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Editors Selection IGR 18-1

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Comment by Keith Martin on:

56225 Glucose-induced temporary visual recovery in primary open-angle glaucoma: a double-blind, randomized study, Casson RJ; Han G; Ebneter A et al., Ophthalmology, 2014; 121: 1203-1211

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In their previous work, the authors have explored the relationship between glucose levels and retinal ganglion cell (RGC) survival in models of acute and chronic retinal ischemia as well as in a rodent model of experimental ocular hypertension. They have demonstrated that elevated vitreous glucose levels appear to correlate with improved RGC survival and they have postulated a mechanism by which elevated glucose could improve the function of 'sick' RGC. The laboratory studies have been carefully performed and thoughtfully analyzed. In the current clinical study, an attempt has been made to start to apply these findings to human glaucoma. The authors aim to test the hypothesis that topically delivered glucose could improve some measures of visual function in aphakic glaucoma patients given 50% glucose eye drops every five minutes for one hour. They interpret their results as demonstrating a possible effect of glucose eye drops on visual performance and they discuss carefully several possible explanations, including an effect of elevated vitreous glucose on retinal function as well as a direct effect on the cornea.

The authors are to be commended for this translational approach and for designing a study which, though unavoidably limited by the constraints of human clinical trials to explore mechanism, nevertheless raises many interesting questions. The possibility that the findings of improved visual function could be due to an osmotic effect on the cornea which differed between the 50% glucose and 0.9% saline drops was addressed by a follow-up study where the drops were matched for osmolarity by using 8% saline. This was a laudable attempt to exclude a corneal explanation for their findings but I do wonder if using 50% L-glucose, a glucose isomer that cannot be metabolized, would have been a better control. As the authors freely acknowledge, the possibility of a non-retinal explanation for their finding remains even though their demonstration of elevated vitreous glucose levels in pseudophakic patients given glucose drops appears convincing.

A further limitation, pointed out by the authors themselves, is the lack of a non-glaucoma control group. This would have been a very interesting addition to the study because, as things stand, it is unclear whether the effect observed is related purely to glaucoma. It would also be interesting to know if a similar effect is observed in other conditions where retinal function is compromised such as macular degeneration. The authors plan further studies using retinal electrophysiology as an endpoint and these studies will hopefully provide complementary information that will help us understand what is going on here better.

Overall, this is a very interesting study performed by careful researchers which builds on solid laboratory work demonstrating an effect of elevated glucose levels on RGC survival. I think more work is needed to prove conclusively that the effect observed is directly caused by an effect on retinal metabolism but, like many pioneering studies, the current work has suggested a whole set of new experiments that I hope will be performed to test this idea further.

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