European journal of ophthalmology · 2012
Impact of ocular hypotensive lipids on clinically significant diabetic macular edema.
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Patel Anu S, Patel Chirag C, Goyal Anju, Anchala Anupama, Adrean Sean, Hughes Bret, Mahmoud Tamer H
Аннотация
PURPOSE: To study the impact of ocular hypotensive lipids (OHL) on the incidence, progression, and response to treatment of clinically significant diabetic macular edema (CSDME).
METHODS: A total of 379 patients (232 female, 147 male) with a history of diabetes mellitus (DM) and primary open-angle glaucoma (POAG) were identified and included in the study. Patients were stratified into groups based on CSDME development and OHL exposure. Main outcome measures included time to development of CSDME, total duration of OHL exposure, and duration of DM and POAG.
RESULTS: Seven patients (1.8%) developed CSDME after OHL exposure (group 1A), 15 (4.0%) developed CSDME prior to OHL exposure (group 1B), and 197 (52.0%) were treated with OHL but never developed CSDME (group 2). Of patients not exposed to OHL, 22 (5.8%) developed CSDME (group 3) and 138 (36.4%) did not (group 4). Mean duration of DM was longer (p<0.0001) in patients who developed CSDME (20.2 years) compared to patients who did not (12.4 years). There was no difference (p=0.67) in the amount of OHL exposure between patients who developed CSDME (4.1 years) and patients who did not (4.6 years). Once developed, there was no difference in the interval until CSDME resolution between OHL treated (17.8 mo) and untreated (12.7 mo) patients (p=0.36).
CONCLUSIONS: The CSDME development correlated most strongly with the duration of diabetes, irrespective of OHL use. Ocular hypotensive lipids treatment of POAG seems not to affect the incidence, progression, or response to treatment of CSDME in diabetes.
METHODS: A total of 379 patients (232 female, 147 male) with a history of diabetes mellitus (DM) and primary open-angle glaucoma (POAG) were identified and included in the study. Patients were stratified into groups based on CSDME development and OHL exposure. Main outcome measures included time to development of CSDME, total duration of OHL exposure, and duration of DM and POAG.
RESULTS: Seven patients (1.8%) developed CSDME after OHL exposure (group 1A), 15 (4.0%) developed CSDME prior to OHL exposure (group 1B), and 197 (52.0%) were treated with OHL but never developed CSDME (group 2). Of patients not exposed to OHL, 22 (5.8%) developed CSDME (group 3) and 138 (36.4%) did not (group 4). Mean duration of DM was longer (p<0.0001) in patients who developed CSDME (20.2 years) compared to patients who did not (12.4 years). There was no difference (p=0.67) in the amount of OHL exposure between patients who developed CSDME (4.1 years) and patients who did not (4.6 years). Once developed, there was no difference in the interval until CSDME resolution between OHL treated (17.8 mo) and untreated (12.7 mo) patients (p=0.36).
CONCLUSIONS: The CSDME development correlated most strongly with the duration of diabetes, irrespective of OHL use. Ocular hypotensive lipids treatment of POAG seems not to affect the incidence, progression, or response to treatment of CSDME in diabetes.