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Addison’s disease (also known as chronic adrenal insufficiency, hypocortisolism or hypocorticism) is a rare endocrine disorder in which the adrenal gland produces insufficient amounts of steroid hormones (glucocorticoids and often mineralocorticoids). It may develop in children as well as adults, and may occur as the result of a large number of underlying causes. The condition is named after Dr Thomas Addison, the British physician who first described the condition in his 1855 publication On the Constitutional and Local Effects of Disease of the Suprarenal Capsules.[1] The adjective “Addisonian” is used for features of the condition, as well as patients with Addison’s disease.[2]
The condition is generally diagnosed with blood tests, medical imaging and additional investigations.[2] Treatment involves replacement of the hormones (oral hydrocortisone and fludrocortisone). If the disease is caused by an underlying problem, it may be possible to address. Regular follow-up and monitoring for other health problems is necessary.[2]
The symptoms of Addison’s disease develop insidiously, and it may take some time to be recognized. The most common symptoms are fatigue, muscle weakness, weight loss, vomiting, diarrhea, headache, sweating, changes in mood and personality and joint and muscle pains. Some have marked cravings for salt or salty foods due to the urinary losses of sodium.[2] Adrenal insufficiency is manifested in the skin primarily by hyperpigmentation.[3]:501
On examination, the following may be noticed:[2]
An “Addisonian crisis” or “adrenal crisis” is a constellation of symptoms that indicate severe adrenal insufficiency. This may be the result of either previously undiagnosed Addison’s disease, a disease process suddenly affecting adrenal function (such as adrenal hemorrhage), or an intercurrent problem (e.g. infection, trauma) in the setting of known Addison’s disease. Additionally, this situation may develop in those on long-term oral glucocorticoids who have suddenly ceased taking their medication. In these people, long term use of synthetic glucocorticoids will have caused further atrophy of the adrenal glands by negative feedback. It is also a concern in the setting of myxedema coma; thyroxine given in that setting without glucocorticoids may precipitate a crisis.
Untreated, an Addisonian crisis can be fatal. It is a medical emergency, usually requiring hospitalization. Characteristic symptoms are:[4]
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