Arachidonic acid pathway in proliferative vitreoretinopathy: the study of the vitreous biomarker in rhegmatogenous retinal detachment

Background: While prompt surgical intervention is still the gold standard, controlling the inflammation may prevent or reduce the progression of PVR, thus increasing the surgical success rate. The arachidonic acid pathway has been reported to play a significant role in the development of PVR. This study aims to investigate the role of the arachidonic acid pathway and assess the related vitreous inflammatory biomarkers in cases of RRD with PVR. Methods: Thirty patients scheduled for a pars plana vitrectomy for RRD with PVR were included in the study. At the beginning of surgery, a sample of undiluted vitreous was collected in each patient to assess vitreous levels of inflammatory biomarkers, including PGE2, COX-2, TGF-β, monocytes (comparison of CD14 and CD45), and total protein. The vitreous inflammatory biomarkers were also analyzed based on the severity of PVR and the onset of RRD. Results: The mean of PGE2 level was 91.77 ± 31.87 pg/mL, the median (range) of COX-2 level was 1.32 (1.25–1.55) ng/mL; TGF-β was 51.83 (15.61–319.58) pg/mL; monocytes were 90.25 (24.85–95.24) %; and total protein was 4.81 (0.19–20.4) mg/dL. A noticeable trend was found towards the elevation of PGE2, COX-2, TGF-β, monocytes, and total protein vitreous levels in conjunction with the severity of PVR, although no significant differences between the groups (p > 0.05 in each group). Conclusion: Inflammation, particularly the arachidonic acid pathway, plays a vital role in the early stage of the pathogenesis of PVR. Inhibition of the arachidonic pathway by the anti-inflammatory agent at the early stage may provide a therapeutic approach for PVR prevention.