Adrenocortical hyperresponsivity to adrenocorticotropic hormone: a mechanism favoring the normal production of cortisol in 21-hydroxylase-deficient nonclassic.

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Presentation transcript:

Adrenocortical hyperresponsivity to adrenocorticotropic hormone: a mechanism favoring the normal production of cortisol in 21-hydroxylase-deficient nonclassic adrenal hyperplasia Raquel Huerta, M.D., Didier Dewailly, M.D., Christine Decanter, M.D., Eric S Knochenhauer, M.D., Larry R Boots, M.D., Ricardo Azziz, M.D. Fertility and Sterility Volume 74, Issue 2, Pages 329-334 (August 2000) DOI: 10.1016/S0015-0282(00)00631-2

Figure 1 Basal (Steroid0) and ACTH-(1-24)-stimulated (Steroid60) levels of 11-deoxycortisol (S) and cortisol (F) in 24 patients with 21-hydroxylase deficient nonclassic adrenal hyperplasia (NCAH) and 37 controls. Depicted are the median values, and brackets represent the range. A statistically significant difference in the basal and stimulated levels between NCAH and controls is observed for S, but not F. Huerta. Adrenocortical hyperresponsivity. Fertil Steril 2000. Fertility and Sterility 2000 74, 329-334DOI: (10.1016/S0015-0282(00)00631-2)