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Early Effects of Intravitreal Triamcinolone Acetonide on Inflammation and Proliferation in Human Choroidal Neovascularization
Olcay Tatar, MD;
Annemarie Adam, MTA;
Kei Shinoda, MD, PhD;
Edwin Kaiserling, MD;
Vicky Boeyden, MD;
Carl Claes, MD;
Claus Eckardt, MD;
Tillmann Eckert, MD;
Grazia Pertile, MD;
Gabor B. Scharioth, MD;
Efdal Yoeruek, MD;
Peter Szurman, MD;
Karl Ulrich Bartz-Schmidt, MD;
Salvatore Grisanti, MD
Arch Ophthalmol. 2009;127(3):275-281.
Objective To evaluate the early effects of triamcinolone acetonide (TA) on inflammation, proliferation, and vascular endothelial growth factor (VEGF) in human choroidal neovascularization (CNV).
Methods Retrospective review of an interventional case series of 29 patients who underwent macular translocation. Fourteen CNV membranes without previous therapy (control CNV group) and 4 CNV membranes excised 3 days after photodynamic therapy (PDT CNV group) comprised the control groups. Eleven patients were treated with intravitreal TA (TA CNV group; n = 5) or PDT and TA combined (PDT+TA CNV group; n = 6) 3 to 9 days preoperatively. The CNV membranes were stained for cytokeratin 18, CD34, VEGF, intercellular adhesion molecule-1 (ICAM-1), E-selectin, CD68, CD45, Ki-67, and Thy-1.
Results Treatment with TA and PDT+TA resulted in increased immunostaining of ICAM-1 in endothelial cells and the stroma and a higher percentage of Thy-1 expression than controls. The density of macrophages was significantly increased in PDT+TA CNV membranes. Leukocyte density and proliferative activity were lower in TA and PDT+TA CNV membranes. The total VEGF score was significantly increased in TA and PDT+TA CNV membranes compared with the control CNV membranes. Evidence of VEGF in the retinal pigment epithelium of PDT+TA CNV membranes was stronger than in control CNV membranes.
Conclusions Triamcinolone acetonide has no inhibitory effect on macrophage infiltration or ICAM-1, Thy-1, or VEGF expression in CNV membranes in the early term. The clinical benefits of TA are probably not based on pure antiinflammatory or VEGF-suppressing mechanisms.
Author Affiliations: University Eye Hospital at the Centre for Ophthalmology of the Eberhard-Karls University, Tuebingen, Germany (Drs Tatar, Yoeruek, Szurman, and Bartz-Schmidt); Department of Pathology, University of Tuebingen, Tuebingen, Germany (Dr Kaiserling and Ms Adam); Laboratory of Visual Physiology, National Institute of Sensory Organs, Tokyo, Japan (Dr Shinoda); AZ-Sint Augustinus, Antwerp, Belgium (Drs Boeyden and Claes); Augenklinik der Staedtischen Kliniken, Frankfurt am Main, Germany (Drs Eckert and Eckardt); Department of Ophthalmology, Sacro Cuore Hospital, Negrar, Italy (Dr Pertile); Augenzentrum Recklinghausen, Recklinghausen, Germany (Dr Scharioth); and Department of Ophthalmology, University Eye Hospital Luebeck, Luebeck, Germany (Dr Grisanti).
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