Platelet derived growth factor and fibroblast growth factor basic levels in the vitreous of patients with vitreoretinal disorders
- aResearch Department, The Royal Victoria Eye & Ear Hospital, Dublin, bDepartment of Ophthalmology, The Royal Victoria Eye & Ear Hospital, Dublin, cNational Ophthalmic Pathology Laboratory, The Royal Victoria Eye & Ear Hospital, Dublin, dUniversity College Dublin, Belfield, Dublin, eDepartment of Nuclear Medicine, St Vincent’s Hospital, Dublin
- Miss Lorraine Cassidy, Ophthalmology Department, Clarendon Wing, Leeds General Infirmary, Belmont Grove, Leeds LS2 9NS.
- Accepted 13 August 1997
Abstract
AIM To determine the potential role of basic fibroblast growth factor (bFGF) and platelet derived growth factor (PDGF) in the pathogenesis of proliferative vitreoretinopathy (PVR).
METHODS An enzyme linked immunosorbent assay technique was used to determine the quantities of bFGF and PDGF in 38 vitreous samples taken from patients undergoing trans pars plana vitrectomy (PPV) for a variety of vitreoretinal disorders.
RESULTS bFGF levels ranged from undetectable to 318.7 pg/ml. The mean concentration was 27.57 pg/ml. PDGF levels ranged from undetectable to 160 pg/ml, the mean concentration being 40.06 pg/ml. Eight of 13 patients with clinical evidence of retinal detachment (RD) and PVR had significantly elevated bFGF concentrations, whereas only one of 11 patients with RD and no PVR had detectable bFGF; seven of eight patients with RD and PVR had elevated PDGF concentrations in the vitreous, whereas all 10 patients with RD and no PVR had no detectable vitreous PDGF. Eight patients with vitreous haemorrhage had raised PDGF concentrations, and the levels were particularly high (>120 pg/ml) in those two patients with active neovascularisation. Two out of nine patients with vitreous haemorrhage had raised bFGF levels.
CONCLUSIONS bFGF and PDGF concentrations are elevated in PVR even in the absence of vitreous haemorrhage, and not in patients with RD uncomplicated by PVR. This observation suggests that both cytokines may be involved in the pathogenesis of PVR.








