ADDISON’S DISEASE (CHRONIC
PRIMARY HYPOADRENALISM)
Addison’s disease can either be caused by
exogenous agents (e.g., infection of the adrenals by Mycobacterium tuberculosis) or be idiopathic. The idiopathic form
is believed to have an immune basis, since 50% of patients have been found to
have antibodies to the micro-somes of adrenal cells (as compared to 5% in the
general population) by immunofluores-cence. The autoantibodies directed against
the adrenal react mainly in the zona glomeru-losa, zona fasciculata, and zona
reticularis and are believed to play the main pathogenic role in this disease,
causing atrophy and loss of function of the adrenal cortex. Biopsy of the
adrenal glands shows marked cortical atrophy with an unaltered medulla.
Abundant in-flammatory mononuclear cells are seen between the residual islands
of epithelial cells.
The autoimmune form of Addison’s disease is
found frequently in association with other autoimmune diseases, such as
thyroiditis, pernicious anemia, and diabetes mellitus; autoantibodies to adrenal
cortex are not found in Addison’s disease caused by tuberculosis of the adrenal
glands.
Symptoms of Addison’s disease or adrenal
insufficiency include weakness, fatigabil-ity, anorexia, nausea, vomiting,
weight loss, and diarrhea. Signs include increased skin pig-mentation and
vascular collapse and hypotension. Addison’s disease is most commonly found in
the fourth and fifth decades of life and is two to three times more frequent in
females.
The diagnosis is confirmed by demonstration of
antiadrenal antibodies by indirect immunofluorescence. Low plasma cortisol
levels and low levels of urine 17-ketosteroids and 17-hydroxycorticoids are
characteristic of the disease. Frequent metabolic abnormali- ties include
acidosis, hyperkalemia, hyponatremia, low levels of chloride and bicarbonate,
and hypoglycemia. Lymphocytosis with eosinophilia may be present.
The treatment of Addison’s disease consists of
replacement of both glucocorticoids and mineralocorticoids.
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