Octave, French physician, 1874-1938. See: Crouzon disease, Crouzon syndrome.
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To the Editor: Crouzon Syndrome (CS), also known as craniosynostosis, is an autosomal dominant genetic disorder linked to single-gene mutation of fibroblast growth factor receptor 2 ( FGFR2 ).[1],[2],[3] The premature fusion of certain skull bones results in a serial of dysmorphic features including underdeveloped maxilla, protruded mandible, shallow orbits, proptosis, and beaked nose.
Steve, from Sunderland, was born with the genetic condition Crouzon Syndrome, which affects the shape of his head and face.
Meanwhile, 31-year-old Steve, who has Crouzon Syndrome, finds himself back on the dating circuit once more.
In 165 cases, there were 38 cases of unilateral coronal synostosis, 127 cases of bilateral deformity, and 45 cases of Crouzon syndrome.
Mutations in FGFRs can also cause several syndromes such as Apert and Crouzon syndromes.
Crouzon syndrome should be differed by hypertelorism, parrot-beaked nose, short upper lip, hypoplastic maxilla, and a relative mandibular prognathism [16].
Craniosynostosis syndromes including Apert, Crouzon, Pfeiffer, Jackson-Weiss, and Beare-Stevenson syndromes, and FGFR2-related isolated coronal synostosis occur as a result of FGFR2 gene mutations localized in the 10q25.3-26 locus (2).
Upper airway endoscopy to optimize obstructive sleep apnea treatment in Apert and Crouzon syndromes.
Variants in FGFR3 have been observed in 100% of individuals with Crouzon syndrome with acanthosis nigricans and in 100% of individuals diagnosed with Muenke syndrome.
The aim of this study was to determine FGFR2 gene mutations in 85 craniosynostosis cases including Apert, Pfeiffer, and Crouzon syndromes, and isolated craniosynostosis patients who were referred to molecular genetics laboratory of Medical Genetics Department, Ege University between 2010 and 2016.
Triplets born with Crouzon syndrome, a genetic disorder characterized by the fusion of skull bones, affecting the shape of the head and face.