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Editors Selection IGR 13-1
Glaucoma and Systemic Diseases: POAG and Glucose Metabolism Disorders
Comment by Rupert Bourne on:
61623 Association of Geroprotective Effects of Metformin and Risk of Open-Angle Glaucoma in Persons With Diabetes Mellitus, Lin HC; Stein JD; Nan B et al., JAMA ophthalmology, 2015; 133: 915-923
Growing interest surrounds long-term calorific restriction and the potential benefits this may have in terms of longevity (geroprotection) but also reduction in risk of age-associated diseases, such as cancer, diabetes and cardiovascular disease. Using 'big data', this study sought to investigate whether metformin, a calorific restriction mimetic drug, reduces the incidence of open-angle glaucoma (OAG) among diabetics. True to the definition the data source was 'big', accessing a health claims database of longitudinal data for 40 million patients in a US managed care network.
This raises intriguing questions as to whether metformin reduces OAG risk through mechanisms beyond glycaemic control, such as inflammatory or neurogenesis pathways
The inclusion criteria that required patients to have been enrolled in the pharmaceutical plan of the network for more than two consecutive years with a diagnosis of diabetes and at least one eye examination in that period to exclude those with a pre-existent diagnosis of glaucoma were met by 150,016 patients aged 40 years and older. Patients were followed-up from the date corresponding to their first eye examination until incident OAG was recorded or the last eye examination, whichever came first. Prescriptions filled for diabetic medications were used as a surrogate for medication consumption and survival analysis was conducted to model the effect of metformin exposure on the risk of developing OAG. Aside from some interesting epidemiological findings (3.9% of these diabetics developed incident OAG, and those of African ancestry had a 95% higher risk of OAG than patients of European ancestry), the analysis revealed that diabetics whose metformin consumption was in the upper quartile had a 25% reduced risk of developing OAG compared with those with no metformin use. Metformin obviously lowers HbA1C (glycaemic control was incident OAG-protective), yet the risk reduction was still evident even when HbA1C was included in the model. This raises intriguing questions as to whether metformin reduces OAG risk through mechanisms beyond glycaemic control, such as inflammatory or neurogenesis pathways.
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