Longitudinal Changes in Retinal Nerve Fiber Layer Thickness after Intravitreal Anti-vascular Endothelial Growth Factor Therapy
1
조회
0
다운로드
1
인용
0
참고문헌
키워드
초록
Purpose: To determine the effects of intravitreal anti-vascular endothelial growth factor (VEGF) on thickness ofthe retinal nerve fiber layer (RNFL) in patients with age-related macular degeneration. Methods: Twenty eyes of 20 patients diagnosed with age-related macular degeneration who underwent intravitrealanti-VEGF injection were studied. Postinjection RNFL thickness was measured using optical coherencetomography. Average thickness, four-quadrant RNFL thicknesses, and intraocular pressure (IOP) in affectedeyes were measured before and 6 and 12 months after anti-VEGF injection for comparison. RNFL thicknessand IOP in affected and normal fellow eyes were also compared. Given that macular lesions can affect RNFLthickness, the changes in thickness were evaluated by dividing the 12 clock-hour RNFL into the pathologic areasadjacent to the lesion and the non-pathologic area. Results: The mean clock-hour segment in the pathologic area was 4.8 hours. A significantly thicker RNFL wasexhibited in temporal quadrants and pathologic areas (p = 0.043 and 0.048, respectively) in affected eyesbefore injection compared to the baseline RNFL thickness in normal eyes. No significant differences werefound in RNFL thickness or IOP between affected and normal eyes after injection. The changes over time inthe temporal and pathologic areas were statistically significant at 6 and 12 months after injection compared tobaseline data (p < 0.05). No significant differences were displayed in RNFL thickness in the other three quadrantsor in non-pathologic areas in either affected or normal eyes. Sequential changes in RNFL thickness inaffected eyes were not significant. Conclusions: Repeat intravitreal anti-VEGF treatment did not have a significant effect on RNFL thickness. RNFL thickness significantly decreased with time in the pathologic areas and in the temporal segment adjacentto exudative macular lesions. The reduction in RNFL thickness was most likely associated with changesin the macular lesion rather than with anti-VEGF injection.
Abstract
Purpose: To determine the effects of intravitreal anti-vascular endothelial growth factor (VEGF) on thickness ofthe retinal nerve fiber layer (RNFL) in patients with age-related macular degeneration. Methods: Twenty eyes of 20 patients diagnosed with age-related macular degeneration who underwent intravitrealanti-VEGF injection were studied. Postinjection RNFL thickness was measured using optical coherencetomography. Average thickness, four-quadrant RNFL thicknesses, and intraocular pressure (IOP) in affectedeyes were measured before and 6 and 12 months after anti-VEGF injection for comparison. RNFL thicknessand IOP in affected and normal fellow eyes were also compared. Given that macular lesions can affect RNFLthickness, the changes in thickness were evaluated by dividing the 12 clock-hour RNFL into the pathologic areasadjacent to the lesion and the non-pathologic area. Results: The mean clock-hour segment in the pathologic area was 4.8 hours. A significantly thicker RNFL wasexhibited in temporal quadrants and pathologic areas (p = 0.043 and 0.048, respectively) in affected eyesbefore injection compared to the baseline RNFL thickness in normal eyes. No significant differences werefound in RNFL thickness or IOP between affected and normal eyes after injection. The changes over time inthe temporal and pathologic areas were statistically significant at 6 and 12 months after injection compared tobaseline data (p < 0.05). No significant differences were displayed in RNFL thickness in the other three quadrantsor in non-pathologic areas in either affected or normal eyes. Sequential changes in RNFL thickness inaffected eyes were not significant. Conclusions: Repeat intravitreal anti-VEGF treatment did not have a significant effect on RNFL thickness. RNFL thickness significantly decreased with time in the pathologic areas and in the temporal segment adjacentto exudative macular lesions. The reduction in RNFL thickness was most likely associated with changesin the macular lesion rather than with anti-VEGF injection.
