Corneal Toxicity Associated With Belantamab Mafodotin Is Not Restricted to the Epithelium: Neuropathy Studied With Confocal Microscopy.
Journal
American journal of ophthalmology
ISSN: 1879-1891
Titre abrégé: Am J Ophthalmol
Pays: United States
ID NLM: 0370500
Informations de publication
Date de publication:
10 2022
10 2022
Historique:
received:
06
04
2022
revised:
12
06
2022
accepted:
13
06
2022
pubmed:
26
6
2022
medline:
28
9
2022
entrez:
25
6
2022
Statut:
ppublish
Résumé
The purpose of this study was to investigate epithelial and neuronal changes in patients with refractory/relapsed multiple myeloma (RRMM) before/during belantamab mafodotin (belamaf) treatment using confocal microscopy. Retrospective case series. RRMM patients underwent best-corrected visual acuity (BCVA) testing and slitlamp examination/photography, followed by corneal confocal microscopy (CCM), to evaluate the epithelium and subbasal nerve plexus (SNP) to measure corneal nerve fiber density (CNFD), branch density (CNBD), and fiber length (CNFL) before and during belamaf treatment. In 14 eyes of 7 patients (4 female, 68 ± 10 years of age) with complete follow-up (4 ± 2 months), the median BCVA dropped from 20/25 (20/25-20/20) to 20/40 (20/200-20/32) in the worse eye at the end of follow-up. Microcystic epithelial changes and ocular surface disease were demonstrated biomicroscopically. CCM showed "grape-like" hyperreflective spots in the central basal epithelium that changed to polymorphous-structured cysts in the superficial epithelium, with no pathology detected at the(peri-)limbal structures. The baseline, normal SNP morphology with a mean CNFD, CNBD, and CNFL of 20.25 ± 7.06/mm This study is the first to illustrate neurotoxic effects of belamaf on the human cornea.
Identifiants
pubmed: 35752319
pii: S0002-9394(22)00245-8
doi: 10.1016/j.ajo.2022.06.009
pii:
doi:
Substances chimiques
Antibodies, Monoclonal, Humanized
0
belantamab mafodotin
DB1041CXDG
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
116-124Informations de copyright
Copyright © 2022 The Author(s). Published by Elsevier Inc. All rights reserved.