The following transcript has been edited for clarity.

Patricio G. Schlottmann, MD: We are here with Alessandro Feo, MD, another of our international speakers invited to our national retina meeting here in Ushuaia, Argentina. Alessandro, you gave some beautiful talks and introduced for many the concept of EMAP. Can you tell us a little bit more about it—what it means, where it comes from?

Alessandro Feo, MD: Absolutely. Thank you so much, Dr. Schlottmann. It’s an honor to be here in Ushuaia today for this amazing and extremely beautiful conference here in Tierra del Fuego, Argentina.

So EMAP, or extensive macular atrophy with pseudodrusen-like appearance, was first described nearly 20 years ago, in 2009, by a French group as a separate disease—as a potentially distinct macular dystrophy.¹ That’s what the French authors initially hypothesized. However, during the following 15 years, mainly French and Italian groups have described and reported this disease in Europe. And nowadays, we are seeing increasing descriptions of this disease also outside of Europe. For example, in South America, Brazil, but also in Asia, in Japan. The main characteristic of this disease include vertical macular atrophy, pseudodrusen-like deposits, and negative genetic testing in conjunction. Together, with new descriptions from the United States that were actually the main focus of my talk, these are indicating that EMAP may actually represent a variant or subtype of late atrophic age-related macular degeneration (AMD) because the main feature is represented by the accumulation of presumed basal laminar deposits. This is a feature that is shared with AMD.

In addition, EMAP is an atrophic disease, and this is extremely relevant in the context of the clinical trials for AMD, the trials that evaluated anticomplement therapies. There is evidence already that the complement is implied in the pathogenesis of EMAP. This was studied already by the French group 15 years ago. So, given the similarities of EMAP with the diffuse trickling pattern of GA as described by Holz and colleagues in 2007,² there is increasing evidence that this phenotype might actually represent a subtype of AMD. And so anticomplement therapies should be at least reevaluated in the trials that have been performed already in which diffuse trickling GA has been included, because a subset of these patients may actually represent EMAP.

Patricio G. Schlottmann, MD: Excellent. That is very important because this description, had it been included in the selection of the patients, may or may not have changed the way we see the results of these new complement-inhibiting therapies for the management of patients with GA. All the research, as always, is oriented to improving the lives of patients with eye diseases, and for that we thank you very much.

Alessandro Feo, MD: Thank you so much. RP

References

1. Hamel CP, Meunier I, Arndt C, et al. Extensive macular atrophy with pseudodrusen-like appearance: a new clinical entity. Am J Ophthalmol. 2009;147(4):609-620. doi:10.1016/j.ajo.2008.10.022

2. Holz FG, Bindewald-Wittich A, Fleckenstein M, et al. Progression of geographic atrophy and impact of fundus autofluorescence patterns in age-related macular degeneration. Am J Ophthalmol. 2007;143(3):463-472. doi:10.1016/j.ajo.2006.11.041