BELANTAMAB TOXICITY MIMICKING KERATOCONUS PROGRESSION

To report belantamab mafotidin ocular toxicity as a cause of pseudo-progression in keratoconus

Belantamab Mafodotin, is a monoclonal antibody-drug conjugate developed for the treatment of relapsed multiple myeloma, demonstrating a clinical response. However, ocular toxicity, such as corneal microcyst-like epithelial changes (MECs) has been observed. This modifies anterior corneal profile by an epithelial thickening, mimicking an ectatic corneal progression when only anterior elevation corneal tomographic maps are used.

The aim is to emphasize the importance of considering the corneal posterior tomographic parameters assessment in the right evaluation of keratoconus. 

Based on the patient´s clinical examinations and follow-up performed in Valladolid Clinical University Hospital, Spain.

A 62-year-old caucasian male with a history of multiple myeloma refractory to five lines of treatment, was referred for ophthalmic evaluation. He was previously diagnosed with keratoconus and after a complete ocular examination, it was decided to start belamaf. 

Baseline ocular exam was significant for Fleischer ring, Vogt striae and subepithelial scarring in both eyes. His best corrected visual acuity (BCVA) with Snellen charts was 0.6 and 0.7 in the right eye (OD) and left eye (OS), respectively.

Ophthalmological follow-up examiantions were performed before each therapeutic cycle. Following the second dose, slit-lamp biomicroscopy revealed multiple bilateral MECs characterized as mild in the periphery and distributed more densely in the inferior cornea. Therapy was maintained looking for a response due to an aggressive form of myeloma.

After the third dose, his BCVA decreased to 0.3 in OU. MECs progressed centripetally and a whorl-like pattern was detected in both corneas. Additional symptoms of ocular discomfort were also experienced.

Corneal elevation tomography, performed with Galilei® G6, showed an increase in keratometric values, with a difference of more than 3 Dioptres (D) in the cone region comparing to the baseline values, what appeared to be a keratoconus progression. Examination showed a thickening in thinnest corneal pachymetry of 13 microns in OD and 17 microns in OS. However, there were no significant changes in posterior elevation corneal maps. AS-OCT confirmed the origin of the epithelium in these changes. These findings allowed to assume that MECs and epithelium changes were the main cause in these topographic changes.

The patient discontinued the treatment not only by his ocular events but also because of myeloma progression. Unfortunately, he passed away weeks later.

Belantamab is associated with significant ocular toxicity. All these changes are reversible when drug is stopped. 

MECs caused by Belantamab may modify epithelial microstructure. These changes can origin modifications in corneal tomography which mimic keratoconus progression. Imaging of the posterior corneal surface by elevation topography scan is useful to differentiate a true progression.