Future Directions in the Study and Management of Congenital Adrenal Hyperplasia due to 21-Hydroxylase Deficiency

Figure 6. Elevations in adrenocorticotropic hormone, increases in neural-adrenomedullary input, and presence of insulin-mediated metabolic input may lead to adrenal hyperandrogenism and premature adrenarche. In turn, adrenal hyperandrogenism, insulin resistance, or both may lead to full-blown polycystic ovary syndrome in a woman with an inherent ovarian vulnerability. ACTH = adrenocorticotropic hormone; CRH = corticotropin-releasing hormone; E = epinephrine; NE = norepinephrine; NPY = neuropeptide Y.
Figure 6. Elevations in adrenocorticotropic hormone, increases in neural-adrenomedullary input, and presence of insulin-mediated metabolic input may lead to adrenal hyperandrogenism and premature adrenarche. In turn, adrenal hyperandrogenism, insulin resistance, or both may lead to full-blown polycystic ovary syndrome in a woman with an inherent ovarian vulnerability. ACTH = adrenocorticotropic hormone; CRH = corticotropin-releasing hormone; E = epinephrine; NE = norepinephrine; NPY = neuropeptide Y. Mechanisms of adrenal hyperandrogenism.

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  1. Ann Intern Med February 19, 2002 vol. 136 no. 4 320-334
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