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Pathogenesis of diabetic retinopathy is multifactorial. Various potential risk factors include hypertension, proteinuria, and duration of diabetes, use of insulin, chronic renal disease, and anaemia. Management of diabetic macular oedema has mainly focused on laser photocoagulation of leaking microaneurysms. While anaemia has been found as an independent risk factor for the development of high risk proliferative diabetic retinopathy,1 its correction has not received due attention in the management of diabetic retinopathy. We report a patient with insulin dependent diabetes mellitus (IDDM) with coexisting nutritional anaemia, who showed spontaneous closure of the microaneurysms on correction of anaemia and metabolic control.
A 39 year man with IDDM for 12 years, presented with bilateral decrease in vision for 3 months. Examination revealed a visual acuity of 20/40 in both eyes and normal anterior segment. Fundus examination showed multiple microaneurysms, cotton wool spots, and superficial retinal haemorrhages scattered throughout the posterior pole in both eyes. Fundus fluorescein angiography showed multiple microaneurysms with focal leakage in both eyes (fig 1). Review of his systems was essentially normal. Laboratory results showed low haemoglobin (4.7 g%), raised erythrocyte sedimentation rate (ESR) (65 mm in the first hour) and hyperglycaemia (fasting blood sugars −242 mg/dl). Peripheral blood film showed moderate anisocytosis and microcytosis of red cells. Total leucocyte count, differential leucocyte count, platelet count, serum electrolytes, urea, creatinine, 24 hours urinary proteins, and bilirubin were within normal limits. Chest x ray, ultrasound abdomen, stool for occult blood, duodenal biopsy, and serum electrophoresis for Waldenstrom’s microglobulinaemia were normal. He was labelled as a case of nutritional (iron deficiency) anaemia. He received blood transfusion (two units) and started on iron, folic acid, vitamin B1, B6, and B12 supplements. His insulin regimen was modified. After 3 months of therapy, his haemoglobin improved to 14 g/dl and blood sugars were normal (fasting blood sugars 110 mg/dl). His visual acuity improved to 20/20 in both eyes. Fundus examination showed spontaneous closure of majority of microaneurysms and resolution of superficial haemorrhages and cotton wool spots in both eyes (fig 2).
In our patient the retinopathy was characterised by multiple microaneurysms, cotton wool spots, and haemorrhages, which were highly suggestive of moderately severe non-proliferative diabetic retinopathy. Anaemia is known to produce a retinopathy that is characterised by haemorrhages and cotton wool spots, and occasionally hard exudates. To our knowledge development of microaneurysms has not been reported in nutritional anaemia. The Diabetes Control and Complications Trial (DCCT)2 has shown that intensive management of diabetes reduces the development and progression of retinopathy in the long run but spontaneous closure of microaneurysms was not noted in this study. A large cross sectional study3 found a twofold increase in risk of retinopathy in patients with haemoglobin less than 12 gm/dl, when controlled for other known risk factors. Shorb et al4 reported three diabetic patients with severe iron deficiency anaemia, who rapidly progressed to severe proliferative retinopathy. Friedman and associates5 reported resolution of macular hard exudates in five patients who were treated with erythropoietin for coexisting anaemia. The authors did not speculate on the mechanism of resolution of hard exudates. It is unlikely that a better metabolic control alone led to spontaneous closure of microaneurysms in our patient. It is more likely that anaemia induced retinal hypoxia played a major part in the development of microaneurysms and other retinopathy changes. We postulate that correction of hypoxia may be the possible mechanism in improvement of the retinopathy.
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