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1 ria that distinguishes it from the classical 21-hydroxylase deficiency.
2 urs in congenital adrenal hyperplasia due to 21-hydroxylase deficiency.
3 alomas may be homozygous or heterozygous for 21-hydroxylase deficiency.
5 n with congenital adrenal hyperplasia due to 21-hydroxylase deficiency (25 children with the salt-was
6 imates of the gene frequency of nonclassical 21-hydroxylase deficiency, also called attenuated, late-
7 ng the CYP21B and TNX genes, that results in 21-hydroxylase deficiency and a connective-tissue disord
8 ss numbers of affected newborns with classic 21-hydroxylase deficiency by contributing to the early d
9 of congenital adrenal hyperplasia caused by 21-hydroxylase deficiency (CAH) and have performed 8,290
10 7.5 million newborns have been screened for 21-hydroxylase deficiency congenital adrenal hyperplasia
12 rplasia; it is unknown whether patients with 21-hydroxylase deficiency have an increased incidence of
17 d out on plasma samples from 117 adults with 21-hydroxylase deficiency receiving their usual glucocor
19 esterone concentrations for classic (severe) 21-hydroxylase deficiency, the most common type of conge
21 multiple members affected with nonclassical 21-hydroxylase deficiency together with the results of q
22 be a far more common disorder than classical 21-hydroxylase deficiency, which occurs in 1/8,000 birth
23 mens obtained from three other patients with 21-hydroxylase deficiency who had undergone bilateral ad
24 diagnosis of congenital adrenal hyperplasia (21-hydroxylase deficiency) with testicular adrenal rest
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