Broadening the Spectrum of Ehlers Danlos Syndrome in Patients With Congenital Adrenal Hyperplasia

J Clin Endocrinol Metab. 2015 Aug;100(8):E1143-52. doi: 10.1210/jc.2015-2232. Epub 2015 Jun 15.

Abstract

Context: The contiguous gene deletion syndrome (CAH-X) was described in a subset (7%) of congenital adrenal hyperplasia (CAH) patients with a TNXA/TNXB chimera, resulting in deletions of CYP21A2, encoding 21-hydroxylase necessary for cortisol biosynthesis, and TNXB, encoding the extracellular matrix glycoprotein tenascin-X (TNX). This TNXA/TNXB chimera is characterized by a 120-bp deletion in exon 35 and results in TNXB haploinsufficiency, disrupted TGF-β signaling, and an Ehlers Danlos syndrome phenotype.

Objective: The objective of the study was to determine the genetic status of TNXB and resulting protein defects in CAH patients with a CAH-X phenotype but not the previously described TNXA/TNXB chimera. Design, Settings, Participants, and Intervention: A total of 246 unrelated CAH patients were screened for TNXB defects. Genetic defects were investigated by Southern blotting, multiplex ligation-dependent probe amplification, Sanger, and next-generation sequencing. Dermal fibroblasts and tissue were used for immunoblotting, immunohistochemical, and coimmunoprecipitation experiments.

Main outcome measures: The genetic and protein status of tenascin-X in phenotypic CAH-X patients was measured.

Results: Seven families harbor a novel TNXB missense variant c.12174C>G (p.C4058W) and a clinical phenotype consistent with hypermobility-type Ehlers Danlos syndrome. Fourteen CAH probands carry previously described TNXA/TNXB chimeras, and seven unrelated patients carry the novel TNXB variant, resulting in a CAH-X prevalence of 8.5%. This highly conserved pseudogene-derived variant in the TNX fibrinogen-like domain is predicted to be deleterious and disulfide bonded, results in reduced dermal elastin and fibrillin-1 staining and altered TGF-β1 binding, and represents a novel TNXA/TNXB chimera. Tenascin-X protein expression was normal in dermal fibroblasts, suggesting a dominant-negative effect.

Conclusions: CAH-X syndrome is commonly found in CAH due to 21-hydroxylase deficiency and may result from various etiological mechanisms.

Trial registration: ClinicalTrials.gov NCT00250159.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, N.I.H., Intramural

MeSH terms

  • Adolescent
  • Adrenal Hyperplasia, Congenital / complications*
  • Adrenal Hyperplasia, Congenital / epidemiology
  • Adrenal Hyperplasia, Congenital / genetics
  • Adult
  • Aged
  • Child
  • Child, Preschool
  • Cohort Studies
  • Ehlers-Danlos Syndrome / classification*
  • Ehlers-Danlos Syndrome / complications*
  • Ehlers-Danlos Syndrome / epidemiology
  • Ehlers-Danlos Syndrome / genetics
  • Female
  • Humans
  • Infant
  • Male
  • Middle Aged
  • Phenotype
  • Young Adult

Supplementary concepts

  • Congenital adrenal hyperplasia due to 21 hydroxylase deficiency

Associated data

  • ClinicalTrials.gov/NCT00250159