Type 1 diabetes and interferon therapy: a nationwide survey in Japan.
Type 1 diabetes and interferon therapy: a nationwide survey in Japan.
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DOI：
10.2337/dc10-2274
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发表时间：
2011-09
期刊：
影响因子：
16.2
通讯作者：
Research Committee on Type 1 Diabetes of the Japan Diabetes Society
中科院分区：
文献类型：
--
作者：
Nakamura K;Kawasaki E;Imagawa A;Awata T;Ikegami H;Uchigata Y;Kobayashi T;Shimada A;Nakanishi K;Makino H;Maruyama T;Hanafusa T;Research Committee on Type 1 Diabetes of the Japan Diabetes Society
干扰素治疗可诱发多种自身免疫性疾病，包括1型糖尿病。为了评估干扰素治疗诱导的1型糖尿病的临床、免疫学和遗传学特征，我们进行了一项全国性的横断面调查。对91例在干扰素治疗期间或治疗后不久出现1型糖尿病的患者的临床特征、抗胰岛自身抗体和HLA-DR分型进行了研究。1型糖尿病发病的中位年龄为56岁（四分位数范围48-63），平均±SD BMI为20.8±2.7 kg/m2。聚乙二醇化干扰素联合利巴韦林治疗的患者从干扰素治疗开始到1型糖尿病发作的时间明显短于非聚乙二醇化干扰素单药治疗的患者（P < 0.05）。94.5%的糖尿病患者在发病时检测到抗胰岛自身抗体。日本人群中的HLA-DRs DR4和DR9也与干扰素治疗相关的1型糖尿病相关。此外，干扰素治疗相关的1型糖尿病患者HLA-DR13的患病率显著高于健康对照组（优势比为3.80 [95% CI 2.20-7.55]; P < 0.0001）和典型1型糖尿病患者（优势比为2.15 [1.17-3.93];P < 0.05）。在干扰素治疗前和治疗期间应检测抗胰岛自身抗体，以确定1型糖尿病的高危人群。较强的抗病毒治疗可能导致1型糖尿病的早期发展。此外，干扰素诱导的1型糖尿病患者在遗传上是易感的。
Interferon therapy can trigger induction of several autoimmune diseases, including type 1 diabetes. To assess the clinical, immunologic, and genetic characteristics of type 1 diabetes induced by interferon therapy, we conducted a nationwide cross-sectional survey. Clinical characteristics, anti-islet autoantibodies, and HLA-DR typing were examined in 91 patients for whom type 1 diabetes developed during or shortly after interferon therapy. Median age at the onset of type 1 diabetes was 56 (interquartile range 48–63) years and mean ± SD BMI was 20.8 ± 2.7 kg/m2. The time period from the initiation of interferon therapy to type 1 diabetes onset in patients receiving pegylated interferon and ribavirin was significantly shorter than that in patients with nonpegylated interferon single therapy (P < 0.05). Anti-islet autoantibodies were detected in 94.5% of patients at diabetes onset. Type 1 diabetes susceptibility HLA-DRs in the Japanese population, DR4 and DR9, were also associated with interferon treatment–related type 1 diabetes. Furthermore, the prevalence of HLA-DR13 was significantly higher in interferon treatment–related type 1 diabetes than in healthy control subjects (odds ratio 3.80 [95% CI 2.20–7.55]; P < 0.0001) and classical type 1 diabetes (2.15 [1.17–3.93]; P < 0.05). Anti-islet autoantibodies should be investigated before and during interferon therapy to identify subjects at high risk of type 1 diabetes. Stronger antiviral treatment may induce earlier development of type 1 diabetes. Furthermore, patients who develop interferon-induced type 1 diabetes are genetically susceptible.