Tenascin-X haploinsufficiency associated with Ehlers-Danlos syndrome in patients with congenital adrenal hyperplasia

J Clin Endocrinol Metab. 2013 Feb;98(2):E379-87. doi: 10.1210/jc.2012-3148. Epub 2013 Jan 2.

Abstract

Context: The gene for congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency, CYP21A2, is flanked by the gene encoding tenascin-X (TNXB), a connective tissue extracellular matrix protein that has been linked to both autosomal dominant and autosomal recessive Ehlers-Danlos syndrome (EDS). A contiguous deletion of CYP21A2 and TNXB has been described.

Objective: The objective of the study was to determine the frequency and clinical significance of TNXB haploinsufficiency in CAH patients.

Design, setting, and participants: A total of 192 consecutive unrelated CAH patients being seen as part of an observational study at the National Institutes of Health Clinical Center (Bethesda, MD) were prospectively studied during 2006-2010. Patients were evaluated for clinical evidence of EDS, including cardiac evaluation. DNA was analyzed by PCR, multiplex ligation-dependent probe amplification, Southern blot, and TNXB sequencing. Tenascin-X expression was evaluated by Western blot analysis of fibroblasts and immunostaining of the skin. CAH patients with TNXB haploinsufficiency were compared with age-matched CAH patients with normal TNXB (controls). Phenotyping of 7 parents with TNXB haploinsufficiency was performed.

Main outcome measures: The frequency of TNXB haploinsufficiency among CAH patients and the frequency of EDS symptomatology among CAH patients with TNXB haploinsufficiency and controls.

Results: TNXB haploinsufficiency, here termed CAH-X syndrome, was present in 7% of CAH patients. Twelve of 91 patients carrying a CYP21A2 deletion (13%) carried a contiguous deletion that extended into TNXB. One patient carried a TNXB premature stop codon. Twelve of 13 patients with CAH-X had EDS clinical features. Patients with CAH-X were more likely than age-matched controls to have joint hypermobility (P < .001), chronic joint pain (P = .003), multiple joint dislocations (P = .004), a structural cardiac valve abnormality by echocardiography (P = .02), and reduced tenascin-X expression by Western blot and immunostaining. A subset of parents had clinical findings.

Conclusions: Clinical evaluation for connective tissue dysplasia should be routinely performed in CAH patients, especially those harboring a CYP21A2 deletion.

Publication types

  • Research Support, N.I.H., Intramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adrenal Hyperplasia, Congenital / genetics*
  • Adrenal Hyperplasia, Congenital / physiopathology
  • Adult
  • Aged
  • Child
  • Child, Preschool
  • Ehlers-Danlos Syndrome / genetics*
  • Ehlers-Danlos Syndrome / physiopathology
  • Female
  • Haploinsufficiency*
  • Humans
  • Infant
  • Joint Dislocations / genetics
  • Joint Dislocations / physiopathology
  • Joint Instability / genetics
  • Joint Instability / physiopathology
  • Male
  • Middle Aged
  • Mutation
  • Pain / genetics
  • Pain / physiopathology
  • Steroid 21-Hydroxylase / genetics*
  • Tenascin / genetics*

Substances

  • Tenascin
  • tenascin X
  • Steroid 21-Hydroxylase