ePoster
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Title:
Recombinant human nerve growth factor (rhNGF)-driven corneal wound healing in a pediatric neurotrophic ulcer refractory to conventional treatments
Poster Details
First Author: C. Bonzano ITALY
Co Author(s): C. Bonzano C. Cutolo D. Sindaco R. Scotto C. Traverso
Abstract Details
Purpose:
To report the clinical presentation and the management of a pediatric neurotrophic ulcer refractory to conventional treatments.
Setting:
Eye Clinic, DiNOGMI, University of Genoa and IRCCS San Martino Polyclinic Hospital, Genoa, Italy.
Methods:
Clinical and imaging description of a clinical case. Slit-lamp examination, anterior segment optical coherence tomography (AS-OCT), anterior segment photography and, corneal in-vivo confocal microscopy (IVCM) were performed during the first examination and at each follow-up visit.
Results:
A 7-year-old male presented with a neurotrophic corneal ulcer in his left eye. Biomicroscopy revealed decreased corneal sensitivity, absent corneal reflex, mild ptosis and decreased lacrimation. The medical record revealed a recent diagnosis of pediatric glioma. Preservative-free artificial tears, a therapeutic contact lens and levofloxacin eyedrops 3-times daily were started. Then, topical autologous serum 40%, 6-times daily, was administered for six weeks without any improvement. Therapy was switched to cenegermin eye drops 6-times daily for eight weeks and the complete healing was achieved at the third week. After the cornea healing, epithelial hyperplasia occurred, and it recovered in three months.
Conclusions:
Early diagnosis and prompt management of pediatric neurotrophic ulcers are mandatory to prevent corneal complications such as scarring, perforation, and amblyopia. Until now, treatment approaches have been limited by the absence of treatments targeting the underlying cause. By stimulating nerve regeneration, recombinant human nerve growth factor promotes corneal healing and may eventually lead to a new standard of care for pediatric patients affected by a neurotrophic ulcer.
Financial Disclosure:
None
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