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العنوان
Vitreous Level Of Tumor Necrosis Factor Alpha In Patients With Retinal Vein Occlusion /
المؤلف
Amira Ahmed Abdel Hamid Taha,
هيئة الاعداد
باحث / Amira Ahmed Abdel Hamid Taha
مشرف / Sherif Aly Gamal El Dien
مشرف / Riham Assem Elessawy
مشرف / Mohamed Ahmed Mohamed Attya
الموضوع
Ophthalmology
تاريخ النشر
2022.
عدد الصفحات
113 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
طب العيون
تاريخ الإجازة
30/5/2022
مكان الإجازة
جامعة القاهرة - كلية الطب - Ophthalmology
الفهرس
Only 14 pages are availabe for public view

from 149

from 149

Abstract

Background: Retinal vein occlusion (RVO) is the second most common retinal
vascular disease and is an important cause of visual loss.
Ischemia triggers the release of inflammatory factors, including cytokines,
chemokines, and vascular endothelial growth factors(VEGF).
TNF- α is an inflammatory cytokine that increase the secretion of VEGF by human
RPE cells and choroidal fibroblasts with VEGF being the most important factor for
initiating pathological ocular neovascularization.
Purpose: To assess TNF- α level in vitreous samples of treatment naïve RVO
patients comparing them Patients with Idiopathic Macular holes and Epiretinal
membranes subjected to vitrectomy, thus evaluating its role in the pathogenesis of
RVO.
Methods: This is a case control study that was conducted on 45 eyes (20 eyes with
not previousely treated RVO as Cases & 25 eyes with Idiopathic Macular Holes and
ERMs as Controls) in the interval between November 2021 and May 2022. Vitreous
samples were collected, frozen and stored at -20c.The level of TNF- α was assessed
using Enzyme-linked Immunosorbent Assay (ELISA) Kits.
Results: Vitreous TNF-α level was higher in RVO subjects [4.92±0.74 (3.80- 6.20)
pg/ml; mean±SD (minimum-maximum)] than subjects without RVO [3.54±0.60
(2.60-5.00) pg/ml; p< 0.001]. There was no significant difference in vitreous TNF-
α level between different RVO subtypes among studied patients (p=0.592).
Conclusion: TNF-α level is increased in vitreous of RVO patients, Thus, it may be involved in its pathogenesis and Anti-TNF-a might be used as treatment targets in
the future.