Immunohistopathologic evaluation of choroidal neovascular membranes following verteporfin-photodynamic therapy.
OBJECTIVE
To evaluate the vascularization and proliferative activity in choroidal neovascular membranes due to age-related macular degeneration after verteporfin photodynamic therapy and submacular removal.


METHODS
Interventional case series.


METHODS
In a retrospective review of seven patients who underwent removal of subfoveal classic choroidal neovascular membranes after treatment with photodynamic therapy 3 to 146 days earlier, membranes were stained for CD 34, CD 105, and Ki-67 and correlated with clinical pictures and fluorescein angiography.


RESULTS
Fluorescein angiography performed on the day of surgery disclosed nonperfusion of the treated area 3 days after photodynamic therapy, but perfusion and leakage were seen at greater post-photodynamic therapy intervals. Membranes excised 3 days after photodynamic therapy showed CD34 and CD105 positive, mostly occluded vessels. The endothelial cells appeared damaged. Ki-67 activity was low. In membranes excised 34 to 146 days after photodynamic therapy, all vessels appeared patent and were lined by healthy endothelial cells with strong expression of CD34 and CD105. Ki-67 expression was elevated after 34 days but decreased thereafter.


CONCLUSIONS
Photodynamic therapy did not cause a general or complete occlusion of vessels within the choroidal neovascular membranes, as suggested by fluorescein angiography 3 days postintervention, but the endothelial cells appeared to be severely damaged. Proliferative activity within these specimens was reduced. At longer intervals after photodynamic therapy, the fibrovascular tissue seemed to recover; perfusion, hyperfluorescence, and leakage of the choroidal neovascular membranes could be detected by fluorescein angiography. The clinical appearance showed a correlation with the immunohistologic characteristics of an increased proliferative activity and patent vascularization.
Grisanti
Salvatore
S
Department of Ophthalmology I, Division of Vitreoretinal Surgery, Eberhard-Karls University of Tuebingen, Schleichstrasse 12-15, 72076 Tuebingen, Germany. salvatore.grisanti@med.uni-tuebingen.de
Tatar
Olcay
O
Canbek
Serap
S
Lafaut
Bart A
BA
Gelisken
Faik
F
Inhoffen
Werner
W
Szurman
Peter
P
Aisenbrey
Sabin
S
Oficjalska-Mlynczak
Jolanta
J
Bartz-Schmidt
Karl Ulrich
KU
D000368:Aged; D000369:Aged, 80 and over; D015703:Antigens, CD; D018952:Antigens, CD34 / Q000378:metabolism; D002199:Capillary Permeability; D002829:Choroid / Q000098:blood supply; D020256:Choroidal Neovascularization / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D000071063:Endoglin; D004730:Endothelium, Vascular / Q000473:pathology; D005260:Female; D005355:Fibrosis; D005451:Fluorescein Angiography; D006801:Humans; D007124:Immunoenzyme Techniques; D019394:Ki-67 Antigen / 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*; D011956:Receptors, Cell Surface; D012189:Retrospective Studies; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism; D000077362:Verteporfin
D015703:Antigens, CD; D018952:Antigens, CD34; C064206:ENG protein, human; D000071063:Endoglin; D019394:Ki-67 Antigen; D017319:Photosensitizing Agents; D011166:Porphyrins; D011956:Receptors, Cell Surface; D019010:Vascular Cell Adhesion Molecule-1; D000077362:Verteporfin