Clinically Significant Macular Edema in Type I Diabetes
Authors: Susan Vitale, Maureen G. Maguire, Robert P. Murphy, Cheryl J. Hiner, Lillian Rourke, Catherine Sackett, Arnall Patz
Journal: Ophthalmology (1995)

Purpose: To examine incidence of and risk factors for clinically significant macular edema in persons with type I diabetes. Methods: A group of 189 persons with type I diabetes, recruited from a summer camp for children with diabetes and from practices of local physicians, were participants in a longitudinal study with annual follow-up visits which included physical and ophthalmologic examinations and color stereo fundus photographs of each eye, centered on the disc and macula. Subjects were free of proliferative retinopathy at study baseline. Ages ranged from 3 to 40 years, duration of diabetes ranged from 0 to 12 years, mean glycosylated hemoglobin (Hgb A1 c) was 12.2% (range, 6.4%–21.5%), and average follow-up was 6.1 years. Presence of clinically significant macular edema was defined as in the Early Treatment Diabetic Retinopathy Study. Results: In a total of 41 persons (62 eyes), clinically significant macular edema developed during study follow-up. Cumulative risk of clinically significant macular edema was 0 until 7 years' duration of diabetes. The cumulative risk of clinically significant macular edema increased linearly for each year of duration between 10 and 20 years, with an average annual increase of approximately 6.7%. Significant risk factors for clinically significant macular edema were older age at diagnosis, male sex, and higher Hgb A1 c level. Systolic and diastolic blood pressure, proteinuria, body mass index, race, initial presence of retinopathy, and use of anti hypertensives did not significantly affect the risk of clinically significant macular edema. Conclusion: Older age at diagnosis of diabetes, male sex, and higher Hgb A1 c levels (poorer control of blood glycemic levels) significantly increase the risk of clinically significant macular edema in persons with type I diabetes. These data extend the evidence implicating worse glycemic control as a cause of clinically significant macular edema, even within a population with relatively loose control. Purpose: To examine incidence of and risk factors for clinically significant macular edema in persons with type I diabetes. Methods: A group of 189 persons with type I diabetes, recruited from a summer camp for children with diabetes and from practices of local physicians, were participants in a longitudinal study with annual follow-up visits which included physical and ophthalmologic examinations and color stereo fundus photographs of each eye, centered on the disc and macula. Subjects were free of proliferative retinopathy at study baseline. Ages ranged from 3 to 40 years, duration of diabetes ranged from 0 to 12 years, mean glycosylated hemoglobin (Hgb A1 c) was 12.2% (range, 6.4%–21.5%), and average follow-up was 6.1 years. Presence of clinically significant macular edema was defined as in the Early Treatment Diabetic Retinopathy Study. Results: In a total of 41 persons (62 eyes), clinically significant macular edema developed during study follow-up. Cumulative risk of clinically significant macular edema was 0 until 7 years' duration of diabetes. The cumulative risk of clinically significant macular edema increased linearly for each year of duration between 10 and 20 years, with an average annual increase of approximately 6.7%. Significant risk factors for clinically significant macular edema were older age at diagnosis, male sex, and higher Hgb A1 c level. Systolic and diastolic blood pressure, proteinuria, body mass index, race, initial presence of retinopathy, and use of anti hypertensives did not significantly affect the risk of clinically significant macular edema. Conclusion: Older age at diagnosis of diabetes, male sex, and higher Hgb A1 c levels (poorer control of blood glycemic levels) significantly increase the risk of clinically significant macular edema in persons with type I diabetes. These data extend the evidence implicating worse glycemic control as a cause of clinically significant macular edema, even within a population with relatively loose control.