Department of Medicine of the UAB, Hospital Universitari Vall d'Hebron, Barcelona 08035, Spain.
Systemic Autoimmune Diseases Unit, Internal Medicine Department, Hospital Universitari Vall d'Hebron, Barcelona 08035, Spain.
World J Gastroenterol. 2021 Aug 14;27(30):5112-5125. doi: 10.3748/wjg.v27.i30.5112.
There is an increased risk of atherosclerosis in patients with chronic hepatitis C or human immunodeficiency virus, but there is scarce data on hepatitis B virus infection. The hypothesis of this study is that hepatitis B virus infection increases the risk of carotid plaques and subclinical atherosclerosis in naïve hepatitis B e antigen (HBeAg) negative subjects.
To assess the rate of carotid plaques and subclinical atherosclerosis in naïve HBeAg negative subjects in comparison with a cohort of healthy controls.
Prospective case-control collaborative study conducted in two tertiary hospitals. Four hundred and two subjects prospectively recruited at the outpatient clinic were included from May 2016 to April 2017: 201 naïve HBeAg-negative hepatitis B virus-infected [49 chronic hepatitis B (CHB) and 152 inactive carriers(ICs)] and 201 healthy controls. Anthropomorphic and metabolic measures, liver stiffness and carotid Doppler ultrasound were performed. Subclinical atherosclerosis was established on an intima-media thickness increase of ≥1.2 mm and/or the presence of carotid plaques. Normally distributed quantitative variables were compared with the Student test and those with a non-normal distribution with the Mann-Whitney test. Categorical variables were compared between groups using the or Fisher exact test.
Carotid plaques were found more often in CHB (32.7%) than ICs (17.1%) or controls (18.4%) ( = 0.048). Subclinical atherosclerosis was also increased in CHB (40.8%) ICs (19.1%) or controls (19.4%) ( = 0.003). No differences in the risk of atherosclerosis were observed between controls and ICs. The factors independently associated with the presence of carotid plaques were age [odds ratio(OR) 1.43, < 0.001] and CHB (OR 1.18, = 0.004) and for subclinical atherosclerosis, age (OR 1.45, < 0.001), CHB (OR 1.23, < 0.001) and diabetes (OR 1.13, = 0.028). In the subset of young subjects (< 50 years), carotid plaques (12.5% 1.1%, = 0.027) and subclinical atherosclerosis (12.5% 2.2%, = 0.058) were more frequent among CHB than ICs.
Untreated HBeAg-negative CHB is an independent risk factor for carotid plaques and subclinical atherosclerosis, while ICs present a similar risk to controls.
慢性丙型肝炎或人类免疫缺陷病毒患者发生动脉粥样硬化的风险增加，但乙型肝炎病毒感染的数据却很少。本研究的假设是乙型肝炎病毒感染会增加 HBeAg 阴性的初治乙型肝炎患者发生颈动脉斑块和亚临床动脉粥样硬化的风险。
评估初治 HBeAg 阴性的乙型肝炎患者发生颈动脉斑块和亚临床动脉粥样硬化的比率，并与健康对照组进行比较。
这是一项在两家三级医院进行的前瞻性病例对照合作研究。2016 年 5 月至 2017 年 4 月，在门诊前瞻性招募了 402 名受试者：201 名初治 HBeAg 阴性乙型肝炎病毒感染者（49 名慢性乙型肝炎患者和 152 名非活动型携带者）和 201 名健康对照者。进行人体测量和代谢指标、肝硬度和颈动脉多普勒超声检查。将内膜中层厚度增加≥1.2mm 和/或存在颈动脉斑块作为亚临床动脉粥样硬化的依据。正态分布的定量变量采用 Student 检验进行比较，非正态分布的定量变量采用 Mann-Whitney 检验进行比较。采用卡方检验或 Fisher 确切概率法比较组间的分类变量。
与非活动型携带者（17.1%）或对照组（18.4%）相比，慢性乙型肝炎患者（32.7%）颈动脉斑块更为常见（ = 0.048）。慢性乙型肝炎患者（40.8%）、非活动型携带者（19.1%）或对照组（19.4%）的亚临床动脉粥样硬化发生率也增加（ = 0.003）。对照组与非活动型携带者之间的动脉粥样硬化风险无差异。与颈动脉斑块相关的独立因素包括年龄[比值比（OR）1.43， < 0.001]和慢性乙型肝炎（OR 1.18， = 0.004）；与亚临床动脉粥样硬化相关的独立因素包括年龄（OR 1.45， < 0.001）、慢性乙型肝炎（OR 1.23， < 0.001）和糖尿病（OR 1.13， = 0.028）。在年轻受试者亚组（<50 岁）中，与非活动型携带者相比，慢性乙型肝炎患者的颈动脉斑块（12.5% 1.1%， = 0.027）和亚临床动脉粥样硬化（12.5% 2.2%， = 0.058）更为常见。
未经治疗的 HBeAg 阴性慢性乙型肝炎是颈动脉斑块和亚临床动脉粥样硬化的独立危险因素，而非活动型携带者与对照组的风险相似。
