Addison's disease

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Related to Adrenal insufficiency: adrenal gland, Adrenal fatigue, adrenal crisis, Adrenal exhaustion

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.

REFERENCES

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]
(medicine)
A primary failure or insufficiency of the adrenal cortex to secrete hormones.
References in periodicals archive ?
Follow-up At 18 months of age: hyperpigmentation of lips and gum Urgent ACTH stimulation test Low serum cortisol High ACTH Normal serum testosterone & DHEA Normal 17 OHP [down arrow] Diagnosis Adrenal insufficiency [down arrow] Management and follow-up Hydrocortisone added to Fludrocortisone OPD: thriving well Gene study at 9 years of age [down arrow] Final Diagnosis DAX-1 gene mutation (AHC) [down arrow] Follow-up Thriving well Still prepubertal Will continue monitoring: FSH, LI 1, Testosterone & gonadal development Figure 3--Timeline summarizing the patient's (Twin B) information, clinical presentation, impression, investigation and management, final diagnosis, and follow-up.
In primary adrenal insufficiency, maintenance therapy requires both glucocorticoids and mineralocorticoid replacement.
This model provides sustained drug release within the therapeutic range and is suitable for the variable drug release patterns required in diseases such as adrenal insufficiency which are affected by circadian rhythm.
Therefore, the clinician will need to balance the risks and benefits for each specific patient but the current study suggests that discontinuation of steroids is feasible and does not result in clinical adrenal insufficiency in patients screened with an AM cortisol measurement.
Bantwal et al., "Adrenal insufficiency in patients with stable non-cystic fibrosis bronchiectasis," Indian Journal of Medical Research, vol.
While its use has been shown to effectively reduce urinary free cortisol in patients with Cushing's syndrome, adrenal insufficiency is a known side effect of therapy [4, 5].
Adrenal insufficiency (AI) stems from inadequate physiologic steroid production and is most commonly a result of discontinuation of long-term glucocorticoid treatment.
If you are diagnosed with adrenal insufficiency, your doctor can give you more information about what to watch out for and how to prepare for an adrenal crisis.
Besides the HPA axis suppression, which is caused by oral or systemic CSs, adrenal insufficiency has been shown to be associated also with inhaled CSs, but with a lower prevalence [15].
Primary adrenal insufficiency due to bilateral adrenal hemorrhage-adrenal infarction in the antiphospholipid syndrome: Long-term outcome of 16 patients.
[3,4] Even minor degrees of adrenal insufficiency increases the mortality in critically ill or injured patients.
One classification of Addison's Disease is called Primary Adrenal Insufficiency, which is where your immune system attacks the body's adrenal glands.