Diabetic retinopathy treated with laser photocoagulation and the indirect effect on glycaemic control.

Anna Praidou,George Karakiulakis,Sofia Androudi,Eleni Papakonstantinou,Stavros Dimitrakos,Ioannis Tsinopoulos,Periklis Brazitikos

doi:10.1155/2014/158251

Abstract

Purpose. To identify any possible relation between glycaemic control and previous laser photocoagulation for diabetic retinopathy. Methods. Seventy-two patients with diabetes were included in the study and were separated into 2 groups according to previous treatment (group A) or not (group B) with argon laser photocoagulation. Glycaemic control was estimated by measuring blood levels of HbA1c in four consecutive measurements. Results. Blood levels of HbA1c in group A were significantly lower 3, 6, and 12 months after laser treatment as compared to blood levels of HbA1c before laser treatment (7.1 ± 0.4% versus 7.6 ± 0.9%, 7.2 ± 0.2% versus 7.6 ± 0.9%, and 7.1 ± 0.2% versus 7.6 ± 0.9%, resp., all P < 0.05). Blood levels of HbA1c in group B did not differ significantly in four consecutive measurements. Conclusion. Our results suggest that we should anticipate a better glycaemic control in cases of patients with diabetes previously treated with laser photocoagulation.

Highlights

Diabetic retinopathy (DR) is the most common microvascular complication of diabetes, which can result even in blindness [1]
In this study we examined the hypothesis that previous treatment with argon laser photocoagulation in patients with diabetes is positively related to their glycaemic control
Patients with diabetes were included in the study and were separated into 2 groups according to treatment or not with argon laser photocoagulation

Summary

Introduction

Diabetic retinopathy (DR) is the most common microvascular complication of diabetes, which can result even in blindness [1]. PDR occurs with severe retinal ischemia and is characterized by the growth of new blood vessels on the optic disc or elsewhere in the retina [2]. Retinal hypoxia is implicated in the pathogenesis of DME and in the development of retinal neovascularization. Hypoxia results in increased expression of vascular endothelial growth factor (VEGF), which is the most potent inducer of increased vascular permeability and the trigger for the formation of abnormal and leaking new vessels [3]. In previously published studies we have already shown the well-established involvement of vascular endothelial growth factor (VEGF) and the contribution of other growth factors [4] in the pathogenesis of PDR [5] and NPDR with DME [3]

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