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目的研究眼眶静脉畸形经平阳霉素联合激光治疗后的组织病理变化并探讨两者联合治疗作用的机制。设计实验研究。研究对象19例非扩张型眼眶静脉畸形病理标本。方法 19例非扩张型眼眶静脉畸形病例中,11例行单纯手术切除,为对照组。8例瘤体注射平阳霉素1.6～8.0 mg,7天后Nd:YAG激光术中照射静脉畸形病灶(能量密度为60～100 J/cm2),然后手术切除,为联合治疗组。两组手术后标本均行HE染色观察内皮损伤并计分,行免疫组化染色观察基质金属蛋白酶(MMP-9)、血管内皮生长因子(VEGF)、α平滑肌肌动蛋白(α-SMA)的表达。主要指标MMP-9和α-SMA的表达水平。结果从联合治疗组的标本可观察到瘤体血管内皮细胞损伤、血栓形成和管腔闭塞表现,两组静脉管壁及内皮细胞损伤计分比较有显著性差异(P=0.044)。两组病例标本细胞中均有不同程度MMP-9和α-SMA表达,其中联合治疗组MMP-9(P=0.001)和α-SMA(P=0.024)表达水平低于对照组。结论 Nd:YAG激光与平阳霉素联合应用治疗眼眶静脉畸形的机制可能是通过损伤瘤体血管内皮和中膜,同时与下调MMP-9和α-SMA的表达水平有关。
Objective To study the histopathological changes of orbital venous malformations after combined with pingyangmycin and laser treatment and to explore the mechanism of the combined treatment. Design experiment research. 19 cases of non-dilated orbital venous malformations pathological specimens. Methods In 19 cases of non-dilated orbital venous malformations, 11 cases underwent simple surgical resection for the control group. 8 cases were injected with 1.6 ~ 8.0 mg of pingyangmycin, 7 days after irradiation Nd: YAG laser venous malformations (energy density of 60 ~ 100 J / cm2), and then surgical resection for the combined treatment group. The specimens of both groups were examined by HE staining and scored by HE staining. The expression of matrix metalloproteinase (MMP-9), vascular endothelial growth factor (VEGF) and alpha-smooth muscle actin (α-SMA) expression. The main indicators of MMP-9 and α-SMA expression levels. Results The tumor vascular endothelial cell injury, thrombosis and lumen occlusion were observed in the combined treatment group. There were significant differences between the two groups in the score of venous wall and endothelial cell injury (P = 0.044). The expression of MMP-9 and α-SMA in both groups were significantly different from those in the control group. The levels of MMP-9 (P = 0.001) and α-SMA (P = 0.024) in the combination group were lower than those in the control group. Conclusion The combination of Nd: YAG laser and pingyangmycin may be related to the treatment of orbital venous malformations by impairing the vascular endothelium and media of the tumor, as well as down-regulating the expression of MMP-9 and α-SMA.