MYXEDEMA

physiological reaction to lack of sufficient thyroid hormone (hypothyroidism) in the adult. It can be brought about by removal of the thyroid for any cause, by a cessation of function of the gland, or simply by glandular atrophy. The changes come on gradually: enlarged tongue; thickened skin with underlying fluid causing puffiness, particularly in the face around the eyelids and in the hands; drowsiness; apathy; sensitivity to cold; failure to menstruate (amenorrhea) or excessive menstrual bleeding (menorrhagia); cardiac enlargement; and lowering of the basal metabolic rate. The outlook for recovery, when treatment is with dessicated thyroid, is excellent. Therapy must be maintained permanently. Excesses of the antidiuretic hormone (vasopressin) in myxedema may produce low blood sodium (hyponatremia). Other endocrine glands may be affected by the shortage of thyroid hormone: the gonadotropins, adrenocorticotropin (ACTH), and growth hormone may be decreased. Ovarian dysfunction in myxedema is different in the primary and secondary types. In the former, menstrual flow may be more frequent, prolonged, and excessive. In the latter, if associated losses of gonadotropins are present, the menses cease. In the male, sexual activity and sperm production decrease. Fertility is reduced in both sexes. Myxedema may also cause delayed sexual maturation (which can be corrected by thyroid replacement), but sexual precocity can also occur. Adrenocortical function may become decreased in myxedema either because of loss of pituitary ACTH, a direct effect of hypometabolism on the adrenals, or as a consequence of decreased utilization of, and therefore decreased need for, cortisol. These are temporary changes. At times, the myxedema is accompanied by permanent primary hypofunction of the adrenal cortices (Addison's disease; also called Schmidt's syndrome). Also, circulatory responses to epinephrine (adrenaline) secreted by the adrenal medulla are decreased in hypothyroidism.