In Addison's disease (sometimes referred to as adrenal insufficiency ), patients lack glucocorticoids and usually also mineralocorticoids. If the adrenal cortex (NNR) no longer produces enough steroids, the cause can either lie directly in the NNR (primary NNR insufficiency) or in the higher-level control organ - the pituitary gland (secondary NNR insufficiency).
Below you will find further information on the causes, symptoms and treatment as well as selected Addison's disease specialists.
When it comes to symptoms, a distinction must be made between long-term insufficiency and a sudden Addisonian crisis. In the primary form, symptoms only occur when over 90% of the NNR has been destroyed. Patients typically have very tanned skin and are often tired and listless. They usually have low blood pressure and often complain of nausea and vomiting. The disease often remains undetected and only becomes noticeable in stressful situations, such as after operations, accidents or other serious illnesses.
An Addison's crisis consists of typical symptoms such as tanned skin, tiredness, nausea, dehydration, reduced excretion and a drop in blood pressure. There is also a drop in blood sugar and severe abdominal pain.
Primary NNR hypofunction is much more common than secondary NNR hypofunction and the primary form is usually caused by destruction of the NNR by autoantibodies, i.e. an autoimmune process. This autoimmune form of the disease is called Addison's disease.
The diagnosis can be easily determined using a few laboratory tests. In primary NNR hypofunction, the concentration of cortisol and mineralocorticoids in the blood is too low. This leads to an increased release of the higher messenger substance ACTH. In the secondary form, there is a reduced release of ACTH, but because the function of the NNR is not impaired, the production of mineralocorticoids is not disturbed.
If NNR hypofunction is suspected, the cortisol level and the electrolytes in the blood are determined. In an acute situation, there is too little sodium and too much potassium in the blood because the messenger substance responsible for electrolyte balance is missing. This messenger substance is the mineralocorticoid aldosterone.
A test is used to confirm the diagnosis. In this test, a messenger substance is injected which stimulates the adrenal gland to produce cortisol in healthy people. If the cortisol level in the blood does not rise, Addison's disease is present. To find out whether it is a primary or secondary form, ACTH is determined. In the primary form, there is an increased ACTH value in the blood and in the secondary form the value is reduced.
The therapy consists of lifelong replacement of cortisol or aldosterone in the case of the primary form. The dose is adjusted so that blood pressure and electrolytes are well regulated and patients feel well.
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