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PURPOSE. To measure vitreous levels of solubleintercellular adhesion molecule-1 (sICAM-1) and soluble vascular cellularadhesion molecule-1 (sVCAM-1) in the eyes of patients with retinal detachment(RD) due to proliferative diabetic retinopathy (PDR) or proliferative vitreoretinopathy(PVR) and to determine whether the levels of these mediators correlated withclinical parameters of disease. METHODS. Undiluted vitreous specimens were collected from 50 eyes of 48patients undergoing vitrectomy for traction RD due to PDR (21 specimens) andrecurrent RD due to PVR (19 specimens). Control vitreous specimens were obtainedfrom patients undergoing macular hole repair (10 specimens). The levels ofsICAM-1 and sVCAM-1 were measured in each sample by specific enzyme-linkedimmunoadsorbent assays. RESULTS. Vitreous levels of sICAM-1 were significantly increased in vitreousspecimens from both PVR (median ± SD; 12.0 ± 76.3 ng/ml; P <0.01) and PDR (8.4 ± 24.0 ng/ml; P < 0.01) when compared to vitreousfrom eyes with macular holes (0.3 ± 4.2 ng/ml). Vitreous levels ofsVCAM-1 were significantly increased in both PVR (36.5 ± 255.2 ng/ml;P < 0.001) and PDR (26.2 ± 93.5 ng/ml; P < 0.01) when comparedto control vitreous (17.7 ± 7.8 ng/ml). The vitreous levels of sICAM-1were higher in cases of PDR which developed recurrent proliferative disease(P < 0.01) and recurrent RD (P = 0.01), whereas the levels of sICAM-1 inPVR and sVCAM-1 in PDR and PVR did not significantly correlate with theseclinical parameters. CONCLUSIONS. Soluble forms of ICAM-1 and VCAM-1 are increased in the vitreouscavity of patients with RD due to PDR or PVR, reflecting the inflammatorynature of these conditions and suggesting a possible role for these mediatorsin the pathogenesis of proliferative retinal disease. The vitreous levelsof these sCAMs at the time of surgery may serve as a marker of inflammation,but their specific levels do not predict the likelihood of recurrent prolife... [ABSTRACT FROM AUTHOR]

Purpose: To determine the influence of lens status on postoperative intraocular pressure (IOP) in eyes undergoing vitrectomy for repair of recurrent retinal detachment (RD) resulting from proliferative vitreoretinopathy (PVR). Design: Retrospective, consecutive, nonrandomized, single-center series. Methods: One hundred and forty-five eyes with recurrent RD resulting from PVR were reviewed retrospectively. In all, 99 eyes underwent relaxing retinotomy at the time of surgery (68.4%). Perfluorocarbon gas (n = 60) or silicone oil (n = 85) were used as postoperative tamponades. For analysis, eyes were subdivided first based on tamponade and retinotomy status. The resultant groups then were divided further by lens status into 2 groups: aphakic eyes (aphakic group) and phakic and pseudophakic eyes (nonaphakic group). Results: Surgical reattachment was achieved in all eyes except one. Eyes receiving both silicone oil and relaxing retinotomy had the worst baseline characteristics compared with those receiving other interventions. In this subset of eyes, a significantly lower proportion of hypotony was found in those eyes that were aphakic after surgery when compared with those eyes that were nonaphakic (P = .037). Conclusions: Surgical management of PVR often results in ultimate retinal reattachment. In eyes receiving both relaxing retinotomy and silicone oil, higher IOPs and a lower proportion of hypotony are found where a native lens or intraocular implant is absent. Removal of the lens or intraocular implant may be considered for those eyes at greatest risk of hypotony. [Copyright &y& Elsevier]

Abstract: We sought to study the presence of the receptor for advanced glycation endproducts (RAGE) and its ligands, advanced glycation endproducts (AGEs), S100/calgranulins and amphoterin (high mobility group box 1 protein; HMGB1), in the vitreous cavity and epiretinal membranes (ERMs) of eyes of patients with proliferative diabetic retinopathy (PDR) and proliferative vitreoretinopathy (PVR). Undiluted vitreous specimens were collected from 30 eyes of 30 patients undergoing pars plana vitrectomy for repair of retinal detachment (RD) secondary to PDR (n=15) or PVR (n=15). The vitreous samples obtained from 10 eyes undergoing macular hole repair were used as controls. Epiretinal membranes were obtained from eight eyes with PDR and from 10 eyes with PVR. The levels of AGEs in the vitreous were measured using ELISA. The vitreous levels of soluble RAGE (sRAGE), S100/calgranulins and amphoterin were measured using Western blot analyses. The localization of RAGE and its ligands in ERMs was determined with immunohistochemistry. The vitreous levels of sRAGE were significantly increased in both PDR and PVR (p≤0.05) compared to control vitreous. In both PDR and PVR, the vitreous levels of AGEs (p≤0.01), S100/calgranulins (p≤0.05), and amphoterin (p≤0.01) were also elevated compared to control eyes. Expression of RAGE was detected in six of eight ERMs from eyes with PDR and eight of 10 ERMs from eyes with PVR. Many cells expressing RAGE also expressed vimentin, suggesting a glial cell origin. Ligands for RAGE were also detected in ERMs, with AGEs detected in five eyes with PDR and eight eyes with PVR. Similarly, S100 and amphoterin ERM expression was observed in six eyes with PDR; these ligands were also expressed in ERMs from eyes with PVR (8 and 7 cases, respectively). We conclude that RAGE and its ligands are increased in the vitreous cavity of eyes with PDR and PVR and are present in ERMs of eyes with these proliferative retinal disorders. These findings suggest a role for the proinflammatory RAGE axis in the pathogenesis of proliferative retinal diseases. [Copyright &y& Elsevier]