Macular atrophy development in patients treated with anti-VEGFs show a clear association with subretinal drusenoid deposits.
Researchers based at New York University School of Medicine have published research confirming an association between subretinal drusenoid deposits (SDD) and macular atrophy (MA) in neovascular AMD patients treated with anti-VEGF medication. The research, conducted on 71 patients with a diagnosis of neovascularisation, but not previously treated with anti-VEGF therapy, showed that SDD was a considerable risk factor in the development of MA. In their study, the researchers reported that, “while only a minority (16%) of eyes with treatment-naïve nAMD had MA at baseline, 51% of eyes lacking MA at baseline developed MA while receiving anti-VEGF therapy”.
The research supports previous investigations of MA in nAMD patients and extends the data to systematically categorize SDD phenotype and location in relation to MA development. The study found that SDD were present in 46 eyes (63%) at baseline measurement and that MA developed in 38 eyes (51%) during the mean of 4.7±1.2 years of follow-up observation. When the data was compared with eyes without SDD, those with SDD at baseline were 3.0 times more likely (95% confidence interval [CI] 1.1–8.5, P=0.0343) to develop MA. In addition, eyes with SDD present in the inferior macula and inferior extramacular fields at baseline were 3.0 times and 6.5 times more likely to develop MA at follow-up compared to eyes without SDD in these locations (95% CI 1.0–8.9, P=0.0461 and 95% CI 1.3–32.4, P=0.0218, respectively). In addition, the research indicated that MA development did not appear to be associated with a specific SDD phenotype, dot or ribbon modality.
While the research paper reviewed current theories around the molecular connection between SDD and MA, the jury still appears undecided in terms of the exact mechanisms of pathology. However, independent of the exact biochemistry at play, the researchers believe that the RPE cells play a critical role in instigating injury to the involved tissues. Consequently, the researcher team proposed “that SDD with their specific morphology, easily recognizable on different imaging modalities, may serve as a clinical biomarker of RPE dysfunction that may help predict eyes at greater risk for MA.” Given the importance and frequency of this issue as reported by clinicians and patients, the availability of a clear measurable biomarker may serve as a valuable tool in clinical management of the disorder. In concluding their studies the New York researchers state that, “the extension of SDD into the inferior fundus, particularly in the inferior extramacular field, appears to be related to subsequent MA development. Histologic studies and accurate SDD and MA models are needed to further refine the biologic relationship between these two clinically important entities”.Back to previous