Abstract
Aim: This study aimed to evaluate the safety and efficacy of intravitreal Ranibizumab 0.5mg in the treatment of macular edema secondary to retinal vein occlusion.
Patients & Methods: This was a prospective interventional analytical study included 39 eyes of 39 patients with retinal vein occlusion. Ophthalmic examination included assessment of visual acuity, measurement of intraocular pressure, and fundus examination. All patients were scanned using Swept source optical coherence tomography (3D DRI OCT Triton [plus], Topcon Corporation, Tokyo, Japan) to assess central macular thickness. The changes of visual acuity, IOP, and central macular thickness were assessed. Data were analyzed via Kolmogorov-Smirnov test and Wilcoxon signed rank.
Results: The mean age was 56.56 ± 9.6, 48.7% were male and 51.3% were females. Hypertension was detected in 69.2%, and hyperlipidemia in 2.6%. The mean best corrected visual acuity was 1.5 logMAR, 1.00 logMAR,1.00 logMAR, preoperative, fourth month, six months postoperative, respectively, (p<0.001). The mean central macular thickness was 675 μ, 306 u, 264 u, preoperative, fourth month, six months postoperative, respectively, (p< 0.001). The OP was 16.5 mmHg, 16.9 mmHg, 17.1 mmHg, preoperative, fourth month, six months postoperative, respectively, (p=0.423). There were no observed significant ocular adverse events such as ocular inflammation, sterile and infectious endophthalmitis, or sustained increase in intraocular pressure with the use of intravitreal ranizumab injections.
Conclusion: Intravitreal Ranibizumab injections as monotherapy have shown promising results with BCVA improvement and a decrease of central macular thickness in patients with macular edema secondary to retinal vein occlusion.
Keywords: Ranibizumab; Macular Thickness; OCT; Visual Acuity
Introduction
Retinal vein occlusion (RVO) is the most common retinal
vascular disease after diabetic retinopathy [1]. Depending on
the area of retinal venous drainage effectively occluded it is
broadly classified as either central retinal vein occlusion (CRVO),
hemispheric retinal vein occlusion , or branch retinal vein occlusion
(BRVO) [2]. Although the exact etiology of RVO remains elusive, it
is likely to follow a thrombotic event. In CRVO this may occur in
the central retinal vein (CRV) at the lamina cribrosa or at a variable
distance in its journey within the optic nerve posterior to the lamina
cribrosa [2]. Hypoxia-induced expression of vascular endothelial
growth factor (VEGF) is thought to be a trigger for macular edema.
High intravitreal levels of VEGF have been found in patients with
retinal vein occlusion [3]. Upregulation of VEGF is associated with
breakdown of the blood-retina barrier with increased vascular
permeability resulting in retinal edema, stimulation of endothelial
cell growth, and neovascularization [4,5]. Macular edema leads to
vision loss in many patients with either central or branch retinal
vein occlusions (CRVO or BRVO). BRVO is the more common of the
two presentations, accounting for approximately 80% of RVO [6].
Recently, there has been interest in the use of vascular
endothelial growth factor (VEGF) inhibition in the treatment of RVO
because of the observation of increased VEGF in the vitreous and
aqueous of patients with these conditions [7].
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