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血脂异常对核苷(酸)类似物治疗的慢性乙型肝炎患者 e 抗原血清学转换的影响。

Effects of dyslipidemia on E antigen seroconversion of patients with chronic hepatitis B treated by nucleoside (acid) analogs.

机构信息

Department of Gastroenterology, Wenzhou People's Hospital, Wenzhou, 325000, China.

Department of Gastroenterology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.

出版信息

Lipids Health Dis. 2021 Oct 30;20(1):148. doi: 10.1186/s12944-021-01582-x.

DOI:10.1186/s12944-021-01582-x
PMID:34717643
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8557562/
Abstract

BACKGROUND

The prevalence of dyslipidemia in China is increasing annually. Current studies suggest that dyslipidemia affects the antiviral efficacy of hepatitis C virus (HCV) therapies, while recent studies suggest that serum lipids influence the response rates of chronic hepatitis B (CHB) patients receiving PEGylated interferon-alpha (Peg IFN-α) treatment. However, the role of dyslipidemia in the efficacy of nucleoside (acid) analogues (NAs) in CHB patients remains unclear.

METHODS

From January 2010 to December 2013, data from 179 treatment-naive patients with CHB who were hepatitis B e antigen (HBeAg)-positive and had visited the first affiliated hospital of Wenzhou Medical University were assessed. Of these patients, 68 were assigned to the dyslipidemia group (diagnosed with CHB complicated with dyslipidemia) and 111 to the normolipidemic group. The following 3 treatment strategies were performed for all CHB patients over a 5-year period: lamivudine (LAM) plus adefovir dipivoxil (ADV) combination therapy, telbivudine (LdT) monotherapy, and entecavir (ETV) monotherapy. Serum assessments, blood biochemistry, HBV serological markers, HBV DNA before treatment and HBeAg serological conversion and virological responses at different timepoints after treatment were compared between the two groups. Measurement data were compared by τ tests and enumeration data by χ tests. Correlation analysis was performed using binary logistic regression analysis.

RESULTS

The rates of HBeAg seroconversion in the dyslipidemia group at years 1, 2, 3, and 4 were 10.3, 13.2, 17.6, and 22.1%, respectively, which were not significantly lower than those of the normolipidemic group (11.7, 16.2, 18.0 and 33.3%; χ = 0.085, 0.293, 0.004, and 2.601, respectively; Ρ > 0.05). However, the rates of HBeAg seroconversion in the dyslipidemia group were significantly lower than those in the normolipidemic group at year 5 (27.9% vs. 43.2%, χ = 4.216, Ρ < 0.05). Univariate logistic regression analysis revealed significant differences in group, gender, PTA, ALT, AST, CR, and LDL-C between groups with and without seroconversion. Multivariate regression analysis demonstrated that dyslipidemia (OR = 1.993, Ρ = 0.038) and male gender (OR = 2.317, Ρ = 0.029) were risk factors associated with HBeAg seroconversion.

CONCLUSIONS

During antiviral therapy, dyslipidemia affects HBeAg seroconversion in CHB patients treated with NAs, but does not affect the virological response.

摘要

背景

中国的血脂异常患病率正逐年上升。目前的研究表明,血脂异常会影响丙型肝炎病毒(HCV)治疗的抗病毒疗效,而最近的研究表明,血清脂质会影响接受聚乙二醇干扰素-α(Peg IFN-α)治疗的慢性乙型肝炎(CHB)患者的应答率。然而,血脂异常在 CHB 患者核苷(酸)类似物(NAs)治疗中的疗效中的作用尚不清楚。

方法

从 2010 年 1 月至 2013 年 12 月,评估了 179 例初治 HBeAg 阳性且就诊于温州医科大学第一附属医院的 CHB 患者的数据。其中 68 例被分配到血脂异常组(诊断为 CHB 合并血脂异常),111 例分配到正常血脂组。所有 CHB 患者在 5 年内均进行以下 3 种治疗策略:拉米夫定(LAM)加阿德福韦酯(ADV)联合治疗、替比夫定(LdT)单药治疗和恩替卡韦(ETV)单药治疗。比较两组患者治疗前和治疗后不同时间点的血清学评估、血液生化学、HBV 血清学标志物、HBV DNA 和 HBeAg 血清学转换及病毒学应答。计量资料采用τ检验比较,计数资料采用χ检验比较。采用二元逻辑回归分析进行相关性分析。

结果

血脂异常组在第 1、2、3、4 年的 HBeAg 血清学转换率分别为 10.3%、13.2%、17.6%和 22.1%,均显著低于正常血脂组的 11.7%、16.2%、18.0%和 33.3%(χ=0.085、0.293、0.004、2.601,均Ρ>0.05)。然而,血脂异常组在第 5 年的 HBeAg 血清学转换率明显低于正常血脂组(27.9%比 43.2%,χ=4.216,Ρ<0.05)。单因素逻辑回归分析显示,两组间 HBeAg 血清学转换与未转换组在组、性别、PTA、ALT、AST、CR 和 LDL-C 方面存在显著差异。多因素回归分析表明,血脂异常(OR=1.993,Ρ=0.038)和男性(OR=2.317,Ρ=0.029)是与 HBeAg 血清学转换相关的危险因素。

结论

在抗病毒治疗期间,血脂异常会影响 CHB 患者接受 NAs 治疗后的 HBeAg 血清学转换,但不会影响病毒学应答。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2783/8557562/18fe66dfb57d/12944_2021_1582_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2783/8557562/9f2ab39edbc7/12944_2021_1582_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2783/8557562/18fe66dfb57d/12944_2021_1582_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2783/8557562/9f2ab39edbc7/12944_2021_1582_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2783/8557562/c94e612787b9/12944_2021_1582_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2783/8557562/03739be1c6ad/12944_2021_1582_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2783/8557562/18fe66dfb57d/12944_2021_1582_Fig4_HTML.jpg

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