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Screening in Primary Care for Diabetic Retinopathy, Maculopathy and Visual Loss in South Africa

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      Abstract

      Objective: The aim of the study was to determine the prevalence of diabetic retinopathy, maculopathy and visual loss in primary care patients and to identify associated risk factors. Research Design and Methods: We conducted a cluster randomised trial at primary care clinics in the Tshwane district in South Africa. Grades of retinopathy and maculopathy (with fundus camera) and visual acuity (Snellen chart) were assessed and, using mobile screening and teleophthalmology, clinical and biochemical testing was conducted to obtain information about glycaemic control and microvascular complications. Results: The prevalence rates for any retinopathy, preproliferative retinopathy and proliferative retinopathy were 24.9, 19.5 and 5.5%, respectively. The prevalence rates of diabetic maculopathy, observable maculopathy and referable maculopathy were 20.8, 11.8 and 9.0%, respectively. The presence of retinopathy was associated with high body mass index, systolic blood pressure, being on insulin treatment, high HbA1c and the presence of neuropathy. High systolic blood pressure, being on insulin treatment, high HbA1c level and high low-density lipoprotein cholesterol level as well as the presence of albuminuria were significant in predicting any diabetic maculopathy. Laser photocoagulation was given to 8.3% of patients from the mobile unit and 12% of patients were referred to the nearest hospital with an outpatient eye clinic for follow-up treatment of various other eye conditions. Using the WHO categories, the study found that 78.1% of diabetes patients had normal vision, 19.3% were visually impaired and 2.2% were severely impaired or blind. Conclusion: High prevalence rates for diabetic retinopathy, maculopathy and visual loss were found and associations were identified.

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      Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD study): randomised controlled trial.

      Patients with type 2 diabetes mellitus are at increased risk of cardiovascular disease, partly owing to dyslipidaemia, which can be amenable to fibrate therapy. We designed the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study to assess the effect of fenofibrate on cardiovascular disease events in these patients. We did a multinational, randomised controlled trial with 9795 participants aged 50-75 years, with type 2 diabetes mellitus, and not taking statin therapy at study entry. After a placebo and a fenofibrate run-in phase, we randomly assigned patients (2131 with previous cardiovascular disease and 7664 without) with a total-cholesterol concentration of 3.0-6.5 mmol/L and a total-cholesterol/HDL-cholesterol ratio of 4.0 or more or plasma triglyceride of 1.0-5.0 mmol/L to micronised fenofibrate 200 mg daily (n=4895) or matching placebo (n=4900). Our primary outcome was coronary events (coronary heart disease death or non-fatal myocardial infarction); the outcome for prespecified subgroup analyses was total cardiovascular events (the composite of cardiovascular death, myocardial infarction, stroke, and coronary and carotid revascularisation). Analysis was by intention to treat. The study was prospectively registered (number ISRCTN 64783481). Vital status was confirmed on all but 22 patients. Averaged over the 5 years' study duration, similar proportions in each group discontinued study medication (10% placebo vs 11% fenofibrate) and more patients allocated placebo (17%) than fenofibrate (8%; p<0.0001) commenced other lipid treatments, predominantly statins. 5.9% (n=288) of patients on placebo and 5.2% (n=256) of those on fenofibrate had a coronary event (relative reduction of 11%; hazard ratio [HR] 0.89, 95% CI 0.75-1.05; p=0.16). This finding corresponds to a significant 24% reduction in non-fatal myocardial infarction (0.76, 0.62-0.94; p=0.010) and a non-significant increase in coronary heart disease mortality (1.19, 0.90-1.57; p=0.22). Total cardiovascular disease events were significantly reduced from 13.9% to 12.5% (0.89, 0.80-0.99; p=0.035). This finding included a 21% reduction in coronary revascularisation (0.79, 0.68-0.93; p=0.003). Total mortality was 6.6% in the placebo group and 7.3% in the fenofibrate group (p=0.18). Fenofibrate was associated with less albuminuria progression (p=0.002), and less retinopathy needing laser treatment (5.2%vs 3.6%, p=0.0003). There was a slight increase in pancreatitis (0.5%vs 0.8%, p=0.031) and pulmonary embolism (0.7%vs 1.1%, p=0.022), but no other significant adverse effects. Fenofibrate did not significantly reduce the risk of the primary outcome of coronary events. It did reduce total cardiovascular events, mainly due to fewer non-fatal myocardial infarctions and revascularisations. The higher rate of starting statin therapy in patients allocated placebo might have masked a moderately larger treatment benefit.
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          Prevalence of diabetic retinopathy in Type 2 diabetes in developing and developed countries.

          As the global prevalence of diabetes increases, so will the numbers of people with diabetic retinopathy. Our review aimed to provide a comprehensive picture of available studies of diabetic retinopathy and how prevalence varies around the developed and developing world.
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            Author and article information

            Affiliations
            aSchool of Health Systems and Public Health, and Departments of bInternal Medicine and cOphthalmology, University of Pretoria, and dPrivate Ophthalmologist, Pretoria, South Africa
            Journal
            OPH
            Ophthalmologica
            10.1159/issn.0030-3755
            Ophthalmologica
            Ophthalmologica
            S. Karger AG (Basel, Switzerland karger@ 123456karger.com http://www.karger.com )
            0030-3755
            1423-0267
            April 2016
            10 March 2016
            : 235
            : 3
            : 141-149
            OPH2016235003141
            10.1159/000443972
            26959502
            Ophthalmologica 2016;235:141-149
            © 2016 S. Karger AG, Basel

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            Tables: 5, References: 31, Pages: 9
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