Different determinants of neovascularization on the optic disc and on the retina in patients with severe nonproliferative diabetic retinopathy.

Almost all patients with type I and many with type II diabetes develop proliferative retinopathy. This entity consists of two components: new blood vessels on the optic disc (NVD), which frequently lead to visual loss, and new blood vessels elsewhere on the retina (NVE), which do not pose such a serious threat to vision. This study examined determinants of neovascularization specifically on the optic disc in eyes with severe nonproliferative retinopathy. The study eyes were under surveillance as the untreated control eyes of participants in the Diabetic Retinopathy Study. During the 5-year follow-up period, NVE developed in almost all of the eyes, whereas the cumulative incidence of NVD in these same eyes was 64% and varied according to several factors. The risk of NVD in a study eye was increased if the contralateral treated eye had NVD rather than NVE or severe nonproliferative retinopathy (odds ratio [OR], 6.1; P < .0001). It was also increased if the study eye had, at the baseline examination, soft exudates and intraretinal microvascular abnormalities (OR, 5.7; P = .002) or soft exudates alone (OR, 4.0; P = .04). Nephropathy and poor glycemic control were each associated with a two-fold increase in risk but neither was statistically significant. Eyes of individuals over 40 years of age were protected from the development of NVD (OR, 0.5; P < .05). The findings of this study support the hypothesis that, in patients with diabetes, the development of NVD is determined by different factors than the development of NVE.

[1]  D L DeMets,et al.  The Wisconsin epidemiologic study of diabetic retinopathy. III. Prevalence and risk of diabetic retinopathy when age at diagnosis is 30 or more years. , 1984, Archives of ophthalmology.

[2]  T. Merimee,et al.  Diabetic retinopathy. A synthesis of perspectives. , 1990, The New England journal of medicine.

[3]  D. Morgan,et al.  STIMULATION OF ENDOTHELIAL CELL GROWTH BY SERA FROM DIABETIC PATIENTS WITH RETINOPATHY , 1988, The Lancet.

[4]  D. DeMets,et al.  The Wisconsin epidemiologic study of diabetic retinopathy. II. Prevalence and risk of diabetic retinopathy when age at diagnosis is less than 30 years. , 1984, Archives of ophthalmology.

[5]  A. Patz,et al.  Demonstration of vasoproliferative activity from mammalian retina , 1980, The Journal of cell biology.

[6]  M. Landers,et al.  Optic disk neovascularization in juvenile rheumatoid arthritis. , 1990, American journal of ophthalmology.

[7]  K Muraoka,et al.  Midperipheral fundus involvement in diabetic retinopathy. , 1981, Ophthalmology.

[8]  L. Rand,et al.  Risk Factors for Progression of Background Retinopathy in Long-Standing IDDM , 1989, Diabetes.

[9]  M. Sanders,et al.  Neovascularisation associated with posterior uveitis. , 1987, The British journal of ophthalmology.

[10]  B. Glaser Extracellular modulating factors and the control of intraocular neovascularization. An overview. , 1988, Archives of ophthalmology.

[11]  Rupert G. Miller,et al.  Survival Analysis , 2022, The SAGE Encyclopedia of Research Design.

[12]  L. Rand,et al.  Factors influencing the development of visual loss in advanced diabetic retinopathy. Diabetic Retinopathy Study (DRS) Report No. 10. , 1985, Investigative ophthalmology & visual science.

[13]  A. Patz Retinal neovascularisation: early contributions of Professor Michaelson and recent observations. , 1984, The British journal of ophthalmology.

[14]  A. Patz Clinical and experimental studies on retinal neovascularization. XXXIX Edward Jackson Memorial Lecture. , 1982, American journal of ophthalmology.

[15]  T. Deckert,et al.  Prognosis of Proliferative Retinopathy in Juvenile Diabetics , 1967, Diabetes.

[16]  P. Henkind Ocular neovascularization. The Krill memorial lecture. , 1978, American journal of ophthalmology.