Abstract
Purpose: :
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.
Methods: :
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.
Results: :
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).
Conclusions: :
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.
Keywords: clinical (human) or epidemiologic studies: natural history • diabetic retinopathy