Early effects of triamcinolone on vascular endothelial growth factor and endostatin in human choroidal neovascularization.
OBJECTIVE
To evaluate the early effects of triamcinolone acetonide as monotherapy or as an adjuvant to ocular verteporfin photodynamic therapy (PDT) on angiogenesis in human choroidal neovascularization (CNV) secondary to age-related macular degeneration.


METHODS
Retrospective review of an interventional series of 55 patients who underwent CNV extraction. Eleven patients were treated with intravitreal triamcinolone acetonide (4 mg) monotherapy (triamcinolone-treated CNV group [n = 5]) or with PDT-triamcinolone combination therapy (PDT-triamcinolone-treated CNV group [n = 6]) 3 to 9 days before surgery. Forty patients who underwent CNV extraction without previous therapy (control CNV group) and 4 patients who underwent CNV extraction 3 days after PDT (PDT CNV group) served as control subjects. The CNV samples were stained for CD34, endostatin, cytokeratin 18, and vascular endothelial growth factor (VEGF).


RESULTS
Vascular endothelial growth factor expression was stronger in the PDT CNV samples (P < .001), triamcinolone CNV samples (P = .01), and PDT-triamcinolone CNV samples (P = .007) compared with the control CNV samples. There were no statistically significant differences in VEGF expression among the PDT CNV samples, triamcinolone CNV samples, and PDT-triamcinolone CNV samples. Endostatin expression was weaker in the PDT CNV samples than in the control CNV samples (P = .008). Endostatin expression was stronger in the triamcinolone CNV samples and the PDT-triamcinolone CNV samples compared with the control CNV samples (P = .001 and P < .001, respectively) and the PDT CNV samples (P < .001 for both).


CONCLUSIONS
To some extent, triamcinolone monotherapy seems to exert its angiogenesis inhibitory effects on CNV by enhancing endostatin expression rather than by suppressing VEGF expression.
Tatar
Olcay
O
Centre for Ophthalmology, University Eye Hospital, Eberhard-Karls University, Schleichstrasse 12-15, 72076 Tuebingen, Germany.
Shinoda
Kei
K
Kaiserling
Edwin
E
Pertile
Grazia
G
Eckardt
Claus
C
Mohr
Andreas
A
Yoeruek
Efdal
E
Szurman
Peter
P
Bartz-Schmidt
Karl U
KU
Grisanti
Salvatore
S
D000368:Aged; D000369:Aged, 80 and over; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D018952:Antigens, CD34 / Q000378:metabolism; D020256:Choroidal Neovascularization / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism; D004359:Drug Therapy, Combination; D043169:Endostatins / Q000378:metabolism*; D005260:Female; D006801:Humans; D007124:Immunoenzyme Techniques; D053538:Keratin-18 / Q000378:metabolism; D008268:Macular Degeneration / Q000150:complications; D008297:Male; D008875:Middle Aged; D010778:Photochemotherapy; D017319:Photosensitizing Agents / Q000627:therapeutic use; D011166:Porphyrins / Q000627:therapeutic use; D012189:Retrospective Studies; D014222:Triamcinolone Acetonide / Q000627:therapeutic use*; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism*; D000077362:Verteporfin
D000893:Anti-Inflammatory Agents; D018952:Antigens, CD34; D043169:Endostatins; D053538:Keratin-18; D017319:Photosensitizing Agents; D011166:Porphyrins; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D000077362:Verteporfin; D014222:Triamcinolone Acetonide