RESUMO
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.
Assuntos
Artrite Reumatoide/complicações , Diabetes Mellitus Tipo 1/complicações , Tireoidite Autoimune/complicações , Idoso , Feminino , HumanosRESUMO
A familial case of generalized resistance to thyroid hormone (GRTH) is described. A 17-year-old man (case 1), who had been treated with methimazole under the diagnosis of Graves' disease and his 11-year old sister (case 2) visited our clinic for the evaluation of their thyroid function. They lacked the signs and symptoms of thyrotoxicosis in spite of extremely high serum thyroid hormone levels. Their plasma TSH levels were not suppressed, but in fact markedly increased after TRH loading. Their peripheral indices of thyroid hormone were within normal limits and were not influenced by exogenous T3 administration. Even 150 micrograms T3 administration for 7 days did not fully suppress the TRH-stimulated TSH level in case 2. The two patients thus were diagnosed to have GRTH. Sera from their father and another sister showed identical abnormalities.