Yoshida H, Inoue T, Hakamata Y, Tamekiyo H, Enomoto T, Koshimura O, Sako Y
Department of Internal Medicine, Shizuoka General Hospital.
Nihon Ronen Igakkai Zasshi. 1998 Jul;35(7):571-6. doi: 10.3143/geriatrics.35.571.
We report a 79-year-old woman case of slowly progressive IDDM (SPIDDM) with rheumatoid arthritis (RA) and Hashimoto disease. High titer of anti-glutamic acid decarboxylase antibody (GAD) with a value of 16,400 U/ml (normal value: less than 5 U/ml) and deteriorated secretion of insulin, and clinical course led to the diagnosis of SPIDDM. Both anti-islet cell and anti-insulin antibodies were negative. One year prior to the diagnosis, at 78 years of age, she was newly diagnosed with NIDDM and had been medicated with sulfonylurea and voglibose, resulting her glucose levels well-controlled. Four months before admission, a gradual increase of plasma glucose was noticed, while oral hypoglycemic agents were fully administrated. On admission, her glycemic control was revealed as follows; a fasting blood glucose level of 458 mg/dl and an HbA1 C level of 14.3%. Urinary CPR was 22.5 micrograms day. Her insulin secretion was proved not to be induced with intravenous glucagon injection. Hyperinsulinemic euglycemic glucose clamp test showed the normal glucose uptake ratio; 9.5 mg/kg/min. Moderate doses of subcutaneous insulin (20 units daily) were effective on her diabetes control. She was newly diagnosed with Hashimoto disease that required thyroid hormone replacement 50 micrograms per day after having developed NIDDM. High titer of anti-thyroglobulin antibody (46.9 U/ml) and anti-thyroid peroxidase antibody (81.5 U/ml) were observed. The patient had been medicated for RA with anti-inflammatory drugs since her early seventieth. Rheumatoid factor was elevated to 127.7 IU/L and, anti-nuclear antibody (x 80) and anti-DNA antibody (x 80) were present. It may be of interest that a specific phenotype of HLA; A24 (9) and DR9 recognized to be susceptible to IDDM was detected in the high-elderly onset SPIDDM. Taken together HLA typing with her history of both RA and Hashimoto disease, our case may provide the information to the mechanism of pathogenesis of SPIDDM. Furthermore, to out knowledge, this is the first case of SPIDDM in the aged; 75-year-old or more.
我们报告了一例79岁患有类风湿关节炎(RA)和桥本氏病的缓慢进展型胰岛素依赖型糖尿病(SPIDDM)女性病例。抗谷氨酸脱羧酶抗体(GAD)滴度高,值为16400 U/ml(正常值:小于5 U/ml),胰岛素分泌恶化,临床病程导致SPIDDM的诊断。抗胰岛细胞抗体和抗胰岛素抗体均为阴性。在诊断前一年,即78岁时,她新诊断出非胰岛素依赖型糖尿病(NIDDM),并一直服用磺脲类药物和伏格列波糖,血糖水平得到良好控制。入院前四个月,尽管已充分服用口服降糖药,但血浆葡萄糖仍逐渐升高。入院时,她的血糖控制情况如下:空腹血糖水平为458 mg/dl,糖化血红蛋白(HbA1C)水平为14.3%。尿C肽释放率为22.5微克/天。静脉注射胰高血糖素未诱导出胰岛素分泌。高胰岛素正常血糖钳夹试验显示葡萄糖摄取率正常;为9.5 mg/kg/min。中等剂量的皮下胰岛素(每日20单位)对控制她的糖尿病有效。在患NIDDM后,她新诊断出桥本氏病,需要每天补充50微克甲状腺激素。观察到抗甲状腺球蛋白抗体(46.9 U/ml)和抗甲状腺过氧化物酶抗体(81.5 U/ml)滴度高。该患者自70岁出头就开始用抗炎药治疗RA。类风湿因子升高至127.7 IU/L,存在抗核抗体(×80)和抗DNA抗体(×80)。在高龄发病的SPIDDM中检测到一种特定的HLA表型;A24(9)和DR9,已知它们易患IDDM,这可能很有意思。结合HLA分型以及她的RA和桥本氏病病史,我们的病例可能为SPIDDM的发病机制提供信息。此外,据我们所知,这是首例年龄在75岁及以上的SPIDDM病例。