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.
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.
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.
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.
A 31 year old woman with essential hypertension grade III and branch retinal vein occlusion with homozygous C677TMTHFR hyperhomocysteinemia and high Lp(a) levels.
The purpose of this study was to investigate the effect of the von Hippel-Lindau (VHL) protein on VEGF gene expression in vitro and to determine whether adenovirus-mediated VHL intraocular gene transfer inhibits the development of angiogenesis in a monkey model of multiple branch retinal vein occlusion (BRVO).
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).
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.
The expressional levels of apoptosis related genes (Bax, Bcl-2) and inflammation related genes (IL-1 β, TNF α, MCP-1 and CCR2) were measured by real-time PCR, the results showed that minocycline treatment upregulated Bcl-2 expression and inhibits TNF α expression since early stage of BRVO.
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).
In 139 patients with CRVO (n = 88) and BRVO (n = 51) and in 40 healthy controls factor VIII, fibrinogen, antithrombin III, protein C, protein S, activated protein C resistance, anticardiolipin antibodies (ACA), homocysteine, factor V Leiden, prothrombin G20210A and methylene tetrahydrofolate reductase (MTHFR) C677T mutation were assessed retrospectively.