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Retinal Vessel Diameter and Diabetic Macular Edema
Author Response: Retinal Vessel Diameter and Diabetic Macular Edema
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Tien Y. Wong
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twong{at}unimelb.edu.au Tien Y. Wong
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We read with interest the article by Sander et al.1 which investigated the progression of diabetic macular edema (DME) in relation to baseline retinal thickness, retinal vascular leakage, and retinal vessel diameters. The authors found that baseline retinal vessel diameter was not associated with progression but that baseline retinal leakage was the strongest predictor of progression from non-clinically significant to photocoagulation for clinically significant macular edema (CSME). There is a general agreement that increased abnormal permeability of the blood-retinal barrier is important in DME progression, but there are fewer data on whether retinal vessel diameter is a structural marker of the pathological processes involved in DME. In this regard, there are now several population-based studies that show retinal arteriolar diameter is strongly related to elevated blood pressure,2 and that in persons with diabetes, larger retinal venular caliber is associated with both the incidence and progression of diabetic retinopathy.3,4 Of the few clinical studies that have investigated structural changes in the retinal vascular diameter in eyes with DME, Kristinsson et al.5 reported a dilation and elongation of retinal vessels before the onset of DME, although this was not found by Sander's study.1 Retinal venular dilation resulting from retinal hypoxia and lactate accumulation is suggested to be one of the earliest changes in the microcirculation of persons with diabetes. These observations support the concept that microvascular disease, as evident in the diabetic retina, plays an important pathogenic role in DME. The failure to find a significant predictive role of retinal vessel diameter for CSME by Sander et al. may be the result of a number of different limitations. First, insufficient power from the small sample size might have limited the study's ability to detect a significant predictive ability for CSME. Second, the study sample was highly selective: patients were included in a multicenter study exploring the effect of ruboxistaurin versus placebo, and almost half of the enrolled eyes were excluded from the vessel diameter assessment without any obvious data of exclusion. Third, the statistical analysis did not take into account factors that might have influenced the retinal vessel diameter. Of particular concern was the fact that ruboxistaurin dosage and photocoagulation features standardization for CSME was not performed. To further examine these issues, we analyzed cross-sectional data in 22 patients (36 eyes) with persistent DME from a multi-centered prospective randomized, placebo-controlled clinical trial of intravitreal triamcinolone and laser treatment versus laser treatment alone for DME.6 Retinal vessel caliber was measured from baseline photographs and central macular thickness was measured from optical coherence tomography using similar methodology as described by Sander et al.1 In models adjusted for age, gender, diabetes duration, HbA1c, mean arterial blood pressure, number of laser treatments prior to baseline examination and diabetic retinopathy severity, we found that retinal arteriolar and venular diameter was not significantly associated with CMT. Our results therefore support Sander's findings that retinal vessel diameter is not associated with DME. However, our study is also limited by inadequate power to detect a significant, but subtle, correlation if one does exist. Furthermore, the lack of more comprehensive information regarding prior laser treatment may have led to residual confounding in our statistical model.7 The lack of a correlation between retinal vessel diameter and DME is surprising but tends to support the concept that the relationship between blood-retinal barrier leakage and retinal edema may be more complex than first thought. Clearly, future larger sample sized studies are needed to verify the hypothesis that changes in measurable retinal vasculature changes are associated with and predictive of DME. Ieva Sliesoraityte1,2 1Centre for Eye Research Australia, University of Melbourne, Australia References 1. Sander B, Thornit DN, Colmorn L, et al. Progression of diabetic macular edema: correlation with blood retinal barrier permeability, retinal thickness, and retinal vessel diameter. Invest Ophthalmol Vis Sci. 2007;48:3983-3987. |
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Birgit Sander
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bisan{at}glo.regionh.dk Birgit Sander
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Sliesoraityte et al. address the compatibility of information from smaller-scale clinical physiology studies applying multiple time-consuming methods of investigation with findings from epidemiological-scale studies comprising a more limited number of methods. Sliesoraityte et al. express concern that failure to identify a predictive role of retinal vessel diameters may be attributable to lack of study power or other technical issues. There are multiple mechanisms whereby vasodilation may be produced and involved in the pathogenesis of diabetic macular edema, including inflammation, vascular endothelial dysfunction, hyperperfusion, and venous congestion.1 The prominent vasoconstriction that follows intravitreal triamcinolone acetonide injection in eyes with diabetic macular edema suggests that vasodilation may be a critical component in the pathogenesis of the edema.2 The Wisconsin Epidemiologic Study of Diabetic Retinopathy showed that baseline venous caliber is significantly associated with incidence and progression of retinopathy, but venous caliber did not predict progression to clinically significant macular edema (CSME) over 4 years after adjusting for covariates. Kristinsson showed a significant increase in both arteriolar end venous caliber preceding CSME in a study of 12 eyes; however, they did not report blood-pressure and HbA1c. Our study included 36 eyes (one eye analyzed in each patient) out of those, 11 eyes progressed during 4 years follow-up. We failed to detect vascular diameter changes both with and without inclusion of covariates and treatment with ruboxistaurin. Thus, a straightforward association of vessel calibers with diabetic macular edema is controversial despite several papers showing constriction of retinal vessels and blood flow after successful photocoagulation treatment. Our study population was rather homogeneous at baseline (retinopathy level < 47) and with stable HbA1c and blood pressure during follow-up. The lack of significant changes might hypothetically be explained by the large interindividual variation in retinal vessel diameters and consequently the need for very large numbers to assess such an effect or lack thereof. The ideal study of retinal vessel calibres and their relation to diabetic macular edema should include data from before the onset of diabetic retinopathy. Our patients had diabetic macular edema at baseline, of a lesser degree than clinically significant macular edema according to the ETDRS. Consequently, we cannot rule out the possibility that significant retinal vessel dilation had occurred before study entry. While vitreous fluorometry is a valuable method in experimental clinical pathophysiology, the need to exclude patients with posterior vitreous detachment limits its applicability in clinical practice. It is not unlikely, however, that current coherence tomography instruments and new methods of grading the distribution and severity of diabetic macular edema layer by retinal layer3 a clinically useful substitute marker of increased blood-retina barrier leakage may be extracted from optical coherence tomography. Birgit Sander1 1Glostrup Hospital - Ophthalmology, Glostrop, Denmark References 1. Larsen M. Unilateral macular oedema secondary to retinal venous congestion without occlusion in patients with diabetes mellitus. Acta Ophthalmol Scand. 2005;83:428-435. |
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