Slowly Progresive IDDM with Rheumatoid Arthritis and Hashimoto Disease in High Elderly.

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  • 慢性関節リウマチと橋本病に合併した後期高齢者のｓｌｏｗｌｙ　ｐｒｏｇｒｅｓｓｉｖｅ　ＩＤＤＭ

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Abstract

We report a 79-year-old woman case of slowly progressive IDDM (SPIDDM) with rheumatoid arthrhtis (RA) and Hashimoto disease. High titer of anti-glutamic acid decarboxylase antibody (GAD) with a value of 16, 400U/ml (normal value: less than 5U/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 458mg/dl and an HbA1C level of 14.3%. Urinary CPR was 22.5μg/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; 9.5mg/kg/min. Moderate doses of subcutaneous insulin (20 units daily) were effective on her diabetes control.<br>She was newly diagnosed with Hashimoto disease that required thyroid hormone replacement 50μg per day after having developed NIDDM. High titer of anti-thyroglobulin antibody (46.9U/ml) and anti-thyroid peroxydase antibody (81.5U/ml) were observed. The patient had been medicated for RA with anti-inflammatory drugs since her early seventieth. Rheumatoid factor was elevated to 127.7IU/L and, anti-nuclear antibody (×80) and anti-DNA antibody (×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 our knowledge, this is the first case of SPIDDM in the aged; 75-year-old or more.

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