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L. J. Ricker, A. Kijlstra, W. de Jager, A. T. A. Liem, F. Hendrikse, E. C. La Heij; The Role of CCL17, CCL19, CCL22, and CXCL10 in the Development of Proliferative Vitreoretinopathy Following Rhegmatogenous Retinal Detachment. Invest. Ophthalmol. Vis. Sci. 2010;51(13):839.
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© ARVO (1962-2015); The Authors (2016-present)
Chemokines have been implicated in the pathogenesis of proliferative vitreoretinopathy (PVR) following rhegmatogenous retinal detachment (RRD). The present study was performed to investigate chemokine expression in patients with primary RRD to gain insight in the early events underlying the future development of PVR.
A multiplex bead-based immunoassay was used to determine 15 different chemokines in subretinal fluid samples obtained from patients undergoing scleral buckling surgery for primary RRD. Based on a medical record study, a selection of subretinal fluid samples was made. Patients who developed a redetachment due to postsurgical PVR within 2½ months (n=25) were compared with controls who had an uncomplicated retinal detachment during the overall follow-up period (n=55). The median follow-up time was 21 months for the PVR group and 6 months for the control group. Controls were matched for gender, age, and storage time. Informed consent was obtained from all patients and the study conformed to the declaration of Helsinki.
Levels of CCL2, CCL11, CCL17, CCL18, CCL19, CCL22, CXCL8, CXCL9, and CXCL10 were significantly higher (P < 0.05) in patients who developed postoperative PVR after primary RRD than in patients with uncomplicated retinal detachment. After correction for multiple comparisons, CCL17 (P = 0.0482), CCL19 (P = 0.0033), CCL22 (P = 0.0039), and CXCL10 (P = 0.0449) remained statistically significant. A significant correlation was observed between CCL17 and CCL22 (r = 0.660; P < 0.0001) and CCL19 and CXCL10 (r = 0.618; P < 0.0001). No significant differences in chemokine expression were demonstrated between patients with different PVR grades.
Various chemokines play a role in the early stages of PVR pathogenesis and represent potential therapeutic targets for prevention of PVR membrane formation following retinal detachment surgery.
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