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Mara Lorenzi, Lucia Sobrin; Pilot Validation of a Marker of Risk for Development of Diabetic Retinopathy. Invest. Ophthalmol. Vis. Sci. 2012;53(14):2850.
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© ARVO (1962-2015); The Authors (2016-present)
To develop a validated marker of risk for diabetic retinopathy, an essential tool for attempting predictable prevention. The ideal marker would make possible what is not possible today: a program of systematic surveillance that identifies patients at risk, and the development of adjunct drugs to be used at the appropriate time in the appropriate patients.
We had found that in patients with well-controlled type 1 diabetes and no retinopathy, the earliest detectable and reproducible abnormality of retinal vessels was a defective myogenic response to pressure. This was evidenced by lack of retinal arterial constriction --or occurrence of vasodilation-- in response to increased perfusion pressure induced by reclining. The abnormality was present in 8 of 17 patients tested (IOVS 2010, 51:6770-6775). Because the abnormality can damage the downstream capillaries via increased blood flow and hydrostatic pressure, we recalled patients studied 4 years earlier to investigate the development of clinical retinopathy. Retinopathy was diagnosed in a masked fashion by dilated ophthalmoscopy and 7 standard field eye photographs.
Four years had elapsed since the original testing for 6 of the patients with defective myogenic response (2.3 ±3.4 % increase in retinal arterial diameter) and 6 of the patients with normal response (- 6.0 ± 4.5% decrease in retinal arterial diameter) (P=0.004). At re-testing, age (34±9 y in the patients with abnormal response and 39±10 in those with normal response), and duration of diabetes (19±4 and 15±4 y, respectively) were similar. Retinopathy (ETDRS 20 or 35) was diagnosed in 4 of the 6 patients (66%) who had a defective myogenic response four years earlier, but in only 1 of the 6 patients (16%) who had a normal response (Chi-Square P=0.07, Fisher’s Exact P= 0.2).
The small size of the sample in which we could collect longitudinal data at this time precludes definitive conclusions. However, the trend for a greater frequency of new cases of retinopathy among diabetic patients who had had a defective myogenic response for at least 4 years (as compared to those who had a normal response four years prior), supports the candidacy of the defective myogenic response to become a marker of retinopathy risk and encourages a fully powered validation study.
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