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.
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).
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.
The genotype distributions or allelic frequencies of ACE I/D, eNOS E298D, and p22phox-242 C/T did not significantly differ between the patients with BRVO and the control subjects.
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.
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.
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.
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>.