摘要
目的 探讨肝癌自发性破裂的病理机制。方法 对肝癌破裂及非破裂患者的标本各30例 ,采用免疫荧光、免疫组化、流式细胞的方法 ,检查患者体内巨噬细胞吞噬功能及其血管壁上有无抗原抗体复合物的沉积。结果 研究发现 ,肿瘤破裂的患者巨噬细胞吞噬功能受损 ,导致体内抗原抗体复合物 (IC)积聚并沉积在血管壁上 ;IC由乙肝病毒e1抗原 (HBeAg/ 1)、免疫球蛋白和补体C1q所组成 ,主要沉积在小动脉壁的弹力膜上 ;在IC的沉积处 ,其小动脉壁存在血管受损现象。结论 患者体内巨噬细胞功能受损导致的IC血管沉积及小动脉受损 ,致使小动脉脆弱 ,在受力情况下极易破裂出血 。
Objective To study the mechanism of spontaneous rupture of hepatocellular carcinoma (HCC). Methods The specimens of 30 patients with ruptured HCC and 30 patients with non ruptured HCC were collected. Immunofluorescence, immunohistochemical and flow cyotmetry techniques were used to detect the phagocytosis of macrophages and the deposition of immune complex (IC) on vascular wall. Results In this study, the poor function of macrophage phagocytosis was found in patients with ruptured HCC, which could results in the cumulating of IC and deposition on vascular wall. The IC, which composed of hepatitis B virus e1 antigen (HBeAg/1), complement C1q and immunoglobulins, was found deposited in the elastic membrane of arteries. Likely as a result of IC deposition, vascular injury occurs mainly in the small arteries where the deposition of IC was present. As the small arteries were the blood vessels with predominant injury, they would likely to be the ones to split and cause hemorrhage and rupture of HCC during vascular load increase. Conclusions We would conclude that the poor function of macrophage phagocytosis, which lead to the IC deposition and vascular injury may be the factors involved in the pathogenesis of ruptured HCC.
出处
《中华外科杂志》
CAS
CSCD
北大核心
2004年第17期1036-1039,共4页
Chinese Journal of Surgery
基金
安徽省自然科学基金资助项目 (0 3 0 43 70 2 )
