Cushing’s glucocorticoid syndrome in the practice of a rheumatologist (A review of literature)

Abstract

Glucocorticoids (GCs) are used to treat different inflammatory and autoimmune diseases due to their anti-inflammatory and immunoregulatory properties. However, GC may lead to the development of many adverse reactions (ARs): hypertension, diabetes mellitus, lipid metabolic disturbances, sleep apnea, osteoporosis, myopathy, and coagulation and fibrinolysis disorders, which are components of the Itsenko – Cushing syndrome. ARs induced by GCs are known to depend on their composition, route of administration, dose, and duration of treatment. However, the major pathogenic mechanisms of ARs are not clearly defined. There is evidence suggesting a role for imbalance between vasoconstriction and vasodilation, and its possible association with nitric oxide, prostanoids (prostaglandins, prostacyclin, and thromboxane), angiotensin II, vasopressin, arginine, endothelins, catecholamines, neuropeptides Y, and atrial natriuretic peptide. Enhanced oxidative stress, activated reninangiotensin system, escalating pressor response, metabolic syndrome, and sleep apnea also make their contribution. It could be ideal to discontinue GC treatment; but this is most commonly impossible because of a further disease exacerbation. In addition, it is necessary to carefully plan the choice of the dose, time, and route of administration of GCs and to evaluate each AR. The design of a GC with marked anti-inflammatory activity and insignificant metabolic effects must hold a central position in its researches.