Abstract
The incidence of overt diabetes in patients with hyperthyroidism has been reported to be 2 to 3 %. Only a few cases of coexisting diabetic ketoacidosis and clinical hyperthyroidism have been reported in Japan.
We describe two young female patients who developed diabetic ketoacidotic precoma after longterm preexisting hyperthyroidism. Case 1: The patient, a 25-year-old female, developed hyperthyroidism at the age of 18 yrs, but had been incompletely treated. She was admitted to our clinic complaining of sudden onset of thirst, general malaise and somnolence. Physical examination on admission revealed a dehydrated lady in somnolence with struma (grade 2), dry skin and mucous membrane. The laboratory data were: urinary glucose and ketone bodies, strongly positive; blood glucose, 636 mg/dl; arterial pH, 7.236; PCO2 20.9 mmHg; base excess (BE)-17 mEq/l; HCO3-8.5 mEq/l; Ht 48%; T3RU 51.5%; T4 17.4 μg/dl; T3 270 ng/dl; TSH below 1 μu/ml; thyroid and microsome tests, both positive. Case 2: The patient, a 37-year-old female, developed hyperthyroidism at the age of 23 yrs, but had received only occasional therapy as in Case 1. She was transferred to our clinic because of vomiting, palpitations and somnolence. Physical examination on admission revealed somnolence (severe), sinus tachycardia (154/min), dry skin and mucous membrane. Goiter was not found. The laboratory data were; urinary glucose and ketone bodies, strongly positive; blood glucose, above 400 mg/dl; arterial pH, 7.176; PCO2 17.5 mmHg; BE -19.9 mEq/l; HCO3- 6.4 mEq/l; Ht 53%; T3RU 51.8%; T4 16.8 μg/dl: T3 280 ng/dl; TSH below 1 μu/ml; microsome test, positive.
Both patients recovered quickly from their impaired consciousness following intravenous administration of saline solution combined with insulin preparation. However, the daily insulin requirement had increased since the serum level of thyroid hormones was elevated during the hospital course until an antithyroid drug was administered. Antithyroid drug therapy resulted in a decrease of the insulin requirement, indicating that the hyperthyroid state had affected the glucose tolerance and actually precipitated diabetic ketoacidosis in these cases.
The present two cases appear to represent a clinical example of the ‘metathyroid diabetes’ proposed by Dr. Houssay. However, according to current concepts of autoimmunity, the possible mechanism common to the coexistence of insulin dependent diabetes and clinical hyperthyroidism may be involved in these cases.
