PURPOSE: To describe bilateral corneal endothelial abnormalities associated with thalidomide toxicity. METHODS: Observational case report. RESULTS: A 30-year-old man, born with bilateral hypoplastic upper limb defects (phocomelia) caused by thalidomide toxicity, presented with bilateral symmetrical corneal endothelial changes resembling guttata without corneal edema. Pachymetry, specular microscopy, and confocal microscopy were performed. Biomicroscopy findings over a 10-year follow-up showed no changes. CONCLUSIONS: Nonprogressive bilateral corneal endothelial changes resembling cornea guttata should possibly be included in the ocular manifestations of thalidomide toxicity. We postulate that thalidomide may have affected the migration and development of the mesenchymal neural crest cells, which are the developmental precursors of the corneal endothelium and stroma.
PURPOSE: To describe bilateral corneal endothelial abnormalities associated with thalidomidetoxicity. METHODS: Observational case report. RESULTS: A 30-year-old man, born with bilateral hypoplastic upper limb defects (phocomelia) caused by thalidomidetoxicity, presented with bilateral symmetrical corneal endothelial changes resembling guttata without corneal edema. Pachymetry, specular microscopy, and confocal microscopy were performed. Biomicroscopy findings over a 10-year follow-up showed no changes. CONCLUSIONS: Nonprogressive bilateral corneal endothelial changes resembling cornea guttata should possibly be included in the ocular manifestations of thalidomidetoxicity. We postulate that thalidomide may have affected the migration and development of the mesenchymal neural crest cells, which are the developmental precursors of the corneal endothelium and stroma.