Causes and pathogenesis of chronic adrenal insufficiency
Last reviewed: 23.04.2024
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The most common causes of primary destruction of the adrenal glands include autoimmune processes and tuberculosis, to rare - tumors (angiomas, ganglioneuromas), metastases, infections (fungal, syphilis ). The adrenal cortex breaks down with thrombosis of veins and arteries. Complete removal of the adrenal glands is used to treat the Itenko-Cushing disease, hypertensive disease. Necrosis of the adrenal gland can occur in the syndrome of acquired immunodeficiency in homosexuals.
Over the past decade, there has been an increase in autoimmune involvement of 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 is assumed in this form of the disease, since there are cases of disease in one family and twins. There are cases of the development of the disease in the presence of antibodies to ACTH receptors. 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 possess organ-specificity, but not species, are more common in women. With the course of the disease, the level of autoantibodies may change. A major role in the violation of immunoregulation is given to T-cells: insufficiency of T-suppressors or impaired 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, hypogonadism, bronchial asthma.
With greater frequency occurs the syndrome described in 1926 by Schmidt, in which there is an autoimmune lesion of the adrenal glands, thyroid gland and gonads. In this case, chronic thyroiditis can proceed without signs of impaired gland function and is detected only with the help of organ autoantibodies. Sometimes thyroiditis is accompanied by hypothyroidism or thyrotoxicosis. It is suggested that, despite the difference in the clinical manifestations of immunopathological conditions, there is a single mechanism of aggression against hormone-producing tissues.
[Pathogenesis of chronic adrenal insufficiency
Decrease in the disease Addison production of glucocorticoids, mineralocorticoids and androgens with the adrenal cortex leads to a violation of all types of metabolism in the body. As a result of a shortage of glucocorticoids that provide gluconeogenesis, glycogen stores in muscles and liver decrease, blood glucose and tissue levels decrease. The sugar content in the blood does not change after glucose loading. A flat glycemic curve is characteristic. Patients often develop hypoglycemic conditions. Reducing the level of glucose in tissues and organs leads to adynamia and muscle weakness. Glucocorticoids actively influence the synthesis and catabolism of proteins, manifesting simultaneously anti-catabolic and catabolic effects. With a decrease in the production of glucocorticoid hormones, the synthesis of proteins in the liver is inhibited, and the insufficient formation of androgens weakens the anabolic processes. For these reasons, in patients with chronic adrenal insufficiency, the body weight decreases, mainly due to muscle tissue.
Glucocorticoids significantly affect the distribution of fluid in tissues and the excretion of water from the body. Therefore, in patients, the ability to rapidly remove fluid after a water load is reduced. The change in mental emotional activity in patients with insufficient production of glucocorticoids is caused by the action of ACTH, which affects various processes in the central nervous system.
Patanatomy of chronic adrenal insufficiency
Morphological changes of the adrenal glands in chronic adrenal insufficiency depend on the cause that caused the disease. In the tubercular process, the entire adrenal gland undergoes destruction, with an autoimmune lesion, only the cortical layer. In either case, the process is two-sided. Tuberculosis changes are characteristic, and tubercle bacilli can be detected. An autoimmune process leads to a significant atrophy of the cortex, sometimes to complete extinction. In other cases, there is abundant infiltration of lymphocytes, proliferation of fibrous tissue.