Intravitreal TNF-α Inhibition in Extensive Macular Atrophy with Pseudodrusen-Like Appearance (EMAP): A Real-World Cohort Study

Purpose To evaluate visual function, visual field preservation, and structural retinal stability in patients with Extensive Macular Atrophy with Pseudodrusen-like Appearance (EMAP) treated with intravitreal adalimumab, a tumor necrosis factor–alpha (TNF-α) inhibitor, in a real-world clinical setting. Methods This retrospective, observational cohort study included adult patients with a clinical diagnosis of EMAP who received three intravitreal injections of adalimumab (2 mg/0.05 mL) at baseline, Month 2, and Month 4. Best-corrected visual acuity (BCVA, logMAR) and automated perimetry parameters—Mean Deviation (MD), Pattern Standard Deviation (PSD), and Field Preservation Deviation Index (FPDI)—were analyzed using paired pre–post comparisons over a 6-month follow-up. Structural outcomes assessed ellipsoid zone (EZ) integrity and central macular thickness on optical coherence tomography (OCT). Full-field electroretinography (ERG) with 30-Hz flicker stimulation was used as a surrogate marker of macular cone function. Nonparametric statistics were applied due to non-normal data distribution. Results Nineteen patients (36 eyes) with paired BCVA data were analyzed. Mean BCVA remained stable from baseline (1.05 ± 0.48 logMAR) to follow-up (1.02 ± 0.42 logMAR), with a mean change of − 0.04 ± 0.25 logMAR (p = 0.28). Clinically, 19.4% of eyes showed a ≥ 0.2 logMAR gain, while 5.6% worsened, and 75% remained stable. Visual field analysis demonstrated no significant changes in MD, PSD, or FPDI, with a modest trend toward functional preservation. OCT analysis showed no significant progression of macular atrophy, EZ disruption, or changes in central macular thickness. ERG flicker responses remained stable in eyes with measurable signals. Conclusions In this real-world EMAP cohort, intravitreal adalimumab was associated with overall functional and structural stability over 6 months, without evidence of accelerated deterioration. These findings support the ocular safety and potential stabilizing role of TNF-α inhibition in EMAP and provide preliminary data to inform future controlled trials targeting inflammatory mechanisms in degenerative macular diseases.