Kaposi's sarcoma has been reported to occur in patients receiving corticosteroid
therapy. Discontinuation of corticosteroids may result in clinical remission.
Although controlled clinical trials have shown corticosteroids to be effective in speeding the resolution of acute exacerbations of multiple sclerosis , they do not show that corticosteroids affect the ultimate outcome or natural history of the disease. The studies do show that relatively high doses of corticosteroids are necessary to demonstrate a significant effect. (See DOSAGE AND ADMINISTRATION .)
Thyroid hormones, gonadal and adrenocortical steroids, are glucoregulatory hormones. Thyroid hormones increase the provision of glucose to meet the enhanced energy demands which they impose. Glucose tolerance is decreased, associated with increased hepatic glucose production, although the glucose-raising effects of thyroid hormones are partially offset by an increased rate of glucose utilization especially in the postabsorptive state. The insulin secretory capacity of the pancreatic B cells is reduced by an excess of thyroid hormones, and the onset of diabetes may be hastened as pancreatic insulin reserves are depleted. Natural estrogens can improve glucose tolerance through a beta-cytotropic effect and enhanced insulin sensitivity. Progesterone may produce similar effects in the absence of estrogens, but progestins appear to antagonize the effects of estrogens. Testosterone exerts only marginal effects on glucose tolerance. Glucocorticoids decrease glucose tolerance by increased hepatic glucose production and impaired peripheral glucose utilization. Glucocorticoids reduce insulin sensitivity and responsiveness in peripheral tissues. However, the diabetogenic influence of glucocorticoid excess is partly compensated by a beta-cytotropic effect and a condition of diabetes develops when the functional reserve of the endocrine pancreas becomes limiting.
Primary aldosteronism is characterized by high blood pressure, caused by increased retention of salt and water by the kidneys, and low serum potassium concentrations (hypokalemia), caused by excess excretion of potassium in the urine. The symptoms and signs of aldosterone excess include not only hypertension but also muscle weakness and cramps and increased thirst and urination. Primary aldosteronism is usually caused by a benign adrenal tumour (adenoma), but some patients have hyperplasia of both adrenal glands. Successful removal of the adrenal tumour usually results in reduction in blood pressure and cessation of potassium loss; patients with bilateral adrenal hyperplasia are treated with antihypertensive drugs.