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OBJECTIVE -Cross-sectional studies have reported that the risk of thyroid dysfunction in patients with type 1 diabetes is two-to threefold higher than in the general population. However, longitudinal studies to determine the natural history of thyroid dysfunction in patients with type 1 diabetes are lacking. RESULTS -A total of 18 patients had hypothyroidism, and 1 patient experienced transient hyperthyroidism. Two subjects developed hypothyroidism 7 and 18 years before the development of diabetes and were excluded from the analysis. The mean age of diagnosis was 19 Ϯ 2 years for type 1 diabetes and 29 Ϯ 3 years for hypothyroidism. Hypothyroidism was more common in female (41%) than in male (19%) subjects and in patients with positive TPO antibodies. Patients who were TPO positive were 17.91 times as likely to develop hypothyroidism as patients who were TPO negative (95% CI 3.89 -82.54). There were no differences in BMI, lipid profile, and HbA 1c between patients with and without thyroid dysfunction. RESEARCH DESIGN AND METHODSCONCLUSIONS -This longitudinal study confirms the association between autoimmune thyroid dysfunction and type 1 diabetes. Our results indicate that all subjects with type 1 diabetes should undergo annual screening by serum TSH measurement to detect asymptomatic thyroid dysfunction, particularly those with positive TPO antibodies.

OBJECTIVE—In this prospective, randomized, open trial, we compared the efficacy and safety of aspart insulin given subcutaneously at different time intervals to a standard low-dose intravenous (IV) infusion protocol of regular insulin in patients with uncomplicated diabetic ketoacidosis (DKA). RESEARCH DESIGN AND METHODS—A total of 45 consecutive patients admitted with DKA were randomly assigned to receive subcutaneous (SC) aspart insulin every hour (SC-1h, n = 15) or every 2 h (SC-2h, n = 15) or to receive IV infusion of regular insulin (n = 15). Response to medical therapy was evaluated by assessing the duration of treatment until resolution of hyperglycemia and ketoacidosis. Additional end points included total length of hospitalization, amount of insulin administration until resolution of hyperglycemia and ketoacidosis, and number of hypoglycemic events. RESULTS—Admission biochemical parameters in patients treated with SC-1h (glucose: 44 ± 21 mmol/l [means ± SD], bicarbonate: 7.1 ± 3 mmol/l, pH: 7.14 ± 0.09) were similar to those treated with SC-2h (glucose: 42 ± 21 mmol/l, bicarbonate: 7.6 ± 4 mmol/l, pH: 7.15 ± 0.12) and IV regular insulin (glucose: 40 ± 13 mmol/l, bicarbonate 7.1 ± 4 mmol/l, pH: 7.11 ± 0.17). There were no statistical differences in the mean duration of treatment until correction of hyperglycemia (6.9 ± 4, 6.1 ± 4, and 7.1 ± 5 h) or until resolution of ketoacidosis (10 ± 3, 10.7 ± 3, and 11 ± 3 h) among patients treated with SC-1h and SC-2h or with IV insulin, respectively (NS). There was no mortality and no differences in the length of hospital stay, total amount of insulin administration until resolution of hyperglycemia or ketoacidosis, or the number of hypoglycemic events among treatment groups. CONCLUSIONS—Our results indicate that the use of subcutaneous insulin aspart every 1 or 2 h represents a safe and effective alternative to the use of intravenous regular insulin in the management of patients with uncomplicated DKA.

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Studies in which plasma osmolality was altered acutely by oral water loading and hypertonic sodium chloride infusion were performed to further identify the mechanisms involved in the pathogenesis of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in a patient with Guillain-Barré syndrome. Although resetting of the osmotic threshold for vasopressin release was demonstrated in these studies, this does not seem to have been a primary factor in the development of SIADH in this patient. Downward resetting of the osmotic threshold by sustained hypoosmolality has been previously demonstrated, and it is possible that this may account for the initially low osmotic threshold identified by our studies. These studies suggest that inappropriate antidiuresis, as shown by the absence of a diuretic response to low threshold suppression of the plasma arginine vasopressin concentration was due either to a vasopressin-independent mechanism or to markedly increased renal tubular sensitivity to vasopressin.