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The IFITM5 Ser40Leu variant can manifest as prenatal Caffey disease.

Jia Ying Celeste YapJiin Ying LimAnju BhatiaVic Khi June TanStephanie KooGen NishimuraShahida MoosaAi Ling KohEne Choo TanNikki FongSaumya Shekhar Jamuar
Published in: American journal of medical genetics. Part A (2023)
We report on a female neonate with a clinico-radiological presentation in keeping with a lethal form of prenatal Caffey disease (PCH). She had antenatal and postnatal features of severely bowed long bones, small chest, diaphyseal hyperostosis and polyhydramnios and died shortly after birth. Initial testing excluded COL1A1-related PCH, as an OI gene panel, consisting of COL1A1, COL1A2, CRTAP, and P3H1 genes, was negative. Targeted sequencing using a gene panel was performed and a de novo heterozygous, likely pathogenic variant in IFITM5: c.119C > T(p.Ser40Leu) was identified, which was previously described to cause a severe form of progressively deforming osteogenesis imperfect (OI). To our knowledge, variants in IFITM5 have not been reported in infantile Caffey disease (ICH) or PCH. Given that the pathogenesis of PCH is largely unknown, we postulate that a subset of PCH may be associated with variants in IFITM5.
Keyphrases
  • copy number
  • pregnant women
  • genome wide
  • early onset
  • healthcare
  • genome wide identification
  • gene expression
  • dna methylation
  • preterm infants
  • single cell
  • transcription factor