To investigate the relations of vascular endothelial growth factor, growth factors, soluble vascular endothelial growth factor receptors, and inflammatory factors to recurrence of macular edema after anti-vascular endothelial growth factor therapy in patients with branch retinal vein occlusion.
Thus, our study indicates that the traditional Chinese medicine HXMM could ameliorate retinal edema and rescue the retinal structure and function in BRVO models through promoting occluded vein recanalization, improving microcirculation, and regulating the expression of VEGF-<i>α</i>.
This suggests that factors or cytokines other than VEGF may be associated with inflammation and retinal hypoxia in BRVO and that the pathogenesis of macular edema is complicated.
Currently the first-line therapies for BRVO include anti-VEGF and dexamethasone implant treatment, however, with direct or indirect damage on retinal neurons, it has limited effect in improving patients visual acuity.
The results showed that adenovirus expressing VHL led to a significant reduction in VEGF expression in vitro under normoxic or hypoxic conditions. adVHL effectively inhibited angiogenesis in retina and iris in laser-induced multiple BRVO in monkey eyes.
A 31 year old woman with essential hypertension grade III and branch retinal vein occlusion with homozygous C677TMTHFR hyperhomocysteinemia and high Lp(a) levels.
Laboratory tests for coagulopathy, including the PT 20210 A variant, should be added to the examination of patients with central or BRVO, especially if most common risk factors for thrombosis have been excluded.
Change over 6 months in retinal ischemia status (central avascular [CA] zone and peripheral nonperfusion [PNP]), mean best-corrected visual acuity (BCVA), the development of shunt vessels and neovascularization, and frequency of laser therapy were assessed in retinal vein occlusion (RVO) patients treated with either ranibizumab 0.5 mg PRN or single dexamethasone 0.7 mg implant, as per European labels, in the COMRADE-B (N = 244; ranibizumab, 126, dexamethasone, 118) or COMRADE-C (N = 243; ranibizumab, 124, dexamethasone, 119) trials.
SEMA3A level was positively correlated with CRT and CV in both BRVO group (CRTr = 0.6535, p = 0.0082; CVr = 0.5190, p = 0.0474) and CRVO group (CRTr = 0.6270, p = 0.0124; CVr = 0.6898, p = 0.0044).
This is the second study in which we showed an increased retinal level of TTR following anti-vascular endothelial growth factor (VEGF) intervention in experimental BRVO.
Histology showed disruption of tissue architecture and temporary swelling with marked hypoxia coinciding with increased VEGF-A and hypoxia inducible factor-1α (HIF-1α) expression and elevation of proinflammatory cytokines within 3 days after experimental BRVO, followed by thinning of the inner retinal layers at later time points.
At the multiple logistic regression analysis, the adiponectin +275 T allele carrier and AGTR1 1166 C allele carrier status were found to be associated with an increased risk of BRVO (TT vs. GG and TG: odds ratio = 2.278, P = 0.002, 95% confidence interval: 1.370-3.789; CC vs. AA and AC: odds ratio = 1.804, P = 0.025, 95% confidence interval: 1.079-3.017).