Nagao Yumiko, Kawaguchi Takumi, Tanaka Kazuo, Kumashiro Ryukichi, Sata Michio
Department of Digestive Disease Information and Research, Kurume University School of Medicine, Asahi-machi, Kurume 830-0011, Japan.
Int J Mol Med. 2005 Aug;16(2):291-6.
Hepatitis C virus (HCV) causes extrahepatic manifestations as well as liver diseases, and contributes to insulin resistance and type 2 diabetes mellitus. The purpose of the present study was to evaluate the relationship of extrahepatic manifestations and insulin resistance in an HCV hyperendemic area. We investigated the incidence of extrahepatic manifestations among 139 inhabitants living in an HCV hyperendemic area in 2002 and compared it to 1999 data for the same inhabitants. Insulin resistance was tested for some non-HCV or HCV-infected inhabitants we had identified during mass screenings in 1999 and 2002. For some of the inhabitants in 2002, we examined records on the prevalence of insulin resistance seven years earlier. The prevalence of extrahepatic manifestations among individuals with positivity for anti-HCV antibodies was higher than among those without HCV in both 1999 and 2002. The prevalence of each extrahepatic manifestation which we identified in 2002 was higher than in 1999. Moreover, in some non-HCV or HCV-infected inhabitants, insulin resistance in 2002 was significantly higher than in 1999. Among inhabitants who had HCV infection with extrahepatic manifestations, fasting insulin levels or HOMA-IR findings seven years prior was significantly higher than for inhabitants who had neither HCV infection nor extrahepatic manifestations (p = 0.03, p = 0.01, respectively). Insulin resistance induces HCV infection, which causes an increase in the incidence of extrahepatic manifestations in HCV-infected individuals.
丙型肝炎病毒(HCV)可导致肝外表现以及肝脏疾病,并与胰岛素抵抗和2型糖尿病有关。本研究的目的是评估HCV高流行地区肝外表现与胰岛素抵抗之间的关系。我们调查了2002年居住在HCV高流行地区的139名居民的肝外表现发生率,并将其与这些居民1999年的数据进行比较。我们对1999年和2002年大规模筛查中确定的一些非HCV感染或HCV感染居民进行了胰岛素抵抗检测。对于2002年的一些居民,我们查看了七年前胰岛素抵抗患病率的记录。1999年和2002年,抗HCV抗体阳性个体的肝外表现患病率均高于无HCV感染个体。我们在2002年确定的每种肝外表现的患病率均高于1999年。此外,在一些非HCV感染或HCV感染居民中,2002年的胰岛素抵抗明显高于1999年。在有肝外表现的HCV感染居民中,七年前的空腹胰岛素水平或稳态模型评估胰岛素抵抗(HOMA-IR)结果显著高于既无HCV感染也无肝外表现的居民(分别为p = 0.03,p = 0.01)。胰岛素抵抗会诱发HCV感染,这会导致HCV感染个体的肝外表现发生率增加。