2/17/2024 0 Comments Downloading Joplin 2.12.16Cell proliferation is indicated by an increase in total DNA the resulting adrenocortical hyperplasia participates in the amplified response of the chronically stimulated gland, and the weight of each gland can be greatly increased. Prolonged in vivo stimulation with ACTH leads to an increase in total adrenal protein and RNA synthesis. Over all, the concomitant rise in cortisol and 11 DOC will more than compensate the loss of aldosterone, and eventually create a state of chronic mineralocorticoid excess, best evidenced by the accompanying suppression of the renin plasma levels, a further contribution to the suppression of aldosterone secretion. Two other mineralocorticoids in man, cortisol and 11 deoxycorticosterone (DOC), at the zona fasciculata, will not escape the long-term effect of chronic ACTH excess and their secretion rates will remain elevated in parallel. Chronic ACTH excess leads to chronic adrenal mineralocorticoid excess and low aldosterone levels: after an acute rise, aldosterone plasma levels resume low values after a few days when ACTH is prolonged. Excess adrenal androgens also occur: in females, they will overcompensate the gonadotrophic loss, inducing high testosterone in males, they will not compensate it, inducing low testosterone. Service des Maladies Endocriniennes et Métaboliques, Centre de Référence des Maladies Rares de la Surrénale, Faculté de Médecine Paris Descartes, Université Paris 5, Hôpital Cochin, Paris, FranceĬhronic ACTH excess leads to chronic cortisol excess, without escape phenomenon, resulting in Cushing’s syndrome.
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