Purpose Topical insulin eye drops are used clinically to promote corneal epithelial healing in persistent epithelial defects. Given these benefits, insulin may also aid epithelial recovery in infectious keratitis. However, it remains unclear whether insulin impacts the growth of common ocular pathogens. This study aimed to evaluate the effect of insulin on microbial growth dynamics in vitro.Methods Regular and rapid insulin were tested at 1 IU/mL and 10 IU/mL in tryptic soy broth (TSB) and lubricating eyedrops. A single clinical isolate of each organism (Staphylococcus aureus, Staphylococcus epidermidis, Pseudomonas aeruginosa, Candida albicans, Fusarium spp. and Aspergillus spp.) was included. Preparations with insulin, TSB alone, and Systane alone were inoculated in triplicate. Growth kinetics were assessed by optical density to calculate area under the curve (AUC), lag phase duration, and maximum specific growth rate (mu).Results Insulin at either concentration in TSB did not enhance microbial growth compared to controls. No growth was observed in artificial tear groups.Conclusion Insulin, whether regular or rapid, at 1 IU/mL or 10 IU/mL, did not increase growth of tested pathogens in vitro. These findings suggest that topical insulin unlikely promotes microbial proliferation in vitro and may be considered a potentially safe adjunct, although in vivo validation remains necessary.
Purpose To report a case of bilateral aggressive Mooren's ulcer (MU) requiring hospitalization, multimodal immunosuppression, and anti-tumor necrosis factor (TNF)-alpha biologic switching guided by therapeutic drug monitoring due to anti-adalimumab antibody (AAA) formation.Methods Observational case report prepared in accordance with the CARE guidelines. A 47-year-old man presented to the emergency department with bilateral corneal ulceration and high perforation risk. Comprehensive infectious and autoimmune evaluation was performed. Treatment included topical and systemic corticosteroids, methotrexate, amniotic membrane grafting, tarsorrhaphy, and sequential biologic therapy.Results Bilateral aggressive MU was diagnosed after exclusion of infectious and systemic autoimmune etiologies, including the absence of scleritis. The patient required escalation from adalimumab to infliximab following AAA formation associated with secondary loss of response. Serum adalimumab trough concentration and AAA were measured by enzyme-linked immunosorbent assay (ELISA) at the time of suspected treatment failure. At two-year follow-up on continuous infliximab therapy, the right eye had dense corneal scarring with hand motion vision, while the left eye achieved 20/20 best-corrected visual acuity following cataract extraction during sustained disease quiescence, with no recurrence observed.Conclusion This case illustrates AAA-associated biologic switching in MU-a phenomenon well described in uveitis but not previously reported in peripheral ulcerative keratitis. Therapeutic drug monitoring may have a role in optimizing biologic therapy for severe corneal autoimmune disease.
PURPOSE T-cell-engaging bispecific therapies are increasingly used in hematologic and solid malignancies. This narrative review aims to summarize reported ocular adverse events associated with these therapies, critically evaluate the strength of available evidence, and propose a practical approach to their recognition and management. METHODS A narrative review of published case reports, clinical series, clinical trial safety findings, pharmacovigilance analyses, and U.S. Food and Drug Administration (FDA) safety communications was conducted to identify ocular adverse events associated with T-cell-engaging bispecific therapies. Available evidence was evaluated with emphasis on clinical presentation, potential causality, differential diagnosis, and management considerations. RESULTS Reported ocular events include uveitis and sclerouveitis during teclistamab therapy, orbital inflammation during xaluritamig treatment, and orbital tumor pseudoprogression during elranatamab treatment. A mosunetuzumab pharmacovigilance analysis identified three uveitis reports among 1,154 primary-suspect reports, although these data do not permit estimation of patient incidence. Uveitis was also reported in a clinical trial evaluating mosunetuzumab combined with polatuzumab vedotin. FDA surveillance has identified uveitis as a potential safety signal for teclistamab and elranatamab. Important differential diagnoses include infection, malignant infiltration, cytokine-associated edema, and neurologic causes of visual symptoms. CONCLUSIONS Ocular inflammatory events have been documented during T-cell-engaging bispecific therapy; however, their incidence, causality, and underlying mechanisms remain uncertain. Current evidence supports clinical vigilance but does not establish a class-wide ocular toxicity syndrome. Prompt ophthalmic evaluation of new ocular symptoms and multidisciplinary collaboration between oncologists and ophthalmologists are recommended as reasonable clinical approaches. Standardized monitoring protocols, corticosteroid treatment strategies, and criteria for treatment rechallenge require further prospective investigation.
