2 ' Current burden Diabetes mellitus is among the leading causes of death, disability and
' economic loss throughout the world (2,3). WHO has estimated that there and trends were 171 million people worldwde with diabetes mellitus in 2000 and predicted that 366 million people will have diabetes mellitus by 2030 (4). The increase will be due mainly to increases in low- and middle-income countries (Figure 1). The International Diabetes Federation has estimated that another 314 million persons have impaired glucose tolerance, and that number will increase to 472 million by 2030 (5). In the United States of America, for example, as much as 6.3% of the population had diabetes mellitus in 2002, and the prevalence and incidence are increasing (6). The United States Centers for Disease Control and Prevention have estimated that 13 million persons in the United States have diagnosed diabetes mellitus and an additional 5.2 million have the disease but it has not yet been diagnosed (7).
The prevalences in other countries are comparable, even in those with newly developing economies, such as India and China. It was estimated that 26 million peope in China had diabetes mellitus in 2001, and the prevalence has increased markedly recently due to population ageing and a rapd increase in incidence (8). Further, while persons with diabetes mellitus in developed countres are mostly elderly, most of those in developing countries are younger (45-64 years), this increasing the impact of diabetes mellitus on those populations and societies (4).
Number of persons with diabetes in the year 2000 and projected increase in 2030
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2.2 Prevention of diabetes mellitus
The two main etiological types of diabetes are type 1 and type 2 (9). Type 1 involves p-cell destruction, which may lead to diabetes mellitus, in which insulin is required for survival. Type 2 is the commonest form of diabetes and is characterized by disorders of insulin resistance and insulin secretion, either of which may be the predominant feature. Several trials have shown that type 2 diabetes mellitus can generally be prevented with diet and physical activity, while persons at high risk (with impaired glucose tolerance) can be treated with drugs (10-15). Prevention of type 2 diabetes mellitus would eliminate a large proportion of the risk for visual loss from diabetic retinopathy To date, no positive results have been obtained in trials for the prevention of type 1 diabetes mellitus.
Diabetic retinopathy is a microvascular complication of both type 1 and type 2 diabetes mellitus. It develops in nearly all persons with type 1 diabetes and in more than 77% of those with type 2 who survive over 20 years with the disease (16). Diabetic retinopathy is a leading cause of new-onset blindness in industrialized countries and a more and more frequent cause of blindness in middle-income countries (18). WHO has estimated that diabetic retinopathy is responsible for 4.8% of the 37 million cases of blindness throughout the world (18).
In the Wisconsin Epidemiologic Study of Diabetic Retinopathy, 13% of the study population who had had diabetes mellitus for fewer than 5 years and 90% of those who had been afflicted for 10-15 years had some degree of diabetic retinopathy when diabetes had been diagnosed when they were less than 30 years of age (presumed to have type 1) (16). Of those with an onset at 30 years or more (presumed to have type 2), 40% who were taking insulin and 24% who were not had some degree of diabetic retinopathy when the duration of diabetes mellitus was fewer than 5 years (17), and 84% taking insulin and 53% not taking insulin had some degree of diabetic retinopathy when the duration of diabetes mellitus was 15-20 years (19).
Of persons who have had insulin-dependent diabetes mellitus for 20 years or more, 60% will have had proliferative retinopathy (16), while of those who have had the condition for 30 years or more, more than 12% are bind (20). Each year in the United States, over 33 000 new cases of diabetic macular oedema, 86 000 cases of prolierative diabetic retinopathy and 12 000-14 000 new cases of blindness occur (20-22). If all patients with diabetes with proliferative retinopathy were to receive timely evaluation and treatment, the rate of blindness (let alone less severe visual loss) would be reduced from 50% to less than 5% after 5 years, a greater than 90% reduction in blindness from this disease (23).
3. EVIDENCE BASE FOR THE PREVENTION AND TREATMENT OF DIABETIC RETINOPATHY
Evidence-based treatment reported from clinical studies spanning more than 30 years can reduce the risk for severe vision loss and blindness from proliferative diabetic retinopathy by more than 90%. Methods are also available to reduce the risk for legal blindness and moderate vision loss significantly Five large multicentre clinical trials conducted in the United Kingdom and the United States provide the scientific basis for the clinical management of diabetic retinopathy.
The Diabetic Retinopathy Study (1971-1975) demonstrated conclusively that scatter (pan-retinal) laser photocoagulation reduces the risk for severe vision loss due to prolierative diabetic retinopathy by as much as 60% (24,25). This study also provided the first and still most widely used classification system for grading the severity of diabetic retinopathy and indications for treatment with scatter laser.
The Early Treatment Diabetic Retinopathy Study (1979-1990) demonstrated that scatter (pan-retinal) laser photocoagulation can reduce the risk for severe vision loss (best corrected vision of 5/200 or worse) to less than 2%. It also showed that focal laser photocoagulation can reduce the risk for moderate vision loss (a doubling of the vsual angle) from diabetic macular oedema by 50%, with no adverse effect on the progression of diabetic retinopathy or risk for vitreous haemorrhage for patients with diabetes mellitus who take up to 650 mg of aspirin per day (26,27).
The Diabetic Retinopathy Vitrectomy Study (1977-1987) provided insight into the timing of vitrectomy surgery to restore useful vision in eyes with non-resolving vitreous haemorrhage (28,29). In particular, it highlighted that, in certain situations, early vitrectomy resulted in better vision. It also drew attention to the poor prognosis of eyes that experience vitreous haemorrhage, regardless of the timing of surgery indicating the desirability of preventing such late complications of diabetic retinopathy
3.4 Diabetes Control and Complications Trial and Epidemiology of Diabetes Interventions and Complications Trial
In the Diabetes Control and Complications Trial (1983-1993), conventional blood glucose control was compared with intensive blood glucose control in patients with type 1 diabetes mellitus and little or no diabetic retinopathy The Trial conclusively demonstrated that, for these patients, intensive control of blood glucose as reflected in measurements of glycosylated haemoglobin reduced the rsk for progression of diabetic retinopathy Those with intensive control showed a 54% reduction in the development of a three-step progression of diabetic retinopathy, a 47% reduction in the development of severe nonproliferative or proliferative diabetic retinopathy, a 56% reduction in the rate of laser surgery and a 23% reduction in the rsk for diabetic macular oedema (30-35). Seven years after completion of the Diabetes Control and Complications Trial, the Epidemiology of Diabetes Interventions and Complications Trial showed that persons in the intensive control group continued to have a substantially lower risk for progression of retinopathy than the conventional control group, despite near convergence of glycosylated haemoglobin levels (35).
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