Addison's disease

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Related to Addison's disease: Cushing's disease, Graves disease

Addison's disease

[for Thomas AddisonAddison, Thomas,
1793–1860, English physician, b. near Newcastle, grad. Univ. of Edinburgh (M.D., 1815). In 1837 he became a physician at Guy's Hospital, London, where he conducted important research on pneumonia, tuberculosis, and other diseases.
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], progressive disease brought about by atrophy of the outer layer, or cortex, of the adrenal glandadrenal gland
or suprarenal gland
, endocrine gland (see endocrine system) about 2 in. (5.1 cm) long situated atop each kidney. The outer yellowish layer (cortex) of the adrenal gland secretes about 30 steroid hormones, the most important of which are aldosterone and
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; it is also called chronic adrenocortical insufficiency. The deterioration of this tissue causes a decrease in the secretion of steroid hormones, many of which are necessary for the maintenance of life. In many cases the cause of the wasting process is not known; in others the predominant cause is the formation and infiltration of tumors, inflammatory disease, or surgery. Symptoms are increasing weakness, abnormal pigmentation of the skin and mucous membranes, weight loss, low blood pressure, dehydration, and gastrointestinal upsets. Secondary Addison's disease is most commonly caused by acute withdrawal of steroids. Once considered inevitably fatal, Addison's disease can now be treated with injections of adrenocortical hormones.

Addison’s Disease


(named after the English physician T. Addison, who first described it in 1855), also known as bronzed skin disease. It is caused by a chronic malfunction of the suprarenal cortex of the adrenal glands and is externally characterized by a bronze coloration of the skin. A relatively rare disease, it manifests itself primarily in the 15–to 30–year age group. Addison’s disease is caused by the destruction of the adrenal glands, usually by tuberculosis or more rarely by syphilis, atrophy of the suprarenal cortex, tumor, or amyloidosis. The disease develops gradually.

As a result of the decreased secretion of adrenocortical hormones (mineralcorticoids), the secretion of sodium and chlorides in the urine increases while their amount in the blood decreases, which, together with retention of potassium, leads to the dehydration of the organism. The blood pressure falls. The lowered glucocorticoid content disrupts carbohydrate and protein exchange, causing muscular weakness, adynamia, rapid fatigue, and weight loss. The dark bronze coloring is caused by a special pigment. Hormone treatment is indicated.


Zefirova, G. S. Addisonova bolezn’. Moscow, 1963. (With bibliography.)
“Bolezni endokrinnoi sistemy.” Edited by V. G. Baranov. (Rukovodstvo po vnutrennim bolezniam, vol. 7.) Leningrad, 1966.

Addison's disease

[′ad·ə·sənz di‚zēz]
A primary failure or insufficiency of the adrenal cortex to secrete hormones.
References in periodicals archive ?
to Signs of Addison's disease include a worsening fatigue and muscle weakness, loss of appetite and weight loss are characteristic of the disease.
Jeffcoate, "Eighty-six cases of Addison's disease," Clinical Endocrinology, vol.
Ffion Jones, of Cardiff, died from Addison's disease in December Will Powell
First, we used broad searches to create large pools of citations for each of the nine possible causes (lead, scurvy, dental caries, coffee/tea, tobacco, starvation, botulism, tuberculosis, and Addison's disease) and then ran those against a set of all citations that refer to a black, hard, bleeding and dry oral condition.
Her bloodwork showed hyperkalemia, hypoglycemia, and hypocortisolism, all lab features of Addison's disease, as compared to the hypercortisolism, hyperglycemia, and hypokalemia seen with eating disorders such as AN [12].
Premature mortality in patients with Addison's disease: A population-based study.
Chronic hypoparathyroidism is the first endocrine disease to occur during the time course of PGA I, usually after chronic mucocutaneous candidiasis and before Addison's disease, and can present between three months to 44 years of age (mean, 7.5 yr).
In suspected Addison's disease cases the conventional 250 ug ACTH dose caused maximum cortisol increment both at 30min and 60min from baseline (p< 0.05) whereas with 1 ug ACTH dose significant cortisol increment was observed only at 30 min (p < 0.05) (Table-1).