Abstract
Deficient 17α-hydroxylation precludes formation of cortisol in the adrenal glands and of sex steroids in the gonads in man, which results in elevated plasma concentrations of deoxycorticosterone (DOC) and corticosterone (B), hypertension, hypokalemia, and suppression of renin and aldosterone production. Subnormal aldosterone levels before and after treatment have suggested an additional enzymatic defect in its formation. To examine this possibility, we studied six patients untreated, on glucocorticoid treatment, and off treatment for short periods of time. To determine the zonal origins of the mineralocorticoid hormones, we measured plasma aldosterone, DOC, B, 18-hydroxycorticosterone (18-OHB), 18-hydroxydeoxycorticosterone, and cortisol along with renin and potassium concentrations at 0800 h and during posture, angiotensin III, and cosyntropin stimulation; after overnight dexamethasone suppressions; and every 4 h during a 24-h period. Elevated DOC (mean ± SEM, 266.7 ± 63.4 ng/dl), B (12,640 ± 3,610 ng/dl...
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: The Journal of Clinical Endocrinology & Metabolism
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
