effects of intravitreous injection on the expression of vascular endothelial growth inhibitor in vitreous of proliferative diabetic retinopathy

effects of intravitreous injection on the expression of vascular endothelial growth inhibitor in vitreous of proliferative diabetic retinopathy

;Rui Shi;Yong Ma;Feng Wang;Jian-Ping Wang
journal of fungi 2015 Vol. 15 pp. 985-988
183
shi2015guojieffects

Abstract

AIM: To explore the effects of intravitreous injection on vascular endothelial growth inhibitor(VEGI)and its relative cytokines in vitreous and to investigate its role in the pathogenesis of proliferative diabetic retinopathy(PDR).

METHODS: Fifty patients with 68 eyes were randomly divided into 2 groups according its treatment situation. Thirty-four patients with 41 eyes were chosen as group one, who were treated with bevacizumab 1.25mg(0.05mL)per eye, and group 2 composed of 16 patients(27 eyes), who were accepted intravitreal injection of triamcinolone acetonide 4mg(0.1mL). Twenty patients(20 eyes), who were diagnosed as macula hole, were chosen for control group. Certain patients were collected as target population according to the inclusion criteria. VEGI, IL-1β and VEGF in vitreous were determined by ELISA, in which the samples of 0.3mL vitreous were collected before intravitreal injection or at 1, 3, 6mo post-injection in the two groups. And the data obtained between groups were compared by SPSS 19.0 statistical software.

RESULTS: Significant difference was found between control group and experimental groups in which VEGI decreased while IL-1β and VEGF increased before injection(P<0.05). However, VEGI increased but IL-1β and VEGF decreased compared with control group after intravitreal injection(P<0.05). The clinical observation showed that the macula edema reduced in experimental groups post-injection, and experimental group 2 was better than experimental group 1 in the long-term results(P<0.05).

CONCLUSION: VEGI is found accompanied with VEGF and IL-1β in the vitreous, and they may play an important role in the pathogenesis of PDR.

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244243
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10.3980/j.issn.1672-5123.2015.6.12
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