What is Addison's disease?
To speak of Addison's disease is to talk about adrenal insufficiency. It is not a common pathology. The incidence, or new cases, is 0.83 per hundred thousand people. The prevalence, or number of cases in a general population, is four to six cases per hundred thousand people.
Some time ago, the most common cause of the disease was tuberculosis, which affected the adrenal glands. Currently, as there is greater control over tuberculosis, The most frequent cause is 'idiopathic': an autoimmune origin in which the body attacks the organs themselves.
While the symptoms may appear at any age, It is more common between thirty and eighty years, having its peak of appearance at forty. Like many endocrine diseases, it is more common among women than among men.
Causes of Addison's disease
We have said that talking about Addison's disease is equivalent to adrenal insufficiency; we must understand then what the adrenal glands are and what function they fulfill.
The adrenal glands are two and are located on top of each kidney, in the abdominal cavity. Internally, each of them is made up of two parts:
- Adrenal medulla: It is the internal part of the gland and is responsible for forming hormones with a structure similar to adrenaline.
- Adrenal cortex: It is the outer layer of each gland and has the function of forming corticosteroid hormones. Within the corticosteroids formed here, we can name:
- Glucocorticoids: cortisol is the most relevant, with metabolic, inflammatory and stress response functions.
- Mineralocorticoids: Aldosterone is the main one, which regulates sodium and body potassium.
- Androgens: male sex hormones.
In Addison's disease, the problem lies in the destruction of the cortex of the adrenal glands. Without bark, the body lacks a sufficient amount of cortisol and aldosterone. The symptoms of the pathology are explained, precisely, by the lack of these hormones.
Are causes of destruction of the adrenal cortex:
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Symptoms of the disease
In Addison's disease, symptoms appear insidiously. That is the most common form of presentation. Slowly, different signs become evident but this generates confusion in the diagnosis. Some symptoms go unnoticed or mimic those of other pathologies.
The problem in the delay of the diagnosis is the gravity that can take the evolution of the Addison, putting in serious danger the life of the person who suffers it. Among the most frequent symptoms are:
- Loss of appetite
- Hyperpigmentation of the skin: darkening in certain areas.
- Low blood pressure.
- HypoglycemiaLow blood sugar
- Asthenia: fatigue, lack of strength.
- Muscle pains.
A special presentation of the disease is the acute crisis, where several symptoms of those listed previously appear suddenly. It is an acute adrenal insufficiency. The outcome can be a deadly shock if not treated properly and immediately. The Addisonian crisis is a vital emergency.
To continue reading: The treatment for the different states of shock
Diagnosis and treatment
The way to diagnose Addison's disease is through the measurement of hormone levels. The simplest test is to measure the cortisol and ACTH hormone circulating in the person's blood early in the morning. In the patient with Addison, the measurement of ACTH is high and cortisol is low.
More specific is to stimulate natural cortisol with an artificial ACTH hormone and measure its levels in the blood before and after stimulation. In people with Addison's disease, cortisol does not increase after stimulation with ACTH.
It is essential that, on suspicion, the doctor requests a first measurement of cortisol in blood. If the results are doubtful or inconclusive, the stimulation test should be done with ACTH in a second instance to point to a diagnostic confirmation.
Along with this etiological tracing, the professional will request the measurement of other biochemical parameters that can be altered.
Once the disease is diagnosed, the basic treatment will consist of artificially supplanting the missing hormones.
Synthetic glucocorticoids are indicated to replace cortisol. Aldosterone is replaced with similar steroids, such as fludrocortisone. Finally, the lack of androgens can be treated with a homolog such as dihydroepiandrosterone.