Vitreous levels of placental growth factor correlate with activity of proliferative diabetic retinopathy and are not influenced by bevacizumab treatment.

PurposePlacental growth factor (PlGF) is a member of the VEGF family that plays an important role in experimental models of diabetic retinopathy and retinal neovascularization. We aimed to investigate whether vitreous levels of PlGF correlated with proliferative diabetic retinopathy (PDR) status, VEGF levels, and bevacizumab treatment. We also analysed PDR membranes to confirm the presence of the PlGF receptor, FLT1, in endothelial cells.MethodsThis was a case-control study: undiluted vitreous fluid samples were obtained from 28 active PDR patients without preoperative bevacizumab treatment, 21 active PDR patients with preoperative bevacizumab treatment, 18 inactive PDR patients, and 21 control patients. PlGF and VEGF levels in samples were determined by enzyme-linked immunosorbent assay. Immunohistochemistry for FLT1 was performed on human PDR membranes.ResultsCompared to control, vitreous PlGF levels were higher in both active PDR without bevacizumab (P<0.0001) and with bevacizumab (P<0.0001). There was no significant difference in PlGF between active PDR patients without and with bevacizumab (P=0.56). Compared to active PDR, PlGF levels were significantly reduced in inactive PDR (P=0.004). PlGF levels were highly correlated with VEGF levels in active PDR. VEGFR1 was expressed in endothelial cells in human PDR membranes.ConclusionThe strong correlation of PlGF levels with PDR disease status and expression of FLT1 in human PDR membranes suggest that PlGF has a pathogenic role in proliferative diabetic retinopathy. Therapeutic targeting of PlGF with agents like aflibercept may be beneficial.

Anterior ischaemic optic neuropathy associated with central retinal vein occlusion.

PURPOSE: To report the unusual association between non-arteritic anterior ischaemic optic neuropathy (NAION) and non-ischaemic central retinal vein occlusion (CRVO) in two patients. METHODS: Case reports are presented. RESULTS: Non-ischaemic CRVO was manifested by dilated, tortuous retinal veins with flame-shape retinal haemorrhages. Fluorescein angiography showed prolonged arteriovenous transit time and normal retinal capillary perfusion without macular oedema. The presence of colour vision abnormalities, relative afferent pupillary defects, pale disc swelling and visual field deficits indicated that the visual loss was attributable entirely to NAION. Laboratory investigations disclosed impaired fibrinolytic function in case 1 and the presence of antiphospholipid antibodies in case 2. CONCLUSIONS: Compression of the central retinal vein by the swollen optic nerve could have predisposed to CRVO. The presence of thrombophilic abnormalities may have contributed to the concomitant occlusion of posterior ciliary arteries and central retinal vein. Ischaemic optic neuropathy needs to be considered in patients with CRVO when the visual acuity is not consistent with the retinal pathology.