Addison disease (or Addison's disease) is adrenocortical insufficiency due to the destruction or dysfunction of the entire adrenal cortex. It affects glucocorticoid and mineralocorticoid function. Almost all patients complain of progressive weakness, fatigue, poor appetite, and weight loss. Prominent gastrointestinal symptoms may include nausea, vomiting, and occasional diarrhoea. Glucocorticoid-responsive steatorrhea has been reported. Dizziness with orthostatic due to hypotension occasionally may lead to syncope. This is due to the combined effects of volume depletion, loss of the mineralocorticoid effect of aldosterone, and loss of the permissive effect of cortisol in enhancing the vasopressor effect of the catecholamine.
Meeting a medical practitioner
Physical examination in long-standing cases most often reveals increased pigmentation of the skin and mucous membranes, with or without areas of vitiligo.Patients show evidence of dehydration, hypotension, and orthostatic.Female patients may show an absence of axillary and pubic hair and decreased body hair. This is due to loss of the adrenal androgens, a major source of androgens in women.Addison disease caused by another specific disease may be accompanied by clinical features of that disease.Calcification of the ear and costochondral junctions is described but is a rare physical finding.
The most common cause of Addison disease is idiopathic autoimmune adrenocortical insufficiency resulting from autoimmune atrophy, fibrosis, and lymphocytic infiltration of the adrenal cortex, usually with sparing of the adrenal medulla. This accounts for more than 80% of reported cases. Idiopathic autoimmune adrenocortical atrophy and tuberculosis (TB) account for nearly 90% of cases of Addison disease.