (all p<0.05). In
multivariate analysis, CAP, raised fasting glucose and BMI
were independently associated with significant fibrosis (odds
ratio 1.005, 2.233 and 1.116 respectively, all p<0.05), while
platelet count was inversely associated with significant fibrosis
(odds ratio 0.982, p<0.001). Conclusion Steatosis and metabolic
abnormalities were independent predictors of significant
fibrosis, implying that they could contribute to the persistence
of fibrosis in CHB patients on NA therapy. Identification and
management of NAFLD and metabolic conditions in on-treatment
CHB patients may potentially assist regression of hepatic
fibrosis.
Disclosures:
Wai-Kay Seto - Advisory Committees or Review Panels: Gilead Science, Bristol-
Myers Squibb; Speaking and Teaching: Gilead Science, Bristol-Myers Squibb,
AstraZeneca, AbbVie, Novartis
Ching-Lung Lai - Advisory Committees or Review Panels: Bristol-Myers Squibb,
Gilead Sciences Inc; Consulting: Bristol-Myers Squibb, Gilead Sciences, Inc;
Speaking and Teaching: Bristol-Myers Squibb, Gilead Sciences, Inc; Stock Shareholder:
Gilead Sciences
Man-Fung Yuen - Advisory Committees or Review Panels: GlaxoSmithKline,
Bristol-Myers Squibb, Pfizer, GlaxoSmithKline, Bristol-Myers Squibb, Pfizer,
GlaxoSmithKline, Bristol-Myers Squibb, Pfizer, GlaxoSmithKline, Bristol-Myers
Squibb, Pfizer; Grant/Research Support: Roche, Bristol-Myers Squibb,
GlaxoSmithKline, Gilead Science, Roche, Bristol-Myers Squibb, GlaxoSmith-
Kline, Gilead Science, Roche, Bristol-Myers Squibb, GlaxoSmithKline, Gilead
Science, Roche, Bristol-Myers Squibb, GlaxoSmithKline, Gilead Science
The following people have nothing to disclose: Rex W. Hui, Sze Hang Kevin Liu,
Ka-Shing Cheung, Lung-Yi Mak, James Fung, Danny Wong

StephenW

AASLD2016 [1854]非酒精性脂肪性肝病对肝脏的影响
纤维化在慢性乙型肝炎患者核苷
模拟治疗：匹配病例对照的结果
研究
非酒精性脂肪性肝病对肝脏的影响
纤维化在慢性乙型肝炎患者核苷
模拟治疗：匹配病例对照的结果
研究。
Rex W. Hui，Wai-Kay Seto，Sze Hang Kevin Liu，Ka-Shing Cheung，
林菲麦，詹姆斯冯，王丹，清龙龙，
凤园医学，香港大学，玛丽皇后
医院，香港，香港
背景非酒精的潜在协同效应
脂肪肝疾病（NAFLD）和慢性乙型肝炎（CHB）
肝纤维化尚未得到充分研究。肝硬度
（LS）和受控衰减参数（CAP）是非侵入性的
量化肝纤维化和脂肪变性的方法
分别。本研究旨在使用LS和CAP来确定
NAFLD对CHB患者长期纤维化的影响
核苷类似物（NA）治疗。方法从12月
2014年，我们招募了CHB患者的NA治疗
无伴随的丙型肝炎或酒精性肝病。肝
生物化学，血清乙型肝炎病毒（HBV）DNA和代谢
参数。招募的患者接受了LS
和CAP测量使用瞬时弹性成像（Fibroscan，
Echosens，Paris）。明显的纤维化定义使用
欧洲肝脏研究协会指南（≥9
kPa对于正常丙氨酸氨基转移酶的患者）。新陈代谢
综合征使用国际糖尿病定义
联盟标准。 CHB患者显着纤维化和
无显着纤维化（对照）匹配
年龄，性别，NA类型和治疗持续时间以1:3的比例。
结果568例CHB患者（平均年龄57.3岁，男性73.2％
90.5％乙型肝炎e抗原阴性），142
纤维化患者和426个对照。中位时间NA
治疗76.7个月（范围6-213个月）。有
无法检测的患者比例无差异
纤维化患者和对照组之间的HBV DNA（92.3％vs
92.5％，p = 0.938）。比较时显着纤维化的患者
到对照，具有显着较高的CAP（255 dB / m vs
240dB / m，p = 0.009），HbA1c（6.0％对5.7％，p <0.001）和
体重指数（BMI）（25.0kg / m 2对23.8kg / m 2，p = 0.001）
并显着降低血小板计数（135对192×109 / L，
p <0.001）。显着纤维化的患者也更多
可能有代谢综合征，中心性肥胖和升高
与对照相比空腹血糖（全部p <0.05）。在
多变量分析，CAP，升高的空腹血糖和BMI
独立相关的显着纤维化（赔率
比值分别为1.005,2.233和1.116，均P <0.05）
血小板计数与显着的纤维化负相关
（优势比0.982，p <0.001）。结论脂肪变性和代谢
异常是显着的独立预测因素
纤维化，这意味着他们可以有助于持久性
的CHB患者的NA治疗。识别和
管理NAFLD和治疗中的代谢条件
CHB患者可能有助于肝的消退
纤维化。
披露：
Wai-Kay Seto - 咨询委员会或审查小组：G​​ilead Science，Bristol-
Myers Squibb;讲座和教学：吉利德科学，百时美施贵宝，
AstraZeneca，AbbVie，Novartis
Ching-Lung Lai - 咨询委员会或审核小组：Bristol-Myers Squibb，
吉利德科学公司咨询：Bristol-Myers Squibb，吉利德科学公司;
演讲和教学：Bristol-Myers Squibb，Gilead Sciences，Inc;股东股东：
吉利德科学
Man-Fung Yuen - 咨询委员会或审核小组：GlaxoSmithKline，
Bristol-Myers Squibb，Pfizer，GlaxoSmithKline，Bristol-Myers Squibb，Pfizer，
GlaxoSmithKline，Bristol-Myers Squibb，Pfizer，GlaxoSmithKline，Bristol-Myers
Squibb，辉瑞;资助/研究支持：Roche，Bristol-Myers Squibb，
GlaxoSmithKline，Gilead Science，Roche，Bristol-Myers Squibb，GlaxoSmith-
Kline，Gilead Science，Roche，Bristol-Myers Squibb，GlaxoSmithKline，Gilead
科学，罗氏，百时美施贵宝，葛兰素史克，吉利德科学
以下人士没有透露：Rex W. Hui，Sze Hang Kevin Liu，
嘉成祥，麦家龙，冯咏仪，黄玉英