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DETERMINATION OF AVERAGE AGE FROM TIME OF ONSET TO DIAGNOSIS OF DIABETIC RETINOPATHY
Abstract
Diabetes mellitus is an enduring disease related with signicant morbidity and mortality. The main pathogenesis behind this disease is its numerous micro- and macrovascular complications. In developing countries, diabetic retinopathy (DR) is one of the major sources of vision impairment in working age population. DR has been classied into two categories: proliferative diabetic retinopathy (PDR) and nonproliferative diabetic retinopathy (NPDR). NPDR is further classied into mild, moderate and severe, while PDR is further classied into early PDR, high risk PDR and advanced diabetic eye disease. DR is a disease caused due to high blood glucose levels which result in vision loss or permanent blindness. High-level advancements in the eld of bio-medical image processing have speeded up the automated process of disease diagnoses and analysis. Much research has been conducted and computerized systems have been designed to detect and analyze retinal diseases through image processing. Similarly, a number of algorithms have been designed to detect and grade DR by analyzing different symptoms including microaneurysms, soft exudates, hard exudates, cotton wool spots, brotic bands, neovascularization on disc (NVD), neovascularization elsewhere (NVE), hemorrhages and tractional bands. The visual examination of the retina is a vital test to diagnose DR-related complications.
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Background Improved blood-glucose control decreases the progression of diabetic microvascular disease, but the effect on macrovascular complications is unknown. There is concern that sulphonylureas may increase cardiovascular mortality in patients with type 2 diabetes and that high insulin concentrations may enhance atheroma formation. We compared the effects of intensive blood-glucose control with either sulphonylurea or insulin and conventional treatment on the risk of microvascular and macrovascular complications in patients with type 2 diabetes in a randomised controlled trial. Methods 3867 newly diagnosed patients with type 2 diabetes, median age 54 years (IQR 48-60 years), who after 3 months' diet treatment had a mean of two fasting plasma glucose (FPG) concentrations of 6.1-15.0 mmol/L were randomly assigned intensive policy with a sulphonylurea (chlorpropamide, glibenclamide, or. glipizide) or with insulin, or conventional policy with diet. The aim in the intensive group was FPG less than 6 mmol/L. in the conventional group, the aim was the best achievable FPG with diet atone; drugs were added only if there were hyperglycaemic symptoms or FPG greater than 15 mmol/L. Three aggregate endpoints were used to assess differences between conventional and intensive treatment: any diabetes-related endpoint (sudden death, death from hyperglycaemia or hypoglycaemia, fatal or non-fatal myocardial infarction, angina, heart failure, stroke, renal failure, amputation [of at least one digit], vitreous haemorrhage, retinopathy requiring photocoagulation, blindness in one eye,or cataract extraction); diabetes-related death (death from myocardial infarction, stroke, peripheral vascular disease, renal disease, hyperglycaemia or hypoglycaemia, and sudden death); all-cause mortality. Single clinical endpoints and surrogate subclinical endpoints were also assessed. All analyses were by intention to treat and frequency of hypoglycaemia was also analysed by actual therapy. Findings Over 10 years, haemoglobin A(1c) (HbA(1c)) was 7.0% (6.2-8.2) in the intensive group compared with 7.9% (6.9-8.8) in the conventional group-an 11% reduction. There was no difference in HbA(1c) among agents in the intensive group. Compared with the conventional group, the risk in the intensive group was 12% lower (95% CI 1-21, p=0.029) for any diabetes-related endpoint; 10% lower (-11 to 27, p=0.34) for any diabetes-related death; and 6% lower (-10 to 20, p=0.44) for all-cause mortality. Most of the risk reduction in the any diabetes-related aggregate endpoint was due to a 25% risk reduction (7-40, p=0.0099) in microvascular endpoints, including the need for retinal photocoagulation. There was no difference for any of the three aggregate endpoints the three intensive agents (chlorpropamide, glibenclamide, or insulin). Patients in the intensive group had more hypoglycaemic episodes than those in the conventional group on both types of analysis (both p<0.0001). The rates of major hypoglycaemic episodes per year were 0.7% with conventional treatment, 1.0% with chlorpropamide, 1.4% with glibenclamide, and 1.8% with insulin. Weight gain was significantly higher in the intensive group (mean 2.9 kg) than in the conventional group (p<0.001), and patients assigned insulin had a greater gain in weight (4.0 kg) than those assigned chlorpropamide (2.6 kg) or glibenclamide (1.7 kg). Interpretation Intensive blood-glucose control by either sulphonylureas or insulin substantially decreases the risk of microvascular complications, but not macrovascular disease, in patients with type 2 diabetes. None of the individual drugs had an adverse effect on cardiovascular outcomes. All intensive treatment increased the risk of hypoglycaemia.
