I am back on “special assignment”. Lin asked me to try to make heads or tails out of a very scientific article entitled “Progression of Geographic Atrophy in Age-Related Macular Degeneration.” It is report number 16 in the AREDS series.
Me thinks she has more confidence in me than I have, but let’s give it a shot. Just remember, social scientist here. My interpretations are always subject to errors.
The article starts with a description of Geographic Atrophy (GA). As many of us know, GA is defined as discrete areas of cell death (atrophy) that eventually grow and come together to form “continents” of damage in the macula. Part of the definition requires the damage to be such that someone examining the eye can see the blood vessels in the next layer (the choroid).
GA usually starts in the macula but generally does not immediately affect the fovea. The fovea is the “prime” area of the macula where the best seeing is actually done. However, as the disease progresses, the fovea is often also involved.
GA involves scotomata, Greek for darkness. Scotomata are those dark islands in our visual fields and result from the death of the cells in those locations.
I am going to skip the methods sections of this article and go right to results….believe me, it is better for everyone that way?.
Okay…because there is no treatment and no cure for GA, science is presently focusing on trying to slow this train down. Worry about actually stopping it once we buy some time. In order to slow it down, we need to know something about it.
The study first calculated how many of their early AMD subjects either went on to develop wet AMD or went on to develop GA. This gave them some idea what the progression of the disease looks like when nothing is done. Basically, they were learning about the natural history of the disease as well as establishing a baseline.
They did make some interesting, incidental discoveries. For example, noncentral lesions grow faster than central ones. Enlargement of lesions occurred more rapidly if the subject had GA in both eyes as opposed to one eye.
Those of us with certain genotypes may be in worse trouble than others. Those who have risk alleles (half a gene pair) on ARMS2, for example, are potentially destined for faster lesion growth. One CFI at-risk allele is another example. Unfortunately, there are several more.
So, on to discussion! What did they actually conclude? Vision loss from GA was steady over the five-year life of the study. Of those in whom there was no central involvement when they were first assessed, 60% developed central involvement within five years. Up to 30% of the eyes with GA developed neovascular AMD within those five years. This was especially true if the companion eye was “wet.” GA lesions may grow more slowly when they are small and when they are large and more rapidly when they are midsized.
There are some genotypes – once again the infamous ARMS2 – that seem to predict both the formation of lesions and their faster growth. If you don’t have those genes, take up smoking. Smoking continues to be found to be a risk factor for both GA presence and growth.
There are three, more pages to go on this thing but I am above my self-imposed word limit here. Also, it is just about nap time. Take this up again tomorrow!
Written September 20th, 2018