Causes and pathogenesis of chronic adrenal insufficiency

The most common causes of primary destruction of the adrenal glands include autoimmune processes and tuberculosis, while rare causes include tumors (angiomas, ganglioneuromas), metastases, and infections (fungal, syphilis ). The adrenal cortex is destroyed by thrombosis of veins and arteries. Complete removal of the adrenal glands is used to treat Itsenko-Cushing's disease and hypertension. Adrenal necrosis can occur in acquired immunodeficiency syndrome in homosexuals.

In recent decades, there has been an increase in autoimmune damage to the adrenal glands. In foreign literature, this disease is described as "autoimmune Addison's disease." Autoantibodies to adrenal tissue are found in most patients. A genetic predisposition to this form of the disease is assumed, since there are cases of the disease in one family and in twins. Cases of the disease developing in the presence of antibodies to ACTH receptors are possible. There are numerous publications on the combination of autoimmune Addison's disease with other autoimmune diseases in one family. Autoantibodies to adrenal tissue are immunoglobulins and belong to class M. They are organ-specific, but not species-specific, and are more common in women. As the disease progresses, the level of autoantibodies may change. A major role in the disruption of immunoregulation is given to T cells: insufficiency of T suppressors or disruption of the interaction of T helpers and T suppressors leads to autoimmune diseases. Autoimmune Addison's disease is often combined with other diseases: chronic thyroiditis, hypoparathyroidism, anemia, diabetes mellitus, hypogonadism, bronchial asthma.

The syndrome described by Schmidt in 1926 is more common, in which there is an autoimmune lesion of the adrenal glands, thyroid gland and sex glands. In this case, chronic thyroiditis can proceed without signs of dysfunction of the gland and is detected only with the help of organ autoantibodies. Sometimes thyroiditis is accompanied by hypothyroidism or thyrotoxicosis. It is assumed that, despite the difference in clinical manifestations of immunopathological conditions, there is a single mechanism of aggression against hormone-producing tissues.

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Pathogenesis of chronic adrenal insufficiency

Reduced production of glucocorticoids, mineralocorticoids and androgens by the adrenal cortex in Addison's disease leads to disruption of all types of metabolism in the body. As a result of a deficiency of glucocorticoids that ensure gluconeogenesis, glycogen reserves in muscles and liver decrease, and glucose levels in blood and tissues decrease. Blood sugar levels do not change after glucose loading. A flat glycemic curve is typical. Patients often experience hypoglycemic conditions. Reduced glucose levels in tissues and organs lead to adynamia and muscle weakness. Glucocorticoids actively influence the synthesis and catabolism of proteins, exhibiting both anticatabolic and catabolic effects. With a decrease in the production of glucocorticoid hormones, protein synthesis in the liver is inhibited, and insufficient formation of androgens weakens anabolic processes. For these reasons, patients with chronic adrenal insufficiency experience a decrease in body weight, mainly due to muscle tissue.

Glucocorticoids significantly affect the distribution of fluid in tissues and the excretion of water from the body. Therefore, patients have a reduced ability to quickly remove fluid after a water load. Changes in mental emotional activity in patients with insufficient glucocorticoid production are caused by the action of ACTH, which affects various processes in the central nervous system.

Pathological anatomy of chronic adrenal insufficiency

Morphological changes in the adrenal glands in chronic adrenal insufficiency depend on the cause of the disease. In the tuberculous process, the entire adrenal gland is destroyed, in the case of autoimmune damage - only the cortex. In both cases, the process is bilateral. Tuberculous changes are characteristic, and tuberculosis bacilli can be detected. The autoimmune process leads to significant atrophy of the cortex, sometimes to complete disappearance. In other cases, abundant lymphocyte infiltration and proliferation of fibrous tissue are detected.