Untreated, adrenal insufficiency is fatal, and indeed this was invariably the case until the advent of synthetic cortisone in 1949. Treatment of Addison's disease is lifelong. The prognosis for any patient with adrenal insufficiency will depend on the underlying cause. In those patients in whom the prognosis is not affected by the underlying pathology, replacement therapy should result in a return to health. However, a Norwegian study found an excess of mortality in patients diagnosed with Addison's disease at a young age, associated with acute adrenal failure, infection and sudden death. [ 16 ]
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.