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

Figure 2. The location and nature of each microconversion and the expected clinical phenotype (salt-losing [ ], non-salt-losing [ ], and nonclassic congenital adrenal hyperplasia [ ]) are shown. The 10 exons and 9 introns of are drawn to scale. Arg = arginine; Asn = asparagine; Asp = aspartate; Glu = glutamate; Ile = isoleucine; Leu = leucine; Lys = lysine; Met = methionine; Pro = proline; Trp = tryptophan; Val = valine.
Figure 2. The location and nature of each microconversion and the expected clinical phenotype (salt-losing [ ], non-salt-losing [ ], and nonclassic congenital adrenal hyperplasia [ ]) are shown. The 10 exons and 9 introns of are drawn to scale. Arg = arginine; Asn = asparagine; Asp = aspartate; Glu = glutamate; Ile = isoleucine; Leu = leucine; Lys = lysine; Met = methionine; Pro = proline; Trp = tryptophan; Val = valine. The 10 most common genetic mutations found in 21-hydroxylase deficiency.SLNSLNCCYP21B

This Article

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