Diabetic macular edema: Passive and active transport of fluorescein through the blood-retina barrier

PURPOSE. TO investigate the passive bidirectional and active outward transp ort of fluorescein through the blood-retina barrier (BRB) in diabetic patie nts with clinically significant macular edema and in healthy controls. METHODS. The passive and active transport of fluorescein through the BRB wa s quantitated by vitreous fluorometry. A previously developed method was us ed to model passive transport. A new simulation model was developed and eva luated for estimation of active transport. The study included 10 eyes of 5 healthy controls and 31 eyes of 20 diabetic patients with clinically signif icant diabetic macular edema (CSME) in at least one eye, totalling 25 eyes with CSME. RESULTS. Passive permeability of fluorescein was increased by a factor of 1 2 in eyes with edema compared to healthy controls (edema, 23.7 nm/sec; heal thy subjects, 1.9 nm/sec, P < 0.01), whereas the active transport was doubl ed (edema, 84.1 nm/ sec; healthy subjects, 43.5 nm/sec, P < 0.01). Unlike a ctive transport, passive permeability was related to the degree of retinopa thy, in that eyes with severe non-proliferative diabetic retinopathy had a passive permeability that was significantly increased compared to moderate retinopathy (32.1 nm/sec and 14.6 nm/sec, respectively, P < 0.05). The pass ive movement quantitated with vitreous fluorometry was larger for diffuse a nd mixed leakage compared to focal (P = 0.07). CONCLUSIONS. insofar as the movement of fluorescein can be taken as a probe for the movement of electrolytes and water, the pathogenesis of diabetic m acular edema seems to involve a disruption of the BRB, presumably its inner component. The active resorptive functions of the blood-retina barrier app ear to be compensatorily increased to counteract edema formation, although the increase is too small to prevent edema in the face of severe leakage th rough the blood-retina barrier.