Insulin sensitivity, metabolic clearance rate of insulin (MCR-I) and basal posthepatic insulin delivery rate (BIDR) were investigated by means of euglycemic clamp technique in 8 normal subjects and 8 patients with hyperthyroid Graves' disease. The mean (±SD) steady-state glucose infusion rate (SSGIR) was lower in hyperthyroid Graves' patients than in normal subjects (228.9±57.0 vs. 290.9±49.4 mg/m2/min, p<0.05). Both MCR-I and BIDR were higher in hyperthyroid Graves' patients than in normal subjects (1162.9+517.1 vs. 463.5±103.9 ml/m2/min, p<0.005; 17.7+12.6 vs. 3.6±0.9 mU/m2/min, p<0.01, respectively).Plasma free T4 levels showed a close correlation with MCR-I (r=0.77, p<0.05) and BIDR (r=0.81, p<0.05), respectively, in Graves' patients. These findings indicate that hyperthyroidism is characterized by not only a decrease in insulin sensitivity, but also an increase in basal insulin secretion and the metabolic clearance rate of insulin, which are correlated with plasma free T4 levels. (Internal Medicine 34: 339-341, 1995)

Abstract.The causes of hyperprolactinemia, the correlation between serum levels of PRL and thyroid function and magnetic resonance imaging (MRI) of the pituitary were studied in patients with chronic thyroiditis.Seventy

Islet cell antibodies were studied in 1,112 non-diabetic adults, 473 normal school children and 162 Type 1 (insulin-dependent) diabetic patients in a Japanese population. The prevalence of islet cell antibodies was 0.5%, 0.4% and 32%, respectively. Most islet cell antibodies positive subjects with Type 1 diabetes had short duration of the disease. No patients who had over 10 years from the onset had islet cell antibodies. Six non-diabetic adults with islet cell antibodies were followed for 4 years. Only one with Hashimoto's thyroiditis showed a diabetic pattern in her oral glucose tolerance test. However, none developed overt insulin-dependent diabetes until 1984. Two out of these six subjects continued to be positive for both islet cell antibodies and antithyroid antibodies or antinuclear antibodies. Islet cell antibodies in the remaining four patients disappeared during the second year. It is difficult to predict the onset of Type 1 diabetes by islet cell antibodies in non-diabetic individuals because they may be transient.

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The responses of both plasma TSH and free T3 (FT3) to TRH were examined in 31 patients with Graves' disease who were euthyroid after treatment with antithyroid drugs, 6 patients with primary hypothyroidism, and 14 control subjects. TSH was measured 0, 15, 30, 60, 90, and 120 min and FT3 was measured 0, 30, 60, 90, 120, 150, and 180 min after TRH injection (500 microgram, iv). The increment in FT3 above the basal level (delta FT3) in normal controls ranged from 1.2-3.7 pmol/L, with a mean +/- SD of 2.2 +/- 0.8 pmol/L. The mean (+/- SD) delta FT3 in patients with primary hypothyroidism was 0.3 +/- 0.2 pmol/L. After the TRH test, antithyroid drugs were stopped in patients with Graves' disease. Nine of 31 Graves' patients relapsed within 6 months after the TRH test. The other 22 patients with Graves' disease were followed while in remission during the observation period of up to 48 months. The mean (+/- SD) delta FT3 were significantly lower in 9 Graves' patients who relapsed than in those who achieved remission (0.5 +/- 0.3 vs. 2.6 +/- 1.1 pmol/L; P less than 0.01). Eight of 9 Graves' patients who relapsed showed lower delta FT3 values than the lowest value (1.1 pmol/L) in 22 Graves' patients in remission. Although the mean increment of TSH above the basal level (delta TSH) was also significantly different between the Graves' patients who relapsed and those in remission (1.4 vs. 12.3 mU/L; P less than 0.01), there was considerable overlap between the 2 groups. These findings suggest that delta FT3 reflects the endocrinological recovery of the pituitary-thyroid axis and is a beneficial indicator for the termination of antithyroid drugs in Graves' disease.

Antinuclear antibodies (ANA) were detected both in type 1 diabetic children and in control subjects. The incidence of ANA in eighty of these diabetics was 16.3%, as determined using two different substrates, human pancreas and human peripheral leucocytes.The incidence and the patterns in the detection of ANA were the same. Four hundred and seventy-three children and one thousand one hundred and twenty-five adults served as the controls.The incidence of ANA in non-diabetic children was 0.8% and that in one adult population was 1.1%.Therefore, the incidence of ANA in childhood diabetics was significantly higher.We studied autoantibodies in childhood diabetics, in normal children and in one adult population.Pancreatic islet cell antibodies (ICA) were detected in 29 out of 80 type 1 diabetics (36.3%) in two out of 473 normal children (0.4%) and in six cases in one population (0.5%).Thyroid microsomal antibodies (MCHA) were detected in 9 out of 80 childhood diabetics and the incidence of MCHA in type 1 diabetics was significantly higher than in the controls.

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