Cheng Jur-Shan, Hu Jing-Hong, Chang Ming-Yu, Lin Ming-Shyan, Ku Hsin-Ping, Chien Rong-Nan, Chang Ming-Ling
From the Clinical Informatics and Medical Statistics Research Center, College of Medicine, Chang Gung University, Taiwan (Cheng, Ku); the Department of Emergency Medicine, Chang Gung Memorial Hospital, Keelung, Taiwan (Cheng); the Department of Gastroenterology and Hepatology, Department of Internal Medicine, Chang Gung Memorial Hospital, Yunlin, Taiwan (Hu); the Division of Pediatric Neurologic Medicine, Chang Gung Children's Hospital, Taoyuan, Taiwan (M.-Y. Chang); the Division of Pediatric General Medicine, Chang Gung Children's Hospital, Taoyuan, Taiwan (M.-Y. Chang); the Department of Cardiology, Heart Failure Center, Chang Gung Memorial Hospital, Taiwan (Lin); the Department of Cardiology, Chang Gung Memorial Hospital, Taoyuan, Taiwan (Lin); the Liver Research Center, Division of Hepatology, Department of Gastroenterology and Hepatology, Chang Gung Memorial Hospital, Taoyuan, Taiwan (Chien, M.-L. Chang); and the Department of Medicine, College of Medicine, Chang Gung University, Taoyuan, Taiwan (Chien, M.-L. Chang).
From the Clinical Informatics and Medical Statistics Research Center, College of Medicine, Chang Gung University, Taiwan (Cheng, Ku); the Department of Emergency Medicine, Chang Gung Memorial Hospital, Keelung, Taiwan (Cheng); the Department of Gastroenterology and Hepatology, Department of Internal Medicine, Chang Gung Memorial Hospital, Yunlin, Taiwan (Hu); the Division of Pediatric Neurologic Medicine, Chang Gung Children's Hospital, Taoyuan, Taiwan (M.-Y. Chang); the Division of Pediatric General Medicine, Chang Gung Children's Hospital, Taoyuan, Taiwan (M.-Y. Chang); the Department of Cardiology, Heart Failure Center, Chang Gung Memorial Hospital, Taiwan (Lin); the Department of Cardiology, Chang Gung Memorial Hospital, Taoyuan, Taiwan (Lin); the Liver Research Center, Division of Hepatology, Department of Gastroenterology and Hepatology, Chang Gung Memorial Hospital, Taoyuan, Taiwan (Chien, M.-L. Chang); and the Department of Medicine, College of Medicine, Chang Gung University, Taoyuan, Taiwan (Chien, M.-L. Chang)
J Psychiatry Neurosci. 2021 Nov 2;46(6):E583-E591. doi: 10.1503/jpn.200154. Print 2021 Nov-Dec.
Whether infection with the hepatitis C virus (HCV) causes schizophrenia - and whether the associated risk reverses after anti-HCV therapy - is unknown; we aimed to investigate these topics.
We conducted a nationwide, population-based cohort study using the Taiwan National Health Insurance Research Database (TNHIRD). A diagnosis of schizophrenia was based on criteria from the , 9th revision (295.xx).
From 2003 to 2012, from a total population of 19 298 735, we enrolled 3 propensity-score-matched cohorts (1:2:2): HCV-treated (8931 HCV-infected patients who had received interferon-based therapy for ≥ 6 months); HCV-untreated (17 862); and HCV-uninfected 17 862) from the TNHIRD. Of the total sample (44 655), 82.81% (36 980) were 40 years of age or older. Of the 3 cohorts, the HCV-untreated group had the highest 9-year cumulative incidence of schizophrenia (0.870%, 95% confidence interval [CI] 0.556%-1.311%; < 0.001); the HCV-treated (0.251%, 95% CI 0.091%-0.599%) and HCV-uninfected (0.118%, 95% CI 0.062%-0.213%) cohorts showed similar cumulative incidence of schizophrenia ( = 0.33). Multivariate Cox analyses showed that HCV positivity (hazard ratio [HR] 3.469, 95% CI 2.168-5.551) was independently associated with the development of schizophrenia. The HCV-untreated cohort also had the highest cumulative incidence of overall mortality (20.799%, 95% CI 18.739%-22.936%; < 0.001); the HCV-treated (12.518%, 95% CI 8.707%-17.052%) and HCV uninfected (6.707%, 95% CI 5.533%-8.026%) cohorts showed similar cumulative incidence of mortality ( = 0.12).
We were unable to determine the precise mechanism of the increased risk of schizophrenia in patients with HCV infection.
In a population-based cohort (most aged ≥ 40 years), HCV positivity was a potential risk factor for the development of schizophrenia; the HCV-associated risk of schizophrenia might be reversed by interferon-based antiviral therapy.
丙型肝炎病毒(HCV)感染是否会导致精神分裂症,以及抗HCV治疗后相关风险是否会逆转,目前尚不清楚;我们旨在研究这些问题。
我们使用台湾国民健康保险研究数据库(TNHIRD)进行了一项全国性的基于人群的队列研究。精神分裂症的诊断基于《国际疾病分类》第9版(295.xx)的标准。
2003 - 2012年,在总计19298735人的总体人群中,我们从TNHIRD中纳入了3个倾向得分匹配队列(1:2:2比例):HCV治疗组(8名接受基于干扰素治疗≥6个月的HCV感染患者);HCV未治疗组(名);以及HCV未感染组(名)。在总样本(44655人)中,82.81%(36980人)年龄在40岁及以上。在这3个队列中,HCV未治疗组的精神分裂症9年累积发病率最高(0.870%,95%置信区间[CI]0.556% - 1.311%;P < 0.001);HCV治疗组(0.251%,95% CI 0.091% - 0.599%)和HCV未感染组(0.118%,95% CI 0.062% - 0.213%)的精神分裂症累积发病率相似(P = 0.33)。多变量Cox分析显示,HCV阳性(风险比[HR]3.469,95% CI 2.168 - 5.551)与精神分裂症的发生独立相关。HCV未治疗队列的总死亡率累积发病率也最高(20.799%,95% CI 18.739% - 22.936%;P < 0.001);HCV治疗组(12.518%,95% CI 8.707% - 17.052%)和HCV未感染组(6.707%,95% CI 5.533% - 8.026%)的死亡率累积发病率相似(P = 0.12)。
我们无法确定HCV感染患者精神分裂症风险增加的确切机制。
在一个基于人群的队列(大多数年龄≥40岁)中,HCV阳性是精神分裂症发生的一个潜在风险因素;基于干扰素的抗病毒治疗可能会逆转与HCV相关的精神分裂症风险。