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• W4387586556 abstract "Cushing’s syndrome is a rare, chronic condition characterized by elevated cortisol levels. Among the many complications associated with the disease, a state of mineralocorticoid excess has been observed due to the enzymatic saturation of type 2 11β-Hydroxysteroid dehydrogenase (11bHSD2) exerted by the excess of circulating glucocorticoids, which in turn allows the binding of cortisol to the mineralocorticoid receptor. The subsequent inappropriate activation of the mineralocorticoid axis induces several alterations in hydro-saline homeostasis, resulting in increased water and sodium retention – with a concomitant increase in blood pressure levels and increased potassium excretion and metabolic alkalosis. Hypertension is one of Cushing syndrome’s most characteristic and frequent complications, its pathogenesis being complex and multifactorial. It has also been shown to be a risk factor for increased mortality in patients with Cushing’s syndrome: therefore, treatment must be initiated early and primarily involves the resolution of hypercortisolism through surgery and eventually cortisol-lowering medical therapy; if the regression of hypertension is not achieved, adjuvant antihypertensive treatment is advocated. Hypokalemia is a less frequent finding – mainly associated with the most severe forms of the disease, as in the case of ectopic ACTH secretion – but it is no less critical, as it can lead to potentially fatal cardiac conduction alterations. Similarly, the first therapeutic approach consists of the swift resolution of hypercortisolism, accompanied by potassium supplements and, possibly, treatment with mineralocorticoid receptor antagonists." @default.
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• W4387586556 date "2023-01-01" @default.
• W4387586556 modified "2023-10-14" @default.
• W4387586556 title "Hydrosaline Alterations in Cushing Disease" @default.
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• W4387586556 doi "https://doi.org/10.1007/978-3-031-27119-9_15" @default.
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