Fabris P, Floreani A, Tositti G, Vergani D, De Lalla F, Betterle C
Department of Infectious Diseases and Tropical Medicine, S. Bortolo Hospital, Vicenza, Italy.
Aliment Pharmacol Ther. 2003 Sep 15;18(6):549-58. doi: 10.1046/j.1365-2036.2003.01681.x.
Type 1 diabetes mellitus is the result of an autoimmune process characterized by pancreatic beta cell destruction. It has been reported that chronic hepatitis C infection is associated with type 2 diabetes mellitus, but not with type 1. Although the prevalence of markers of pancreatic autoimmunity in hepatitis C virus-positive patients is not significantly different to that reported in the general population, it increases during alpha-interferon therapy from 3 to 7%, probably due to the immunostimulatory effects of this cytokine. To date, 31 case reports of type 1 diabetes mellitus related to interferon treatment have been published. Type 1 diabetes mellitus occurs more frequently in patients treated for chronic hepatitis C than for other conditions and is irreversible in most cases. In 50% of these patients, markers of pancreatic autoimmunity predated treatment, the majority of cases having a genetic predisposition. Thus, in predisposed individuals, alpha-interferon can either induce or accelerate a diabetogenic process already underway. We suggest that islet cell autoantibodies and glutamic acid decarboxylase autoantibodies should be investigated before and during interferon treatment in order to identify subjects at high risk of developing type 1 diabetes mellitus.
1型糖尿病是一种以胰腺β细胞破坏为特征的自身免疫过程的结果。据报道，慢性丙型肝炎感染与2型糖尿病有关，但与1型糖尿病无关。尽管丙型肝炎病毒阳性患者中胰腺自身免疫标志物的患病率与普通人群中报道的患病率无显著差异，但在α干扰素治疗期间，该患病率从3%增至7%，这可能归因于这种细胞因子的免疫刺激作用。迄今为止，已发表了31例与干扰素治疗相关的1型糖尿病病例报告。1型糖尿病在接受慢性丙型肝炎治疗的患者中比在接受其他疾病治疗的患者中更频繁发生，并且在大多数情况下是不可逆的。在这些患者中，50%的胰腺自身免疫标志物在治疗前就已存在，大多数病例具有遗传易感性。因此，在易感个体中，α干扰素可诱导或加速已在进行的致糖尿病过程。我们建议在干扰素治疗前和治疗期间应检测胰岛细胞自身抗体和谷氨酸脱羧酶自身抗体，以识别有发生1型糖尿病高风险的个体。
