Basic fibroblast growth factor, glutamine synthetase, and interleukin-6 in vitreous fluid from eyes with retinal detachment complicated by proliferative vitreoretinopathy

被引:35
作者
La Heij, EC
Van De Waarenburg, MPH
Blaauwgeers, HGT
Kessels, AGH
Liem, ATA
Theunissen, C
Steinbusch, H
Hendrikse, F
机构
[1] Univ Hosp Maastricht, Dept Ophthalmol, NL-6202 AZ Maastricht, Netherlands
[2] Univ Hosp Maastricht, Dept Clin Epidemiol & Med Technol Assessment, NL-6202 AZ Maastricht, Netherlands
[3] Univ Hosp Maastricht, Dept Basic Neurosci, NL-6202 AZ Maastricht, Netherlands
关键词
D O I
10.1016/S0002-9394(02)01536-2
中图分类号
R77 [眼科学];
学科分类号
100212 ;
摘要
PURPOSE: To investigate the presence of basic fibroblast growth factor (bFGF), glutamine synthetase (GS), and interleukin-6 (IL-6) in vitreous fluid from eyes with retinal detachment complicated by proliferative vitreoretinopathy (PVR). DESIGN: Comparative case series; experimental study. METHODS: In a prospective study, we measured bFGF, GS, IL-6, and total protein in vitreous fluid samples from 53 eyes from 53 consecutive patients with PVR operated on in our hospital. As controls, vitreous fluid samples from eyes with a macular hole (n = 9) or pucker (n = 11) were used. MAIN OUTCOME MEASURES: Laboratory data of the patient group were compared with the control group and correlated with various clinical data, especially with visual recovery and redetachment. RESULTS: For IL,6, bFGF, and total protein we found significantly higher levels in PVR patients' eyes than in control eyes (P = .039 P = .046, and P < .0001, respectively). Within the PVR group, no significant correlation was found for IL-6, bFGF, GS, or total protein with the various tested clinical variables. CONCLUSIONS: We found increased levels of IL-6, FGF, and total protein in vitreous fluid from patients' eyes with PVR. Whether the increased levels of 11 6, bFGF, and total protein are the result of an injury-induced upregulation of these proteins as part of a self,protective mechanism of the retina to minimize photoreceptor damage after the mechanical injury induced by retinal detachment is, at present, not known. (C) 2002 by Elsevier Science Inc. All rights reserved.
引用
收藏
页码:367 / 375
页数:9
相关论文
共 34 条
[1]   Pathogenic mechanisms in proliferative vitreoretinopathy [J].
Campochiaro, PA .
ARCHIVES OF OPHTHALMOLOGY, 1997, 115 (02) :237-241
[2]  
Cao W, 1997, INVEST OPHTH VIS SCI, V38, P1358
[3]   Platelet derived growth factor and fibroblast growth factor basic levels in the vitreous of patients with vitreoretinal disorders [J].
Cassidy, L ;
Barry, P ;
Shaw, C ;
Duffy, J ;
Kennedy, S .
BRITISH JOURNAL OF OPHTHALMOLOGY, 1998, 82 (02) :181-185
[4]   PROLIFERATIVE VITREORETINOPATHY - PATHOBIOLOGY, SURGICAL-MANAGEMENT, AND ADJUNCTIVE TREATMENT [J].
CHARTERIS, DG .
BRITISH JOURNAL OF OPHTHALMOLOGY, 1995, 79 (10) :953-960
[5]   Inhibition of glutamine synthetase decreases proliferation of cultured rat intestinal epithelial cells [J].
DeMarco, V ;
Dyess, K ;
Strauss, D ;
West, CM ;
Neu, J .
JOURNAL OF NUTRITION, 1999, 129 (01) :57-62
[6]  
DONATI G, 1995, INVEST OPHTH VIS SCI, P2228
[7]  
El-Asrar Ahmed M. Abu, 1997, American Journal of Ophthalmology, V123, P599
[8]  
Geller SF, 2001, INVEST OPHTH VIS SCI, V42, P1363
[9]  
GELLER SF, 1995, INVEST OPHTH VIS SCI, V36, P737
[10]   Glutamine synthetase protects against neuronal degeneration in injured retinal tissue [J].
Gorovits, R ;
Avidan, N ;
Avisar, N ;
Shaked, I ;
Vardimon, L .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (13) :7024-7029