corticosteroid

corticosteroid /kôr′tikōstir″oid/ [L, cortex + steros, solid] , any one of hormones elaborated by the adrenal cortex (excluding the sex hormones of adrenal origin) that influence or control key processes of the body. These processes include carbohydrate and protein metabolism, maintenance of serum glucose levels, electrolyte and water balance, and functions of the cardiovascular system, the skeletal muscle, the kidneys, and other organs. The corticosteroids synthesized by the adrenal glands include the glucocorticoids and the mineralocorticoids. The principal glucocorticoids are cortisol and corticosterone. The only physiologically important mineralocorticoid in humans is aldosterone. These hormones may be manufactured and administered exogenously. The glucocorticoids tend to cause the cells of the body to shift from carbohydrate catabolism to fat catabolism, to accelerate the breakdown of proteins to amino acids, and to help maintain normal blood pressure. The secretion of these hormones increases during stress, especially that produced by anxiety and severe injury. Chronic overproduction of these substances is associated with various disorders, such as Cushing’s syndrome. A high blood level of glucocorticoids markedly increases the number of eosinophils and decreases the size of lymphatic tissues, especially the thymus and the lymph nodes. The decrease in lymphocytes slows antibody formation and affects the body’s immune system. Aldosterone is the most powerful of the natural mineralocorticoids in the regulation of electrolyte balance, especially in the balance of sodium and potassium. Cortisol induces sodium retention and potassium excretion, but less effectively than aldosterone. The effects of the corticosteroids on the cardiovascular system, which are not precisely understood, are most evident in hypocortisolism, when the reduction in blood volume, accompanied by increased viscosity, may cause hypotension and cardiovascular collapse. The absence of corticosteroids decreases capillary permeability, decreases vasomotor response of small vessels, and reduces cardiac size and output. The skeletal muscles require adequate amounts of corticosteroids to function normally; excessive amounts cause them to function abnormally. Cortisol and its synthetic analogs can prevent or reduce inflammation by inhibiting edema, leukocytic migration, and disposition of collagen and by causing other complications associated with inflammatory processes. The antiinflammatory actions of synthetic hormones can be harmful, however, because they mask the disease process and prevent accurate observation of its progress. Hypoadrenalism may result from the too rapid withdrawal of such drugs after prolonged therapy. Toxic effects associated with prolonged large dose corticosteroid therapy include fluid and electrolyte imbalance, hyperglycemia and glycosuria, increased susceptibility to infections, myopathy, arrested growth, ecchymoses, Cushing’s syndrome, acne, and behavioral disturbances. Myopathy, characterized by weakness of the proximal musculature of the arms and the legs and associated shoulder and pelvic muscles, may also develop. Corticosteroid therapy may also produce behavioral changes, such as schizophrenia, suicidal tendencies, nervousness, and insomnia. See also adrenal crisis.