Intravitreal bevacizumab in inflammatory ocular neovascularization.
OBJECTIVE
To assess the role of bevacizumab in inflammatory ocular neovascularization.


METHODS
Retrospective, multicenter, consecutive case series of inflammatory ocular neovascularization.


METHODS
Patients with inflammatory ocular neovascularization of varying causes for whom standard therapy failed were treated with intravitreal injection of bevacizumab. Main outcome measures included improvement of best-corrected visual acuity (BCVA) expressed in logarithm of minimum angle of resolution units, response of inflammatory ocular neovascularization by funduscopy and angiography, and decrease in central foveal thickness as measured by optical coherence tomography at the three-month follow-up.


RESULTS
At the three-month follow-up, 84 eyes of 79 patients had been treated with a mean of 1.3 injections (range, one to three). Thirty-four eyes showed juxtafoveal choroidal neovascularization (CNV), 34 eyes showed subfoveal CNV, eight eyes showed peripapillary CNV, and 11 eyes showed neovascularization of the disc (NVD) or neovascularization elsewhere (NVE). BCVA improved 2.4 lines from 0.68 (6/28 or 20/94) to 0.44 (6/17 or 20/55) (P < .001). BCVA improved by one to three lines in 34.5% of the eyes, by four to six lines in 16.7% of the eyes, and by more than six lines in 14.2% of the eyes. Function was unchanged in 23.8% of the eyes. BCVA worsened in 10.7% (zero to three lines in 7.1%, more than four lines in 3.6%). Central foveal thickness decreased from baseline 346 to 252 microm (P < .001). For CNV, 32 eyes (43.2%) had complete regression after the injection, 27 (36.5%) had partial regression, five (6.8%) had no response, and 10 eyes (13.5%) were not evaluated by the contributors. For NVD or NVE, seven eyes (63.6%) had complete regression of new vessels and four eyes (36.4%) had partial regression after the injection.


CONCLUSIONS
Intravitreal bevacizumab led to short-term significant visual improvement and regression of inflammatory ocular neovascularization in a wide variety of inflammatory ocular diseases.
Mansour
Ahmad M
AM
Department of Ophthalmology, American University of Beirut and Rafic Hariri University Hospital, Beirut, Lebanon. dr.ahmad@cyberia.net.lb
Mackensen
Friederike
F
Arevalo
J Fernando
JF
Ziemssen
Focke
F
Mahendradas
Padmamalini
P
Mehio-Sibai
Abla
A
Hrisomalos
Nicholas
N
Lai
Timothy Y Y
TY
Dodwell
David
D
Chan
Wai-Man
WM
Ness
Thomas
T
Banker
Alay S
AS
Pai
Sivakami A
SA
Berrocal
Maria H
MH
Tohme
Rania
R
Heiligenhaus
Arnd
A
Bashshur
Ziad F
ZF
Khairallah
Moncef
M
Salem
Khalil M
KM
Hrisomalos
Frank N
FN
Wood
Matthew H
MH
Heriot
Wilson
W
Adan
Alfredo
A
Kumar
Atul
A
Lim
Lyndell
L
Hall
Anthony
A
Becker
Matthias
M
D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D020533:Angiogenesis Inhibitors / Q000627:therapeutic use*; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized; D000068258:Bevacizumab; D002648:Child; D020256:Choroidal Neovascularization / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D005128:Eye Diseases / Q000150:complications; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007267:Injections; D008297:Male; D008875:Middle Aged; D009898:Optic Disk / Q000098:blood supply; D015861:Retinal Neovascularization / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D012189:Retrospective Studies; D041623:Tomography, Optical Coherence; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors; D014792:Visual Acuity / Q000502:physiology; D014822:Vitreous Body
D020533:Angiogenesis Inhibitors; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D042461:Vascular Endothelial Growth Factor A; D000068258:Bevacizumab