Background:
We investigated whether intensive glycemic control, combination therapy for dyslipidemia, and intensive blood-pressure control would limit the progression of diabetic retinopathy in persons with type 2 diabetes. Previous data suggest that these systemic factors may be important in the development and progression of diabetic retinopathy.
Methods:
In a randomized trial, we enrolled 10,251 participants with type 2 diabetes who were at high risk for cardiovascular disease to receive either intensive or standard treatment for glycemia (target glycated hemoglobin level, <6.0% or 7.0 to 7.9%, respectively) and also for dyslipidemia (160 mg daily of fenofibrate plus simvastatin or placebo plus simvastatin) or for systolic blood-pressure control (target, <120 or <140 mm Hg). A subgroup of 2856 participants was evaluated for the effects of these interventions at 4 years on the progression of diabetic retinopathy by 3 or more steps on the Early Treatment Diabetic Retinopathy Study Severity Scale (as assessed from seven-field stereoscopic fundus photographs, with 17 possible steps and a higher number of steps indicating greater severity) or the development of diabetic retinopathy necessitating laser photocoagulation or vitrectomy.
Results:
At 4 years, the rates of progression of diabetic retinopathy were 7.3% with intensive glycemia treatment, versus 10.4% with standard therapy (adjusted odds ratio, 0.67; 95% confidence interval [CI], 0.51 to 0.87; P=0.003); 6.5% with fenofibrate for intensive dyslipidemia therapy, versus 10.2% with placebo (adjusted odds ratio, 0.60; 95% CI, 0.42 to 0.87; P=0.006); and 10.4% with intensive blood-pressure therapy, versus 8.8% with standard therapy (adjusted odds ratio, 1.23; 95% CI, 0.84 to 1.79; P=0.29).
Conclusions:
Intensive glycemic control and intensive combination treatment of dyslipidemia, but not intensive blood-pressure control, reduced the rate of progression of diabetic retinopathy. (Funded by the National Heart, Lung, and Blood Institute and others; ClinicalTrials.gov numbers, NCT00000620 for the ACCORD study and NCT00542178 for the ACCORD Eye study.)
Diabetic retinopathy (DR) was the leading cause of severe visual impairment (VI) in subjects 25–64 years of age in the U.S. 30 to 40 years ago (1,2). At that time, severe VI (best corrected visual acuity of 20/200 or worse in the better eye) was 25 times as common in subjects with diabetes compared with those without diabetes. VI in subjects with diabetes resulted mainly from vitreous hemorrhage, tractional detachment of the macula due to proliferative diabetic retinopathy (PDR), and from macular edema involving the foveal area due to leakage from the breakdown of the blood-retinal barrier. Cataract and glaucoma also contributed to VI in individuals with diabetes.
Poor glycemic control was common in subjects with diabetes at that time (3,4). This was due, in part, to the fact that intensive appropriate insulin treatment was difficult to achieve. This was related to the technology that was available for monitoring glucose levels (self-monitoring of glycemic control was done by testing of spot urines; no glycosylated hemoglobin A1c was available) and to the way insulin was administered (no pump, treatment with one injection per day of a long-acting insulin). There was no definitive evidence that achieving good glycemic control would actually result in less DR; thus, there was a lack of consensus on optimal glucose levels among physicians caring for individuals with diabetes. Some clinicians believed that high blood glucose was less likely to result in the development of severe DR in subjects with type 2 diabetes than in those with type 1 diabetes (5). Blood pressure was also poorly controlled in individuals with diabetes at that time (3,4).
In 1972, the efficacy of photocoagulation had not yet been demonstrated to prevent visual loss due to PDR or macular edema. Vitrectomy, a surgical intervention to …
BACKGROUND
Long-term microvascular and neurologic complications cause major morbidity and mortality in patients with insulin-dependent diabetes mellitus (IDDM). We examined whether intensive treatment with the goal of maintaining blood glucose concentrations close to the normal range could decrease the frequency and severity of these complications.
METHODS
A total of 1441 patients with IDDM -- 726 with no retinopathy at base line (the primary-prevention cohort) and 715 with mild retinopathy (the secondary-intervention cohort) were randomly assigned to intensive therapy administered either with an external insulin pump or by three or more daily insulin injections and guided by frequent blood glucose monitoring or to conventional therapy with one or two daily insulin injections. The patients were followed for a mean of 6.5 years, and the appearance and progression of retinopathy and other complications were assessed regularly.
