Addison's disease (after the English physician Thomas Addison) is also called autoimmune adrenalitis or primary adrenal insufficiency. Previously, tuberculosis was the most common cause of progressive destruction of the adrenal cortex, but today autoimmune attack on the adrenal cortex tissue, is the most common cause of Addison's disease.
The symptoms are only felt when nearly 90% of the adrenal cortex has been destroyed, causing a shortage of the hormones produced by the adrenal cortex for cortisol and aldosterone. A variety of symptoms such as weight loss, abdominal discomfort, nausea, vomiting, diarrhea, anemia, fatigue / collapse on exertion, muscle weakness, hyperpigmentation of the skin and mucous membranes, low blood pressure, low pulse, etc is caused by lack of these hormones. Addison's disease can occur either alone or as a so-called autoimmune poly glandular syndrome (APS).
Autoantibodies directed against the 21-hydroxylase is the marker of the autoimmune form of Addison's disease. The antibodies are of predictive value as they can be detected even before symptoms are noted. In the advanced stage of disease the presence of autoantibodies fall. As Addison's disease (predominantly as part of APS) is often associated with other autoimmune diseases such as autoimmune thyroiditis, type 1 diabetes mellitus and celiac disease, there may be reason to check the autoantibodies present in these conditions.