Expanding the phenotype of a neurofibromatosis type 1-like syndrome: a patient with a SPRED1 mutation and orbital manifestations

Ophthalmic Plast Reconstr Surg. 2009 Sep-Oct;25(5):399-401. doi: 10.1097/IOP.0b013e3181b59eea.

Abstract

A 4-year-old child with no medical history presented for evaluation of a small, palpable nodule near the left inferolateral rim. The lesion had a bluish hue and had been slowly enlarging over the course of several months. MRI of the orbits revealed a heterogenous and infiltrative preseptal and extraconal mass which enhanced with gadolinium, and sphenoid wing dysplasia on the left. A complete ophthalmic and physical examination failed to reveal any other stigmata of neurofibromatosis type 1 (NF1) or neurofibromatosis type 2 (NF2). An incisional biopsy of the palpable mass revealed a plexiform neurofibroma. Molecular sequencing of the NF1 and NF2 genes did not reveal causative mutations. Further investigation revealed a loss of function mutation in SPRED1 on chromosome 15. Although loss of function mutations in the SPRED1 gene are known to cause several dermatologic changes associated with the NF1-like phenotype, to our knowledge, this is the first description of a SPRED1 gene mutation resulting in ophthalmic abnormalities.

Publication types

  • Case Reports
  • Retracted Publication

MeSH terms

  • Adaptor Proteins, Signal Transducing
  • Child, Preschool
  • Chromosomes, Human, Pair 15 / genetics*
  • DNA Mutational Analysis
  • Humans
  • Intracellular Signaling Peptides and Proteins / genetics*
  • Magnetic Resonance Imaging
  • Male
  • Membrane Proteins / genetics*
  • Mutation / genetics*
  • Neurofibromatosis 1 / diagnosis
  • Neurofibromatosis 1 / genetics*
  • Orbital Neoplasms / diagnosis
  • Orbital Neoplasms / genetics*
  • Phenotype
  • Polymerase Chain Reaction

Substances

  • Adaptor Proteins, Signal Transducing
  • Intracellular Signaling Peptides and Proteins
  • Membrane Proteins
  • SPRED1 protein, human