RESULTS
In the primary-prevention cohort, intensive therapy reduced the adjusted mean risk for the development of retinopathy by 76 percent (95 percent confidence interval, 62 to 85 percent), as compared with conventional therapy. In the secondary-intervention cohort, intensive therapy slowed the progression of retinopathy by 54 percent (95 percent confidence interval, 39 to 66 percent) and reduced the development of proliferative or severe nonproliferative retinopathy by 47 percent (95 percent confidence interval, 14 to 67 percent). In the two cohorts combined, intensive therapy reduced the occurrence of microalbuminuria (urinary albumin excretion of ≥ 40 mg per 24 hours) by 39 percent (95 percent confidence interval, 21 to 52 percent), that of albuminuria (urinary albumin excretion of ≥ 300 mg per 24 hours) by 54 percent (95 percent confidence interval, 19 to 74 percent), and that of clinical neuropathy by 60 percent (95 percent confidence interval, 38 to 74 percent). The chief adverse event associated with intensive therapy was a two-to-threefold increase in severe hypoglycemia.
CONCLUSIONS
Intensive therapy effectively delays the onset and slows the progression of diabetic retinopathy, nephropathy, and neuropathy in patients with IDDM.
Data from the Diabetic Retinopathy Study (DRS) show that photocoagulation, as used in the Study, reduced the rate of development of severe visual loss and inhibited the progression of retinopathy. These beneficial effects were noted to some degree in all those stages of diabetic retinopathy which were included in the Study. Some deleterious effects of treatment were also found, including losses of visual acuity and constriction of peripheral visual field. The risk of these harmful effects was considered acceptable in eyes with retinopathy in the moderate or severe proliferative stage when the risk of severe visual loss without treatment was great. In early proliferative or severe nonproliferative retinopathy, when the risk of severe visual loss without treatment was less, the risks of harmful treatment effects assumed greater importance. In these earlier stages, DRS findings have not led to a clear choice between prompt treatment and deferral of treatment unless and until progression to a more severe stage occurs. The purpose of this interim report is to present the data on which these conclusions are based. More detailed reports of Study findings will appear in the future.
Diabetic macular changes in the form of yellowish spots and extravasations that permeated part or the whole thickness of the retina were observed for the first time by Eduard Jaeger in 1856. This was only possible as a result of the newly developed direct ophthalmoscope that was first described in 1855. Jaeger's findings were controversial at the time and Albrecht von Graefe openly claimed that there was no proof of a causal relationship between diabetes and retinal complications. It was only in 1872 that Edward Nettleship published his seminal paper "On oedema or cystic disease of the retina" providing the first histopathological proof of "cystoid degeneration of the macula" in patients with diabetes. In 1876, Wilhelm Manz described the proliferative changes occurring in diabetic retinopathy and the importance of tractional retinal detachments and vitreous haemorrhages. In the early years of the 20th century, the debate continued whether macular changes were directly related to diabetes or whether they were due to hypertension and arteriosclerosis. It was not until the second half of the century that the work of Arthur James Ballantyne in Glasgow provided more evidence that suggested that diabetic retinopathy represents a unique vasculopathy.
To evaluate factors related to the incidence of diabetic retinopathy (DR) in a population of African descent, after 9 years of follow-up.
Population-based cohort study; 81% participation after 9 years.
Three hundred twenty-four participants of the Barbados Eye Studies, with diabetes mellitus (DM) at baseline and at risk for developing DR during follow-up.
Diabetes-related changes were assessed by masked gradings of baseline and follow-up photographs using a standardized system. The 9-year cumulative incidence of DR was based on participants with DM and free of retinopathy at baseline; incidence rates were estimated by the product-limit approach. Cox regression models for discrete-time data were used to evaluate risk factors associated with the 9-year incidence of DR.
Multivariate analyses revealed that older age at DM onset decreased the 9-year risk of DR development; for each 10 years of older age at onset, the risk of DR decreased by 30% (risk ratio [RR], 0.7; 95% confidence interval [CI], 0.56-0.96). The risk of DR doubled among persons with DM duration between 5 and 9 years (RR, 2.1; 95% CI, 1.2-3.6) versus those with shorter durations; it also doubled in those treated with oral medications or insulin at baseline versus those treated with diet only. Antihypertensive treatment halved the risk of DR versus no treatment (RR, 0.5; 95% CI, 0.3-0.9) and high systolic or diastolic blood pressure (BP) increased risk. Thus, DR risk increased by 30% for every 10 mmHg of higher systolic BP at baseline (RR, 1.3; 95% CI, 1.1-1.4) or of BP increase from baseline to the 4-year follow-up (RR, 1.3; 95% CI, 1.1-1.4). Diabetic retinopathy risk similarly increased with each 1% of higher glycosylated hemoglobin level at baseline (RR, 1.3; 95% CI, 1.2-1.5).
The long-term follow-up of persons with DM in this population of African origin, where disease prevalence is high, identified important potentially modifiable risk factors for DR. Findings suggest that efforts to achieve optimal glycemic and BP control may reduce the vision-threatening complications of DM.
Photocoagulation for diabetic macular edema Early treatment of diabetic retinopathy study report number 1
Photocoagulation for diabetic macular edema Early treatment of diabetic retinopathy
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