Addison's disease: symptoms and treatment of salt starvation diseaseIn Addison's disease, the production of vital hormones in the adrenal cortex is disturbed. The disease progresses insidiously. Can lead to death if left untreated. Which symptoms indicate Addison's disease and which therapy helps.
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In Addison's disease (also known as Addison's disease, bronchial skin disease or salt starvation disease), the adrenal cortex produces progressively fewer hormones. Doctors speak of an insufficiency, i.e. a weakness or underactivity of the adrenal cortex. The disease is rare, occurs in all age groups and affects both sexes equally often.
Hormones of the adrenal cortex
Every person has two adrenal glands. The small organs lie above the kidneys and consist of an inner adrenal medulla and an outer adrenal cortex. The cortices of the adrenal glands produce hormones that act as messengers and perform vital functions in the human body. Medical experts distinguish three groups of hormones:
Glucocorticoids like cortisone, boost energy supply in stressful situations, have an anti-inflammatory effect and suppress the body's own defenses. They are important for the metabolism of bones, skin, muscles and connective tie. They also affect appetite, sex drive and psyche.
Mineralocorticoids such as aldosterone regulate the body's salt and water balance and thus control blood volume and blood prere.
Androgens such as testosterone influence bone growth, increase muscle mass, lower cholesterol levels and increase protein build-up. Also control the development of male sexual characteristics and spermatogenesis. In men, in addition to the adrenal cortex, the testes also produce androgens.
Causes of adrenal cortex weakness
Most often, the adrenal cortex is underactive because its ties are destroyed (Primary adrenocortical insufficiency). Strictly speaking, the term "Addison's disease" is used to describe the symptoms of Addison's disease only this primary form of adrenocortical insufficiency.
Most sufferers experience tie atrophy with no apparent cause. Physicians suspect a faulty reaction of the immune system, in which the body's own defenses attack the cells of the adrenal glands. Other possible causes are infections, inherited diseases, tumors or bleeding into the adrenal glands (for example, after years of taking anticoagulant medication).
The brain controls the adrenal cortex via messenger substances such as CRH (corticotropin-releasing hormone) or ACTH (adrenocorticotropic hormone). Therefore, brain dysfunction can also inhibit hormone production in the adrenal cortex, such as after a stroke, brain tumors, injury, or surgery (secondary adrenocortical insufficiency).
Long-term use of high-dose cortisone preparations also suppresses the formation in the brain of the messenger substances that stimulate hormone production in the adrenal cortex (tertiary adrenocortical insufficiency). After cortisone therapy is discontinued, the adrenal cortex is extremely slow to start producing hormones again. Therefore, it is important to phase out high-dose cortisone very slowly.
Symptoms of hypofunction in Addison's disease
A deficiency of adrenal cortical hormones normally develops insidiously. Many people with impaired adrenal cortex function have no symptoms under normal living conditions. Only significant physical and physical stress causes symptoms, such as surgery, infection, burns, or severe illness. Presumably, persistent signs of disease do not occur until at least 90 percent of the adrenocortical tie has already been destroyed.
Typical symptoms of Addison's disease are:
Hyperpigmentation (brown discoloration) of skin and mucous membranes: The body responds to cortisol deficiency by producing more melatonin, which is responsible for skin pigmentation. The skin discolors especially in the area of skin folds, scars, nipples, on the extensor sides of arms and legs, over bony elevations and in areas exposed to the sun. Black spots may appear on the forehead, neck, face and shoulders. In exceptional cases, Addison's disease may also lead to white spot disease (vitiligo).