Physiopathology of Hypogonadism

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Cushing's disease is characterized by chronic glucocorticoid excess secondary to hypersecretion of adrenocorticotropic hormone (ACTH) and other proopiomelanocortin peptides. It is commonly caused by a pituitary corticotroph adenoma. Hypogonadism is common in Cushing's disease. High levels of glucocorticoids decrease serum testosterone levels in men through several mechanisms (see Fig. 3). Excessive production of glucocorticoids may produce gonadotropin deficiency by acting at the pituitary and hypothalamic levels (58). Two regions of the mouse GnRH promoter (distal and proximal negative glucocorticoid response elements) regulate transcriptional repression by glucocorticoids. Glucocorticoid receptors induce glucocorticoid repression of GnRH gene transcription by their association within a multiprotein complex at the negative glucocorticoid response element (59). In addition, elevated glucocorticoid levels directly suppress testicular function, inducing apoptosis in Leydig cells (60), inhibiting LH receptor signal transduction, decreasing the oxidative activity of 11P-hydroxys-teroid dehydrogenase, and impairing Leydig cell steroidogenesis (61).

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