The spectrum of clinical, hormonal and molecular findings in 280 individuals with nonclassical congenital adrenal hyperplasia caused by mutations of the CYP21A2 gene

Clin Endocrinol (Oxf). 2015 Apr;82(4):543-9. doi: 10.1111/cen.12543. Epub 2014 Aug 3.

Abstract

Background: Nonclassical congenital adrenal hyperplasia (NC-CAH) is caused by mutations of the CYP21A2 gene. The clinical manifestations and hormonal derangements of NC-CAH are quite variable.

Objectives: (i) To define the phenotype and its relation to genotype according to gender and age and (ii) to evaluate the validity of currently applied hormonal criteria for establishing the diagnosis of NC-CAH.

Patients and methods: The clinical, hormonal and molecular data of 280 subjects (235 female) with NC-CAH and a median age of 17·6 years were analysed. CYP21A2 genotyping was performed in all subjects.

Results: The majority of females aged less than 8 years presented with premature pubarche (88·3%), while those older than 8 presented with a polycystic ovary-like phenotype (63·2%). A total of 7·7% of the females and 51·1% of the males were asymptomatic at the time of diagnosis. In the total group, 50·4% of the subjects were compound heterozygotes for one classical (C) and one nonclassical (NC) mutation, while 46% of the alleles studied carried the p.V281L mutation. Basal 17OHP values were below 6 nm (2 ng/ml) in 2·1% of the subjects with NC-CAH, but none had peak 17OHP values post-ACTH lower than 30 nm (10 ng/ml).

Conclusions: NC-CAH has a variable phenotype depending on the age, gender and the presence of a classical mutation. A peak cut-off value of 17OHP post-ACTH lower than 30 nm excludes the diagnosis of NC-CAH, whereas basal 17OHP <6 nm may represent a false-negative result. A significant number of patients harboured a classical mutation, a finding which requires genotyping of the partner for genetic counselling.

MeSH terms

  • Adolescent
  • Adrenal Hyperplasia, Congenital / genetics*
  • Adult
  • Aged
  • Alleles
  • Child
  • Child, Preschool
  • Female
  • Genotype
  • Heterozygote
  • Humans
  • Infant
  • Male
  • Middle Aged
  • Mutation*
  • Phenotype
  • Polycystic Ovary Syndrome / physiopathology
  • Steroid 21-Hydroxylase / genetics*
  • Young Adult

Substances

  • CYP21A2 protein, human
  • Steroid 21-Hydroxylase