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永存原始玻璃体增生症晶状体后纤维血管膜组织病理学观察 被引量:5

Histopathological study of retrolental membranes secondary to persistent hyperplastic primary vitreous
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摘要 目的研究永存原始玻璃体增生症(PHPV)患者晶状体后纤维血管膜的组织病理学特点,以期探讨其可能发病机制。方法实验研究。对手术获取的6例(6只眼)PHPV患者晶状体后纤维血管膜HE染色和PAS染色,光镜下观察;应用I型胶原抗原、Ⅷ因子相关抗原、平滑肌肌动蛋白、上皮膜抗原、神经元特异性烯醇化酶、胶原纤维酸性蛋白及增殖细胞核抗原进行免疫组织化学染色,观察其组织病理学特点和细胞增殖情况;应用TUNEL染色法观察其细胞凋亡情况。结果HE染色可见PHPV晶状体后纤维血管膜含有致密的纤维结缔组织,其中可见淋巴细胞、肥大细胞等炎性细胞;PAS染色该组织内含有大量黏多糖成分;免疫组织化学染色可见PHPV晶状体后纤维血管膜中存在I型胶原、上皮组织、平滑肌组织、血管组织和神经组织,并存在大量增殖细胞;TUNEL染色证实纤维血管膜中存在凋亡细胞,晶状体后囊膜下亦存在凋亡的晶状体上皮细胞。结论PHPV晶状体后纤维血管膜组织构成与原始玻璃体细胞构成存在一致性,其形成机制可能系晶状体后纤维血管组织过度增殖及退化不足。炎症因素在其退化过程中扮演重要角色。 Objective To study the pathological characteristics of retrolental membranes (RLMs) secondary to persistent hyperplastic primary vitreous ( PHPV), and to discuss the possible pathogenesis of PHPV. Methods Experimental study. Six RLMs obtained from six patients with PHPV during vitrectomy were examined by light microscopy ( HE & PAS staining). All of them were observed with proliferating cell nuclear antigen (PCNA) immunostaining, together with collagen I , factor VI related antigen, smooth muscle actin (SMA), epithelial membrane antigen (EMA), neuron specific enolase (NSE) and glial fibrillary acidic protein (GFAP) staining. Apoptosis were detected by terminal deoxynucleotidyl transferasemediated deoxyuridine 5-triphosphate nick-end labeling (TUNEL). Results Light microscopy showed that the RLM was a dense connective tissue with numerous inflammatory cells including mast cells and lymphoeytes. PAS staining showed that RLMs contained a larger amount of polysaccharides. Histopathology and immunohistochemistry showed that there were vascular channels, smooth muscle cells, nervous cells and epithelial cells scattered in RLMs. Collagen I was the main component of RLMs. PCNA-positive nuclei were widely found in RLMs. TUNEL-positive nuclei were also found in all RLMs, as well as in the posterior subcapsular epithelial cells of lens. Conclusions The cell types of RLMs secondary to PHPV are similar to those of the primary vitreous. It is possible that the mechanism of the progression of RLMs is the overdevelopment and incomplete regression of the retrolental vascular system. Inflammation may play an important role in the regression of RLMs.
出处 《中华眼科杂志》 CAS CSCD 北大核心 2010年第4期317-322,共6页 Chinese Journal of Ophthalmology
关键词 永存原始玻璃体增生症 纤维血管膜 晶状体后 细胞增殖 细胞凋亡 Persistent hyperplastic primary vitreous Retrolental membrane Cell proliferation Apoptosis
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