Background: Mirvetuximab soravtansine (MIRV) improves outcomes in FRα-positive, platinum-resistant ovarian cancer; however ocular adverse events (OAEs), particularly corneal epithelial toxicity, are frequent and warrant structured ophthalmologic monitoring. Methods: In this retrospective observational study, 31 consecutive patients receiving MIRV for FRα-positive gynecologic malignancies underwent standardized ophthalmic assessments at baseline and prior to each treatment cycle (every 21 days). The protocol included best corrected visual acuity (BCVA), slit-lamp biomicroscopy, anterior-segment optical coherence tomography (AS-OCT), corneal topography, and tear film analysis. OAEs were graded according to the Common Terminology Criteria for Adverse Events (CTCAE) v5.0, based on symptom severity and functional impairment. Results: OAEs occurred in all patients (31/31, 100%), predominantly grade 1–2. Corneal epithelial toxicity was documented in 28/31 patients (90.3%), while no grade ≥ 3 events were observed. Symptoms typically developed 7–14 days after the second infusion. AS-OCT and corneal topography consistently revealed epithelial microcysts and surface irregularities, which were usually detected during scheduled pre-cycle ophthalmologic evaluations. Tear-film instability (break-up time ≤ 5 s) developed in 19/31 patients (61.3%), generally within 10 days after the second infusion, and improved in all but 2 patients (6.5%) following prophylactic lubrication. Transient refractive changes occurred in 28/31 patients (90.3%) and were associated with a temporary BCVA reduction (mean nadir ~20/32 Snellen), followed by recovery during follow-up. Conclusions: MIRV-related ocular alterations are frequent but reversible and clinically manageable. Multimodal imaging combined with functional and refractive assessment provides sensitive markers of corneal epithelial toxicity and supports integrated ophthalmologic monitoring to preserve visual function and maintain oncologic treatment continuity.

Background/Objectives: Nicotinamide (NAM), a form of vitamin B3 and precursor of nicotinamide adenine dinucleotide (NAD), has emerged as a potential metabolic and neuroprotective strategy in glaucoma. This systematic review aimed to evaluate the available human evidence on NAM-containing and NAD-targeted strategies in glaucoma, integrating interventional, observational, and mechanistic evidence with particular attention to clinical outcomes, methodological quality, and safety. Methods: A systematic literature search was conducted in PubMed, Scopus, and the Cochrane Central Register of Controlled Trials (CENTRAL), with the search updated through 22 August 2026. Eligible studies included randomized and non-randomized interventional studies evaluating NAM-containing or NAD-targeted supplementation strategies, as well as observational human studies investigating NAM/NAD-related biomarkers or mitochondrial metabolic alterations in relation to glaucoma. Risk of bias was assessed according to study design using RoB 2 for randomized trials, ROBINS-I for non-randomized interventional studies, and a domain-based assessment for observational exposure and biomarker studies. Owing to substantial clinical and methodological heterogeneity, findings were synthesized narratively without quantitative pooling. Results: Thirteen eligible reports representing eight unique human studies were included. Randomized trials provided preliminary evidence that NAM-containing interventions may produce short-term functional and electrophysiological effects. NAM supplementation was associated with improvement in inner retinal electrophysiological function in randomized crossover studies, whereas effects on visual field outcomes were inconsistent. A trial combining NAM with pyruvate reported favorable short-term visual field changes, although the specific contribution of NAM could not be isolated. Non-randomized studies provided complementary evidence on vascular, metabolic, structural, electrophysiological, and patient-reported outcomes but were limited by potential confounding and uncontrolled study designs. Observational studies reported associations between glaucoma and altered circulating NAM concentrations and systemic mitochondrial dysfunction. Available studies were generally small and of limited duration, and the evidence was insufficient to establish sustained neuroprotection or modification of glaucoma progression. Conclusions: Human evidence supports the biological plausibility of targeting NAM/NAD metabolism in glaucoma and provides preliminary signals of short-term biological and functional effects. However, current evidence remains insufficient to support routine high-dose NAM supplementation in clinical practice. Larger, adequately powered, long-term randomized controlled trials are required to establish sustained efficacy, optimal dosing, patient selection, and long-term safety.