Abstract
Our purpose was to evaluate the concentrations of vitreous cytokines in patients with rhegmatogenous retinal detachment (RRD). We hypothesized that patients with macula on RRD have lower levels of cytokines compared to patients with macula off RRD and proliferative vitreoretinopathy (PVR). Vitreous fluids were collected during 23G pars plana vitrectomy from 58 eyes of 58 patients. Indication for vitrectomy included macula off and macula on RRD, PVR, and idiopathic epiretinal membrane (ERM). A multiplex chemiluminescent immunoassay was performed to measure the concentrations of 48 cytokines, chemokines, and growth factors. Levels of HGF, IL-6, IL-8, IL-16, IFN-gamma, MCP-1, and MIF were significantly higher in all groups of retinal detachment compared to ERM. Levels of CTACK, eotaxin, G-CSF, IP-10, MIG, SCF, SCGF-beta, SDF-1alpha were significantly higher in PVR compared to macula on RRD and ERM. Levels of IL-1ra, IL-5, IL-9, M-CSF, MIP-1alpha, and TRIAL were significantly higher in PVR compared to macula on RRD. Our results indicate that the position of macula lutea and the presence of PVR significantly influence vitreous cytokine expression. The detected proteins may serve as biomarkers to estimate the possibility of PVR formation and may help to invent personalized therapeutic strategies to slow down or prevent PVR.
Highlights
In rhegmatogenous retinal detachment (RRD), liquified vitreous enters under the neurosensory retina through a retinal break, which leads to the separation of the photoreceptor outer segment from the underlying retinal pigment epithelium (RPE)
Four groups of patients were formed as follows: a control group consisting of patients without RRD who underwent vitrectomy for the management of epiretinal membrane (ERM), patients with macula off RRD with proliferative vitreoretinopathy (PVR)-C [15], patients with macula off and patients with macula on RRD without PVR
We performed a prospective clinical study in 42 patients with RRD and 16 age-matched controls with ERM to evaluate the concentrations of vitreous cytokines, chemokines and growth factors and to investigate if there is a difference in the cytokine profile of macula off, macula on RRD and PVR
Summary
In rhegmatogenous retinal detachment (RRD), liquified vitreous enters under the neurosensory retina through a retinal break, which leads to the separation of the photoreceptor outer segment from the underlying retinal pigment epithelium (RPE). [6] Many groups try to explore the possible non-surgical treatment of PVR, e.g. Pennock et al proposed that ranibizumab might be potential prophylaxis for PVR They discovered that ranibizumab reduced the bioactivity of vitreous of patients and experimental animals with PVR, and protected rabbits from developing the disease. Kunikata et al investigated the role of intravitreal injection of triamcinolone acetonide (IVTA) in preventing photoreceptor apoptosis in eyes with RRD. [10] Kawahara et al suggested that statins could be potent inhibitors of cicatricial contraction in proliferative vitreoretinal diseases They found that intravitreal injection of simvastatin dose-dependently prevented the progression of diseased states in an in vivo model of PVR. Markus et al studied the role of transglutaminase 2 in a knockout mouse model of PVR, and they found that the lack of transglutaminase 2 did not prevent the formation of PVR. [12] Despite these findings, there is no available cure or prophylaxis for PVR as of yet, apart from the surgical approach. [13]
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