| Literature DB >> 25899317 |
Hanneke Basart1,2, Annekatrien van de Kar2, Lesley Adès3, Tae-Joon Cho4, Erin Carter5, Saskia M Maas1, Louise C Wilson6, Chantal M A M van der Horst2, Emma M Wade7, Stephen P Robertson7, Raoul C Hennekam1,8.
Abstract
Frontometaphyseal dysplasia (FMD) is a distinctive sclerosing skeletal dysplasia associated with a number of non-skeletal manifestations including hearing loss, cardiac malformations, and stenosis, particularly of the upper airway and urinary tract. Some, but not all, patients have mutations in FLNA causing the condition. Consonant with the X chromosomal location of FLNA males are generally more severely affected than females. FLNA mutations can be detected in 82% of affected males. We describe seven patients (one male, six females) all of whom have the major clinical and radiological features of FMD, but without detectable mutations in FLNA. The females in our cohort are affected to a similar degree as is usually found in males. In addition, all patients have marked keloid formation at various body sites, including the eye, from an early age. Other features that may indicate a different etiology in these patients are the increased frequency of cleft palate, Robin sequence, tracheal stenosis, and mild intellectual disability, which all occur in three of more patients in the present group. All patients are isolated. We hypothesize that the presently reported patients represent further evidence that phenotypes strongly resembling FMD exist that are not accounted for by mutations in FLNA. Since the frequency of several of the manifestations, their sporadic presentations, and the presence of keloid formation differ from the X-linked form of this condition we propose de novo autosomal dominant acting mutations in a gene functionally related to FLNA, underpin this disorder.Entities:
Keywords: Robin sequence; cleft palate; filamin A; frontometaphyseal dysplasia; hypertrophic scar; intellectual disability; keloid; otopalatodigital spectrum disorder
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Year: 2015 PMID: 25899317 DOI: 10.1002/ajmg.a.37044
Source DB: PubMed Journal: Am J Med Genet A ISSN: 1552-4825 Impact factor: 2.802