Addison's disease occurs when the adrenal cortex is impaired. This disease is diagnosed both in men and in women, mainly of middle age (from 30 to 40 years). This is a fairly rare disease that is recorded in one person per 100 thousand people. Addison Birmer's disease can develop as a result of autoimmune processes, infectious diseases (syphilis, adrenal tuberculosis and typhoid), as well as in amyloidosis and malignant tumors. In 70% of patients, the disease occurs due to malfunctions in the immune system (antibodies begin to take body cells for foreign bodies, attack and destroy them). When cells of the adrenal cortex are destroyed, the synthesis of gluco- and mineralocorticoids (cortisol, 11-deoxycorticosterone, aldosterone) decreases. Scientists have proven that glucocorticoids regulate a variety of biochemical processes in the body (regulates blood pressure, insulin concentration, is involved in the regulation of protein, lipid and carbohydrate synthesis).
Often hypocorticism is observed in patients taking hormones of the adrenal cortex. In most cases, the etiology of the disease remains unclear. Adrenal insufficiency is classified into primary and secondary. Primary insufficiency develops with damage to the adrenal tissue, and secondary - due to insufficient stimulation of their adrenocorticotropic hormone.
Addison's disease: symptoms
Clinical signs of the disease are due to a lack of mineral and glucocorticoids in the body. The most characteristic signs are adynamia, hypotension, dysfunction of the gastrointestinal tract (nausea, decreased appetite, vomiting, constipation, which are often replaced by diarrhea). In some patients, hypochlorhydria is observed.
Addison's disease is accompanied by increased irritability or depression, frequent headaches and insomnia. A chest x-ray shows a decrease in heart size. An electrocardiogram records signs of hyperkalemia (increased blood potassium concentration). Skin pigmentation does not reflect the severity of the disease, however, an increase or decrease in its treatment indicates the effectiveness of therapeutic actions.
Addison's disease with secondary origin is characterized by less severe symptoms. Very rarely, the disease manifests itself without skin pigmentation (the so-called "white addison"). The main cause of this disease is adrenal tuberculosis. In the absence of appropriate treatment, Addison's disease is complicated. Clinical signs are aggravated: nausea, vomiting, diarrhea, blood pressure decreases sharply, the concentration of potassium in the blood increases. In the peripheral blood, the amount of residual nitrogen, the number of red blood cells, and the hemoglobin content increase. Therefore, if the patient is not provided with timely assistance during the Addison crisis, he dies with signs of renal and cardiovascular failure.
The most significant laboratory parameters for diagnosis are the content of 17-ACS in plasma and 17-CS in the urine, as well as a decrease in blood glucose. A morphological blood test indicates lymphocytosis, eosinophilia, and delayed ESR.
Addison's disease is differentiated from the following diseases: bronze diabetes, pellagra, poisoning with arsenic, bismuth and argentum. This disease, as a rule, has a chronic course with periodic exacerbation. The severity of Addison Birmer's disease is determined by the severity of the main signs of the disease, as well as by the number of drugs that are necessary to compensate for adrenal insufficiency.