Moshfeghi Darius M, Kaiser Peter K, Grossniklaus Hans E, Sternberg Paul, Sears Jonathan E, Johnson Mark W, Ratliff Norman, Branco Andre, Blumenkranz Mark S, Lewis Hilel
Cole Eye Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
Am J Ophthalmol. 2003 Mar;135(3):343-50. doi: 10.1016/s0002-9394(02)01936-0.
To report the clinicopathologic findings after submacular removal of choroidal neovascular membranes (CNV) treated with verteporfin ocular photodynamic therapy.
Interventional case series.
Retrospective review of eight eyes of eight patients who underwent submacular surgery for CNV after having previously received verteporfin ocular photodynamic therapy for presumed ocular histoplasmosis (one patient), age-related macular degeneration ([AMD] three patients) pathologic myopia (two patients), punctate inner choroiditis (one patient), and idiopathic CNV (one patient). All cases had undergone ocular photodynamic therapy with verteporfin using standard protocols. Six of eight patients suffered a submacular hemorrhage after ocular photodynamic therapy, and two of eight patients refused further ocular photodynamic therapy. All patients subsequently had submacular surgery with removal of the CNV. One membrane was routinely processed, sectioned, and stained with hematoxylin and eosin. Five membranes were stained with toluidine blue for light microscopic examination. Semithin (1.0 microm) sections were cut and stained with uranyl acetate-lead citrate for transmission electron microscopy.
Choroidal neovascular membranes were removed at 3 days (presumed ocular histoplasmosis), 29 days (punctate inner choroiditis), 63 days (AMD, pathologic myopia), 66 days (AMD), 107 days (pathologic myopia), 116 days (AMD), and 152 days (idiopathic) after verteporfin ocular photodynamic therapy. Histopathologic and ultrastructural examination showed areas of vascular occlusion at 3 days that were not seen at later time points. All specimens had patent CNV. There were signs of vascular damage with extravasated erythrocytes and fibrin, pigment clumping in cells, and inflammatory cells in all but the 3-day specimen.
This case series presents data only from patients who refused repeat treatment with ocular photodynamic therapy or who developed submacular hemorrhage after initial photodynamic therapy. Histopathologic evaluation of CNV 3 days after verteporfin ocular photodynamic therapy showed partial vascular occlusion that was not present in later specimens. These later specimens demonstrated evidence of vascular damage. Verteporfin ocular photodynamic therapy does not appear to lead to permanent and complete occlusion of the CNV. Thus, treatments that lead to permanent closure of CNV without damage to the retinal pigment epithelium and sensory retina are still needed.
报告经维替泊芬眼内光动力疗法治疗后脉络膜新生血管膜（CNV）进行黄斑下切除术后的临床病理结果。
干预性病例系列。
回顾性分析8例患者的8只眼，这些患者在先前接受维替泊芬眼内光动力疗法治疗推测性眼组织胞浆菌病（1例患者）、年龄相关性黄斑变性（[AMD]3例患者）、病理性近视（2例患者）、点状内层脉络膜炎（1例患者）和特发性CNV（1例患者）后接受了黄斑下手术切除CNV。所有病例均按照标准方案接受了维替泊芬眼内光动力疗法。8例患者中有6例在眼内光动力疗法后发生黄斑下出血，8例患者中有2例拒绝进一步的眼内光动力疗法。所有患者随后均接受了黄斑下手术切除CNV。1个膜常规处理、切片并用苏木精和伊红染色。5个膜用甲苯胺蓝染色用于光镜检查。切取半薄（1.0微米）切片并用醋酸铀-柠檬酸铅染色用于透射电子显微镜检查。
在维替泊芬眼内光动力疗法后3天（推测性眼组织胞浆菌病）、29天（点状内层脉络膜炎）、63天（AMD、病理性近视）、66天（AMD）、107天（病理性近视）、116天（AMD）和152天（特发性）进行了脉络膜新生血管膜切除。组织病理学和超微结构检查显示3天时存在血管闭塞区域，而在后期时间点未见。所有标本的CNV均通畅。除3天标本外，所有标本均有血管损伤迹象，包括红细胞和纤维蛋白外渗、细胞内色素团块以及炎症细胞。
本病例系列仅呈现了拒绝重复眼内光动力疗法治疗或在初次光动力疗法后发生黄斑下出血的患者的数据。维替泊芬眼内光动力疗法后3天对CNV的组织病理学评估显示存在部分血管闭塞，而后期标本中不存在。这些后期标本显示有血管损伤的证据。维替泊芬眼内光动力疗法似乎不会导致CNV永久性和完全闭塞。因此，仍需要能导致CNV永久性闭合且不损伤视网膜色素上皮和感觉视网膜的治疗方法。
