Abstract
To investigate the semophorin 3A (SEMA3A) level in aqueous humor of patients with retinal vein occlusion (RVO) and explore the correlation of SEMA3A with macular oedema and ganglion cell degeneration in RVO. This comparative study prospectively included 41 consecutive patients (41 eyes) with RVO who had intravitreal anti-VEGF injections from March 2014 to March 2015 for cystoid macular oedema (CME) or neovascular glaucoma (NVG). The patients were divided into three groups according to the fluorescein angiograghy (FFA): central retinal vein occlusion (CRVO) group (n=15), branch retinal vein occlusion (BRVO) group (n=15) and NVG group (secondary to CRVO, n=11). The patients who had undergone cataract surgery (n=16) during the same period served as controls. The SEMA3A concentration in aqueous humor collected before the initial anti-VEGF injection was determined by enzyme-linked immunosorbent assay (ELISA). Central retinal thickness (CRT), cube volume (CV) and ganglion cell-inner plexiform layer (GC-IPL) thickness was analysed by spectral-domain optical coherence tomography (SD-OCT). Semaphorin 3A level in CRVO group (1.52±1.23ng/ml) and NVG group (1.67±0.98ng/ml) were significantly higher than the control group (0.66 ± 0.58ng/ml; both p<0.05). Moreover, SEMA3A level in CRVO group was higher than BRVO group (1.52±1.23ng/ml versus 0.53±0.37ng/ml; p<0.05). 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). In RVO patients, the GC-IPL thickness of affected eyes were significantly reduced compared with the normal follow eyes (CRVOt=4.55, p=0.006; BRVOt=4.54, p=0.004). Meanwhile, negative correlation of SEMA3A level with GC-IPL thickness was found in both BRVO group (r=-0.5906, p=0.0205) and CRVO group (r=-0.6100, p=0.0157). Semaphorin 3A level is increased in aqueous humor of RVO patients. Positive correlation of CRT as well as negative correlation of GC-IPL thickness with SEMA3A may suggest a pathological role of SEMA3A in macular oedema and ganglion cell degeneration during RVO.
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