Choroidal neovascularization (CNV) occurring in the setting of pre-existing geographic atrophy (GA) represents a complex and clinically challenging scenario in age-related macular degeneration (AMD). While anti-vascular endothelial growth factor (anti-VEGF) therapy has revolutionized the management of nAMD, its impact on eyes with coexisting GA remains uncertain. This study aimed to evaluate the anatomical and functional outcomes of intravitreal ranibizumab treatment in patients with unilateral CNV and established GA over a 12-month follow-up period.
Fifty-four eyes from 27 patients were included in this retrospective analysis. All participants had a confirmed diagnosis of GA based on multimodal imaging, including near-infrared (NIR) reflectance and spectral-domain optical coherence tomography (SD-OCT), with lesions measuring at least 1.27 mm² within one disc diameter of the fovea. CNV was classified as subfoveal (66.7%), juxtafoveal (33.3%), or extrafoveal (0%). Treatment consisted of an initial loading phase of three monthly intravitreal ranibizumab injections (0.5 mg/0.05 mL), followed by pro re nata (PRN) retreatment based on recurrence of fluid, hemorrhage, or persistent hyperreflective material on OCT.
At baseline, mean best-corrected visual acuity (BCVA) was 54.41 ± 14.7 ETDRS letters. By month 12, BCVA remained stable in treated eyes (54.81 ± 15.9 letters; p = 0.9), while fellow eyes showed a minor decline (-2 letters; p = 0.3). Central macular thickness (CMT) significantly decreased from 360.11 ± 88.40 μm to 249.00 ± 93.04 μm (p = 0.002), indicating effective control of exudative changes. In contrast, CMT in fellow eyes changed minimally (275.19 ± 43.3 μm to 268.5 ± 29.5 μm; p = 0.4).
Geographic atrophy progressed in both groups: treated eyes showed an increase from 5.42 ± 3.74 mm² to 8.10 ± 5.90 mm² (p < 0.001), while fellow eyes increased from 7.59 ± 5.59 mm² to 10.18 ± 7.88 mm² (p < 0.01). The absolute growth rate was nearly identical (treated: +2.68 mm²; untreated: +2.59 mm²), suggesting that GA expansion is independent of anti-VEGF treatment. A significant inverse correlation was observed between baseline GA area and progression rate (Tau-Kendall: -0.546, p < 0.001), indicating that smaller lesions grow faster. OCT features revealed marked resolution of subretinal fluid (SRF) and intraretinal fluid (IRF), which were present in 77.TACC1 Antibody Purity 7% and 62.ACSM5 Antibody Cancer 9% of cases at baseline, respectively, but reduced to 11.PMID:35239546 1% and 33.3% at month 12. Hyperreflective material (HRM), initially predominantly subretinal and undefined (70.3%), evolved into well-defined, sub-RPE deposits by month 12—consistent with ongoing tissue remodeling and repair processes.
Subfoveal choroidal thickness (SCT) remained stable in both eyes (treated: 143.11 ± 69.9 μm to 141.7 ± 87.3 μm; p = 0.9; fellow: 128.5 ± 73.2 μm to 123.7 ± 80.3 μm; p = 0.8), suggesting no significant effect of treatment on choroidal structure.
These findings demonstrate that anti-VEGF therapy effectively reduces exudation and stabilizes vision in eyes with CNV and pre-existing GA. The parallel progression of GA in treated and untreated eyes strongly argues against a causative role for anti-VEGF agents in accelerating atrophy. Instead, the data support the view that GA progression is driven by underlying AMD pathology rather than treatment-related factors. Future studies with extended follow-up are needed to assess long-term outcomes and potential cumulative effects of repeated injections.MedChemExpress (MCE) offers a wide range of high-quality research chemicals and biochemicals (novel life-science reagents, reference compounds and natural compounds) for scientific use. We have professionally experienced and friendly staff to meet your needs. We are a competent and trustworthy partner for your research and scientific projects.Related websites: https://www.medchemexpress.com