Diabetes 2000.
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Biomedical subjects
Publications and source records attributed to A Patz.
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OBJECTIVE: To describe the interval between first appearance of mild nonproliferative diabetic retinopathy (NPDR) and first appearance of neovascularization (NV) in type I diabetes. SETTING: A longitudinal study of 269 patients followed up annually. PARTICIPANTS: Participants had insulin-dependent diabetes and were free of proliferative diabetic retinopathy in both eyes at the baseline visit. MAIN OUTCOME MEASURE: Stereoscopic color fundus photographs of each eye at each study visit, graded for features of retinopathy. RESULTS: Among the 305 eyes for which the duration of diabetes at the first appearance of mild NPDR could be determined, NV developed in 28 by the end of the study. Survival analysis showed that the later the onset of mild NPDR was, the shorter the time from onset of mild NPDR to onset of NV (relative hazard for each additional year to onset of mild NPDR, 1.22; 95% confidence interval, 1.10-1.35). Adjustment for systolic and diastolic blood pressure, proteinuria, and glycosylated hemoglobin (Hgb A10) levels did not change the relative hazard estimate for onset of mild NPDR. Higher levels of Hgb A10 were associated with a shorter time from onset of mild NPDR to onset of NV (relative hazard, 1.26; 95% confidence interval, 1.05-1.51 [after adjusting for time at onset of mild NPDR]), as were higher levels of diastolic blood pressure, although not significantly (relative hazard for 10-mm Hg increase in diastolic blood pressure, 1.52; 95% confidence interval, 0.82-2.83 [adjusting for onset of mild NPDR, Hgb A10 level, systolic blood pressure, and proteinuria]). Neither proteinuria nor systolic blood pressure had an effect on time from onset of mild NPDR to onset of NV, after adjustment for time at onset of mild NPDR, Hgb A10 level, and diastolic blood pressure. CONCLUSION: Later onset of mild NPDR is not necessarily associated with delayed development of NV in patients with type I diabetes. Caution must therefore be used in assessing the value of interventions that delay the onset of mild NPDR without evidence of delayed onset of NV.
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 A1c) 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 A1c level. Systolic and diastolic blood pressure, proteinuria, body mass index, race, initial presence of retinopathy, and use of antihypertensives did not significantly affect the risk of clinically significant macular edema. CONCLUSION: Older age at diagnosis of diabetes, male sex, and higher Hgb A1c 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.
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"Diabetes 2000" will parallel a major diabetic retinopathy public information campaign recently announced by the National Eye Institute. The NEI's National Eye Health Education Program (NEHEP), which targets both diabetic retinopathy and glaucoma, is fashioned along the lines of earlier federal initiatives against smoking and high blood pressure. By continuously updating our medical knowledge and skills related to this multisystem disorder, and by forging partnerships between physicians in the effective and efficient management of diabetic patients, we have a unique and important opportunity--we can reduce preventable blindness from diabetes by the year 2000.
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The presence of background and preproliferative retinopathy in 70 patients with type I diabetes was correlated with their pubertal development. Pubertal status was assessed by pediatricians using the sexual maturity ratings of Tanner. In young diabetics with comparable disease duration (5 to 10 years), postpubertal children had a greater prevalence of retinopathy than those who were not sexually mature. After adjusting for duration of diabetes and sex, the relative odds of having retinopathy in the postpubescent group relative to the prepubescent or pubescent groups was 4.8 (95% confidence interval: 1.5 to 15.3). This study suggests that minimal retinopathy in children is not rare and that postpubescent children have a greater prevalence of diabetic retinopathy than do prepubescent children with similar diabetes duration.
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The authors observed three cases (6 eyes) of vaso-occlusive retinopathy associated with the lupus anticoagulant and the related antiphospholipid antibody anticardiolipin. The disease occurred in patients who had no definable autoimmune disease such as systemic lupus erythematosus (SLE) and was characterized by severe bilateral retinal vascular occlusion. There was profound visual loss from intraretinal ischemia as well as vitreous hemorrhage from preretinal neovascularization. Results of laboratory testing showed a prolonged partial thromboplastin time (PTT) in two patients, and the presence of the lupus anticoagulant in all. Treatment with panretinal photocoagulation appeared to stabilize the neovascularization. The role of systemic anticoagulation and immunosuppressive therapy is uncertain.
The tuneable dye laser was used to simulate treatment of choroidal neovascularization and panretinal photocoagulation (PRP) in monkey retina. The histopathologic effects of wavelengths from 560 to 630 nm in juxtafoveal, papillomacular bundle, and nonfoveal areas were investigated. An unexpected observation using high-intensity burns in juxtafoveal and, to a lesser extent, in papillomacular bundle areas was inner retinal damage with 600-nm light. At moderate energy levels, the effect of 600 nm were more comparable with those with other wavelengths and included much less damage to the inner retinal layers. At mild energy levels, the effects were comparable with other wavelengths. During and after the application of the burns, the energy levels and ophthalmoscopic appearances were comparable for each wavelength for the high-, moderate-, and mild-intensity burns. The histopathologic effects of 630-nm light (tuneable dye red) were comparable with those of the standard krypton red (647 nm) laser. Nonmacular and PRP effects were similar with all wavelengths. These results indicate that power levels may need to be reduced when placing 600-nm (orange) laser burns in the macula.
The authors report the occurrence of occlusive retinal arterial disease and retinal neovascularisation in a 44-year-old woman with systemic lupus erythematosus (SLE). Two days after uncomplicated panretinal photocoagulation the patient developed an acute anterior segment ischaemic syndrome. To our knowledge this complication has not been reported in any other patient following laser photocoagulation or in association with SLE.
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The Diabetic Retinopathy Study (DRS) demonstrated that prompt argon laser photocoagulation, in comparison to indefinite delay in treatment, could reduce by more than 50% the risk of severe visual loss from proliferative diabetic retinopathy. The DRS also enlightened two generations of ophthalmologists about the value of the randomized controlled clinical trial as a way of assessing new and existing treatments for unsolved therapeutic problems. After the example of the DRS, laser treatment was shown to be effective in reducing vision loss in selected patients with branch retinal vein occlusion, age-related macular degeneration, ocular histoplasmosis, and diabetic macular edema. Existing trials, supported by the National Eye Institute, are seeking to determine the appropriate treatment for selected patients with newly diagnosed glaucoma, vascularized corneas, retinopathy of prematurity, proliferative vitreoretinopathy and complicated retinal detachment, and choroidal melanoma. Clinical practice has benefited enormously from these studies all of which owe their existence, at least in part, to the prototypical clinical trial, the DRS. This symposium discusses the DRS and places it in today's perspective, with a look to the past as well.