Two brothers with non-classical 21-hydroxylase deficiency: to treat or not to treat?

Horm Res. 2004;62(5):241-4. doi: 10.1159/000081622. Epub 2004 Oct 18.

Abstract

Variations in phenotype in 21-hydroxylase deficiency (21OHD) have cautioned against initiating treatment in the absence of abnormal clinical features. We report 2 Caucasian brothers with compound heterozygous mutations of the CYP21 gene and mild clinical and biochemical features of late-presenting 21OHD. The index case presented aged 8.5 years with mild genital virilization and bone age advanced by 5 years. Elevated basal and synacthen-stimulated 17-hydroxyprogesterone (17OHP; 22.4 and 246 nmol/l) and androstenedione (10.9 and 19.9 nmol/l) levels confirmed 21OHD. His younger brother was investigated at age 7.3 years, and although examination showed normal pre-pubertal genitalia, basal and synacthen-stimulated 17OHP (32.4 and 281 nmol/l) and androstenedione (6.2 and 9.0 nmol/l) were abnormal, and bone age was advanced by 1.5 years. Because of actual or incipient virilization, both patients were treated with glucocorticoid replacement 8-12 mg/m(2)/day. This decision is discussed in the context of published guidelines for the management of 21OHD.

Publication types

  • Case Reports

MeSH terms

  • Adrenal Hyperplasia, Congenital / drug therapy*
  • Adrenal Hyperplasia, Congenital / enzymology*
  • Adrenal Hyperplasia, Congenital / genetics
  • Bone Development
  • Child
  • Genotype
  • Heterozygote
  • Humans
  • Hydrocortisone / therapeutic use
  • Male
  • Mutation
  • Phenotype
  • Sexual Maturation
  • Steroid 21-Hydroxylase / genetics*
  • Steroid 21-Hydroxylase / metabolism*

Substances

  • Steroid 21-Hydroxylase
  • Hydrocortisone