In Addison's disease a combined autoantibody and cell-mediated immune reaction against adrenocortical cells ultimately results in fibrous cortical replacement with relative sparing of the medulla. Clinical signs and symptoms do not become manifest until at least 90 per cent of the adrenocortical tissue is destroyed. In other conditions (e.g. tuberculosis, adrenal hemorrhage) the medulla is also affected. However, there is no distinct clinical syndrome of adrenal medullary insufficiency. This could be explained by the fact that catecholamines are produced by other tissues such as the sympathetic nerves. In primary hypoadrenalism both glucocorticoid and mineralocorticoid secretion are deficient. In secondary/tertiary hypoadrenalism primarily glucocorticoid deficiency occurs. In both conditions adrenal androgen secretion is also affected which has some clinical implications in women (e.g. loss of pubic and axillary hair).

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