男性慢性乙型肝炎患者吸烟对肝纤维化的影响及其治疗后的

StephenW

Liver Int. 2019 Mar 28. doi: 10.1111/liv.14108. [Epub ahead of print]
Impacts of cigarette smoking on liver fibrosis and its regression under therapy in male patients with chronic hepatitis B.
Xiong M1, Li J1, Yang S1, Zeng F1,2, Ji Y1, Liu J1, Wu Q1, He Q1, Tang X1, Jiang R1, Zhou F1, Chen Y1, Wen W1, Chen J1, Hou J1.
Author information

1
    Hepatology Unit, Department of Infectious Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, China.
2
    Department of Infectious Diseases, Guangzhou Women and Children's Medical Center, Guangzhou, China.

Abstract
BACKGROUND & AIMS:

The role of cigarette smoking in the development of chronic hepatitis B (CHB) remains poorly understood. We assessed the potential contributions of cigarette smoking to liver fibrosis and its regression after starting antiviral therapy in CHB patients.
METHODS:

In this cohort study, 2144 consecutive male CHB patients under no antiviral therapy were evaluated and 206 patients with significant liver fibrosis (≥F2) initiating antiviral therapy had longitudinal follow-up. Liver fibrosis was measured by liver stiffness measurement using transient elastography. To adjust for imbalances between smoking history and never smoking groups, propensity score (PS) matching model with 1:1 ratios were performed. Cigarette smoking history and intensity (pack-years) were collected and documented using a standardized questionnaire.
RESULTS:

Before PS matching, 432/2144 patients had advanced fibrosis in prevalence cohort. Patients with smoking history (n=1002) had a greater prevalence of advanced fibrosis than those without (n=1142) (24.4% vs. 16.5%, p=0.001). Multivariate logistic regression analysis demonstrated that smoking contributed to advanced fibrosis (OR, 1.458; 95% CI, 1.114-1.908). In longitudinal cohort, multivariate logistic regression analysis demonstrated retarded fibrosis regression in patients with history of smoking ≥10 pack-years (OR, 0.288; 95% CI, 0.1-0.825). After PS matching, patients with smoking history had higher prevalence of advanced fibrosis (22.8 vs. 18%, p=0.024) than those non-smokers. In post-PS-matching logistic regression, the effect of smoking on advanced fibrosis persisted (OR, 1.415; 95% CI, 1.047-1.912; p=0.024).
CONCLUSIONS:

Cigarette smoking in male CHB patients aggravated liver fibrosis prior to and delayed fibrosis regression under antiviral therapy. This article is protected by copyright. All rights reserved.

This article is protected by copyright. All rights reserved.
KEYWORDS:

Cigarette smoking; advanced liver fibrosis; fibrosis regression; hepatitis B virus infection

PMID:
    30920714
DOI:
    10.1111/liv.14108

StephenW

肝脏国际2019年3月28日doi：10.1111 / liv.14108。 [印刷前的电子版]
男性慢性乙型肝炎患者吸烟对肝纤维化的影响及其治疗后的消退
熊M1，李J1，杨S1，曾F1，Ji Y1，刘J1，吴Q1，何Q1，唐X1，江R1，周F1，陈Y1，文武1，陈J1，侯J1。
作者信息

1
    南方医科大学南方医院感染科肝病科，广州
2
    广州市妇女儿童医学中心传染病科，广州

抽象
背景与目的：

吸烟在慢性乙型肝炎（CHB）发展中的作用仍然知之甚少。我们评估了在CHB患者开始抗病毒治疗后吸烟对肝纤维化的潜在影响及其消退。
方法：

在该队列研究中，对未经抗病毒治疗的2144名连续男性CHB患者进行了评估，206名具有显着肝纤维化（≥F2）的患者开始进行抗病毒治疗，进行了纵向随访。通过使用瞬时弹性成像的肝硬度测量来测量肝纤维化。为了调整吸烟史与从不吸烟组之间的不平衡，进行了1：1比例的倾向评分（PS）匹配模型。使用标准化问卷收集并记录吸烟史和强度（包年）。
结果：

在PS匹配之前，432/2144名患者在患病率组中具有晚期纤维化。有吸烟史的患者（n = 1002）晚期纤维化患病率高于无患者（n = 1142）（24.4％对16.5％，p = 0.001）。多变量logistic回归分析表明，吸烟导致晚期纤维化（OR，1.458; 95％CI，1.114-1.908）。在纵向队列中，多因素logistic回归分析显示吸烟史≥10包年的患者的纤维化退行缓解（OR，0.288; 95％CI，0.1-0.825）。 PS匹配后，有吸烟史的患者晚期纤维化患病率较高（22.8％对18％，p = 0.024），而非吸烟者则较高。在PS后匹配逻辑回归中，吸烟对晚期纤维化的影响持续存在（OR，1.415; 95％CI，1.047-1.912; p = 0.024）。
结论：

男性CHB患者的吸烟在抗病毒治疗前加重肝纤维化并延迟纤维化消退。本文受版权保护。版权所有。

本文受版权保护。版权所有。
关键词：

吸烟;晚期肝纤维化;纤维化消退;乙型肝炎病毒感染

结论：
    30920714
DOI：
    10.1111 / liv.14108