Clinical Features of the Diabetic Syndrome Appearing after Steroid Therapy.

IN 1930 Britton showed that extracts of the adrenal cortex administered to norma-l or adrenalectomised animals caused elevation of the blood sugar and increased the glycogen content of muscle and liver tissue. Subsequently Ingle (1941) reported the occurrence of glycosuria when cortisone was administered to normal rats. Sprague and colleagues, (1950a) described diabetic responses to glucose tolerance tests in patients given 90 to 200 mg. of cortisone daily. Since then it has been shown that ostensibly normal human subjects given large doses of corticotrophin or adrenal cortical steroids 'may show hyperglycemia and glycosuria (Conn and Fajans, 1956). The term "steroid" diabetes was first applied to man by Sprague and colleagues (1950b) to designate the diabetes occurring in a boy with Cushing's syndrome. It has since been suggested (Bastenie, 1956) that the nosological use of the term should be extended to include (1) the diabetes occurring in association with conditions where severe endocrine disorders obviously exist, i.e., in Cushing's syndrome, Achard-Thiers' syndrome and acromegaly; (2) the diabetes in patients with no definite clinical signs of hyperfunction of the adrenal cortex but in whom there is biochemical evidence of hypercorticism,-i.e., certain cases of fat diabetes and the obesity occurring in prediabetes; (3) the aggravation of the diabetic state characterised by increased insulin requirements occurring in the acidosis of insulindependent diabetics following an interruption of insulin supply or as a result of surgical shock or trauma. Selye (1946) postulated that such aggravation might be due to a temporary over-production of the gluco-regulatory corticoids of a defensive nature. To these examples of diabetes produced or aggravated by an increased endogenous supply of adrenal cor-