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Addison's Disease



Addison's disease (adrenal insufficiency) usually results from an autoimmune response in wchich circulating antibodies react specifically against the adrenal gland and destroy it. Addison's disease occurs when more than 90% of both adrenal glands are destroyed. Other causes include tuberculosis (once the chief cause), bilateral adrenalectomy, neoplasms and infections (histoplasmosis, cytomegalovirus). Rarely, a family history of autoimmune disease predisposes th patien to Addison's disease and other endoctine system disoders.

SYMPTOMS
Addison's disease typically produces such effects as weakness, fatigue, weight loss, and various GI disturbances, such as nausea, vomiting, loss of appetite (anorexia), and chronic diarrhea.

A simple, noninvasive saliva test known as the Adrenal Stress Index (ASI) can determine whether an imbalance in the adrenal gland exists. Te ASI test also evaluates how well the adrenal glands function by tracking their 24-hour circadian rhythm. Based on the laboratory results, medicl practitiones can prescribe the appropriate treatment to restore the balance of hormones.

The disorder also usually causes a conspicuous bronze coloration of the skin. The patient appears to be deeply suntanned, especially in the creases of the hands, elbows, and the knees. He also may exhibit a darkening of scars, areas of vitiligo (absence of pigmentation), and increased pigmentation of the mucous membranes. Such abnormalities result from decreased secretion of cortisol (one of the glucocorticoids), which causes the pituitary gland to simultaneously secrete excessive amounts of corticotropin and melanocyte-stimulating hormone (MSH).

Additional symptoms include low blood pressure (hypotension) and weak, irregular pulse. Other clinical effects include decreased tolerance of even minor stress, poor coordination, fasting hypoglycemia, and a craving for salty food.

TREATMENT
For all patients with Addison's disease lifelong corticosteroid replacement, usually with cortisone or hydrocortisone (both of which also have a mineralocorticoid effect), is the primary treatment.


References to materials used for this publication are available upon request.

 



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