참고문헌 (22)
- Rosenfeld PJ, "Ranibizumab for neovascular age-related macular degeneration", N Engl J Med, 355, pp.1419~1431 (2006)
- Gunther JB, "Bevacizumab (Avastin) for the treatment of ocular disease", Surv Ophthalmol, 54, pp.372~400 (2009)
- el Matri L, "Intravitreal injection of triamcinolone combined with bevacizumab for choroidal neovascularization associated with large retinal pigment epithelial detachment in age-related macular degeneration", Graefes Arch Clin Exp Ophthalmol, 248, pp.779~784 (2010)
- Jager RD, "Risks of intravitreous injection: a comprehensive review", Retina, 24, pp.676~698 (2004)
- Angulo Bocco MC, "Intravitreous injection: retrospective study on 2028 injections and their side effects", J Fr Ophtalmol, 31, pp.693~698 (2008)
- Sampat KM, "Complications of intravitreal injections", Curr Opin Ophthalmol, 21, pp.178~183 (2010)
- Day S, "Ocular complications after anti-vascular endothelial growth factor therapy in Medicare patients with age-related macular degeneration", Am J Ophthalmol, 152, pp.266~272 (2011)
- Hollands H, "Short-term intraocular pressure changes after intravitreal injection of bevacizumab", Can J Ophthalmol, 42, pp.807~811 (2007)
- Falkenstein IA, "Changes of intraocular pressure after intravitreal injection of bevacizumab (Avastin)", Retina, 27, pp.1044~1047 (2007)
- Kim JE, "Short-term intraocular pressure changes immediately after intravitreal injections of anti-vascular endothelial growth factor agents", Am J Ophthalmol, 146, pp.930~934 (2008)
- Sharei V, "Course of intraocular pressure after intravitreal injection of 0.05 mL ranibizumab (Lucentis)", Eur J Ophthalmol, 20, pp.174~179 (2010)
- Kahook MY, "Sustained elevation in intraocular pressure associated with intravitreal bevacizumab injections", Ophthalmic Surg Lasers Imaging, 40, pp.293~295 (2009)
- Bakri SJ, "Persisent ocular hypertension following intravitreal ranibizumab", Graefes Arch Clin Exp Ophthalmol, 246, pp.955~958 (2008)
- Adelman RA, "Persistent ocular hypertension following intravitreal bevacizumab and ranibizumab injections", J Ocul Pharmacol Ther, 26, pp.105~110 (2010)
- Jalil A, "Intravitreal bevacizumab (Avastin) causing acute glaucoma: an unreported complication", Eye (Lond), 21, pp.1541~ (2007)
- Sondell M, "Vascular endothelial growth factor has neurotrophic activity and stimulates axonal outgrowth, enhancing cell survival and Schwann cell proliferation in the peripheral nervous system", J Neurosci, 19, pp.5731~5740 (1999)
- Zachary I, "Neuroprotective role of vascular endothelial growth factor: signalling mechanisms, biological function, and therapeutic potential", Neurosignals, 14, pp.207~221 (2005)
- Nishijima K, "Vascular endothelial growth factor-A is a survival factor for retinal neurons and a critical neuroprotectant during the adaptive response to ischemic injury", Am J Pathol, 171, pp.53~67 (2007)
- Horsley MB, "Retinal nerve fiber layer thickness in patients receiving chronic anti-vascular endothelial growth factor therapy", Am J Ophthalmol, 150, pp.558~561 (2010)
- Seth RK, "Assessment of optic nerve cup-to-disk ratio changes in patients receiving multiple intravitreal injections of antivascular endothelial growth factor agents", Retina, 29, pp.956~959 (2009)
- Martinez-de-la-Casa JM, "Retinal nerve fiber layer thickness changes in patients with age-related macular degeneration treated with intravitreal ranibizumab", Invest Ophthalmol Vis Sci, 53, pp.6214~6218 (2012)
- Hwang DJ, "Effect of diabetic macular edema on peripapillary retinal nerve fiber layer thickness profiles", Invest Ophthalmol Vis Sci, 55, pp.4213~4219 (2014)