Belantamab-mafodotin

Abstract

Superficial keratopathy: 2 case reports In a report, a 56-year-old man and a 77-year-old man was described who developed superficial keratopathy during treatment with belantamab mafodotin for relapsed and refractory multiple myeloma (RRMM). Case 1: A 56-year-old man, who had a history of hypertension and type 2 diabetes mellitus, was diagnosed with RRMM. He showed no response to multiple prior therapies three and a half years prior. Therefore, he started receiving belantamab mafodotin infusion 2.5 mg/kg (day 0). Subsequently, he was referred for baseline evaluation which showed no ocular symptoms, previous ocular disease or surgery. He received second infusion on day 21. One week after the second infusion, he reported visual loss in both eyes (OU), ocular discomfort, blurriness and dryness in eyes. At the follow-up visit on day 42, his pinhole visual acuity (VA) had decreased in OU. Slit lamp examination (SLE) showed a ring-shaped, moderate amount of superficial keratopathy in the form of diffuse microcystic-like epithelial changes (MECs) in the paracentral cornea in OU. The central portion of the cornea was clear in OU. At the same time, corneal topography revealed irregular astigmatism which was greater in right eye (OD) than in left eye (OS). Anterior segment optical coherence tomography (AS-OCT) showed increased heterogeneous signal intensity and hyperreflective lesions in the paracentral corneal epithelium with uninvolved central cornea. Several disruptions in the line of the Bowman’s layer (BL) were observed in OD. In addition, the mean of the full corneal epithelial thickness (CET) increased. The indicated bilateral corneal findings were recorded as grade 2 superficial keratopathy. Therefore, the third infusion was withheld. He was treated with prednisolone acetate and preservative-free artificial tears. Despite profound changes observed in OD compared to OS, MECs clinically improved. After discussion with the hematology team, he received the third dose of belantamab mafodotin on day 62. At the most recent visit on day 82, there was residual mild superficial keratopathy in OU, which improved further with prednisolone acetate. Except for corneal epithelium and BL, no abnormality of the stromal layer or other components of the cornea in OU was observed on OCT throughout the clinical course. Case 2: A 77-year-old man, who had a history of anaplastic large cell non-Hodgkin’s lymphoma and RRMM, was referred for ophthalmic evaluation before belantamab mafodotin administration. He was initially treated with multiple unspecified therapies. On current presentation, baseline evaluation revealed normal VA in OU, clear corneas and no abnormality of the anterior and posterior segments except mild nuclear sclerosis. He denied any ocular symptoms, previous ocular disease or surgery. He received the first belantamab mafodotin infusion 2.5 mg/kg (day 0) and the second infusion on day 21. Subsequently, one week after the second infusion, he reported bilateral decrease in his vision despite using preservative-free artificial tears. At the follow-up visit on day 41, his pinhole VA had decreased in OU. An SLE and VA assessment showed grade 2 diffuse superficial keratopathy with involvement of the entire cornea in OU. The findings were more severe in the peripheral cornea. AS-OCT revealed increased heterogeneous signal intensity and hyperreflective lesions in the corneal epithelium in the paracentral region in OU, which was more severe in OD. The mean of full CET also increased in OD, while there was no change in OS. Therefore, his belantamab mafodotin infusions were held. There were no abnormal findings in corneal stroma or other components of the cornea except corneal epithelium, and no changes in corneal thickness without CET was observed in OU throughout the clinical cause. Given the decreased vision with moderate diffuse superficial keratopathy in OU, he was treated with prednisolone acetate and artificial tears. He did not experience any other AEs during his follow-up.