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LISBON -- Women who receive long-term glucocorticoid treatment for congenital adrenal hyperplasia due to 21-hydroxylase deficiency are at risk for decreased bone mineral density, Jeremy A. King, M.D., reported in a poster presentation at the 12th International Congress of Endocrinology.
The risk of decreased bone mineral density (BMD) is particularly high among postmenopausal women with the salt-losing form of 21-hydroxylase-deficient congenital adrenal hyperplasia (CAH). The best way to prevent the problem is to avoid oversuppression of adrenal androgens via careful monitoring, said Dr. King of Johns Hopkins University, Baltimore.
Morphologic measurements, serum hormone assays, and BMD assessments were performed in 11 adult women with the salt-losing (SL) form of CAH who had been receiving glucocorticoid replacement therapy since infancy, and in 15 women with the simple virilizing (SV) form of CAH, who had begun glucocorticoid treatment at ages varying from infancy to 22 years. The measurements were also performed in 15 controls, 9 of whom were unaffected sisters (US) of the subjects, and 6 with polycystic ovarian syndrome (PCOS).
Subjects from both CAH groups were significantly shorter than the controls. (See table.) All bone parameters, including Z-score, T-score, and L-spine, were lower in the CAH group.
In addition, levels of 17-hydroxyprogesterone, androstenedione, dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEAS) were also all significantly lower in ...