Simó Rafael, Lecube Albert, Genescà Joan, Esteban Joan Ignaci, Hernández Cristina
Diabetes Research Unit, Endocrinology Division, Hospital Universitari Vall d'Hebron, Pg. Vall d'Hebron 119-129, 08035 Barcelona, Spain.
Diabetes Care. 2006 Nov;29(11):2462-6. doi: 10.2337/dc06-0456.
There is evidence to suggest that hepatitis C virus (HCV) infection is a high-risk condition for developing type 2 diabetes. However, there are no interventional studies that confirm that HCV infection causes diabetes. The main aim of this study was to compare the incidence of glucose abnormalities (diabetes plus impaired fasting glucose) between HCV-infected patients with or without sustained virological response (SVR) after antiviral therapy.
Patients with normal fasting glucose (<100 mg/dl) with biopsy-proven chronic hepatitis C without cirrhosis and with at least 3 years of follow-up after finishing antiviral therapy were included in the study (n = 234). Patients received interferon alpha-2b (alone or with ribavirin) for 6 or 12 months according to genotype. Cumulative incidence of glucose abnormalities was evaluated by using the Kaplan-Meier method comparing subjects with and without a SVR to antiviral treatment. A multivariate Cox proportional hazards analysis was performed to explore the variables independently associated with the development of glucose abnormalities.
During follow-up, 14 of 96 (14.6%) patients with SVR and 47 of 138 (34.1%) nonsustained responders developed glucose abnormalities (P = 0.001). Patients with SVR did not develop diabetes during follow-up, whereas nine cases of diabetes were detected in nonsustained responders (P = 0.007). After adjustment for the recognized predictors of type 2 diabetes, the hazard ratio for glucose abnormalities in patients with SVR was 0.48 (95% CI [0.24-0.98], P = 0.04).
Our results provide evidence that eradication of HCV infection significantly reduces the incidence of glucose abnormalities in chronic hepatitis C patients. In addition, this study supports the concept that HCV infection causes type 2 diabetes.
有证据表明丙型肝炎病毒(HCV)感染是发生2型糖尿病的高危因素。然而,尚无干预性研究证实HCV感染会导致糖尿病。本研究的主要目的是比较抗病毒治疗后获得或未获得持续病毒学应答(SVR)的HCV感染患者中血糖异常(糖尿病加空腹血糖受损)的发生率。
本研究纳入空腹血糖正常(<100 mg/dl)、经活检证实为无肝硬化的慢性丙型肝炎且抗病毒治疗结束后至少随访3年的患者(n = 234)。患者根据基因型接受6或12个月的α-2b干扰素(单独或联合利巴韦林)治疗。采用Kaplan-Meier方法评估血糖异常的累积发生率,比较抗病毒治疗有或无SVR的受试者。进行多变量Cox比例风险分析,以探索与血糖异常发生独立相关的变量。
随访期间,96例有SVR的患者中有14例(14.6%)出现血糖异常,138例无持续应答者中有47例(34.1%)出现血糖异常(P = 0.001)。有SVR的患者在随访期间未发生糖尿病,而在无持续应答者中检测到9例糖尿病(P = 0.007)。在对公认的2型糖尿病预测因素进行校正后,有SVR的患者发生血糖异常的风险比为(0.48)(95% CI [0.24 - 0.98],P = 0.04)。
我们的结果提供了证据,表明根除HCV感染可显著降低慢性丙型肝炎患者血糖异常的发生率。此外,本研究支持HCV感染导致2型糖尿病这一概念。