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目的 肝癌自发性破裂在亚洲的发病率较高 ,且发病机理不详。在我们既往的研究中 ,首次发现抗原抗体复合物血管壁沉积及血管受损与其破裂有关。该研究中 ,对小动脉周围的弹性硬蛋白进行了深入的探讨 ,以进一步核实我们的前期发现。方法 采用免疫组化及投射电子显微镜的方法 ,对 2 3例肝癌破裂及 30例肝癌非破裂的手术标本进行检测。结果 在肝癌破裂组 ,患者小动脉的周围弹性硬蛋白厚度明显增厚 ,弹性硬蛋白增生、弹性蛋白酶异常分别及胶原纤维降解现象广泛存在 ;同时亦可发现弹性硬蛋白中的电子密度沉积物及中性粒细胞由血液浸入血管壁的现象 ;弹性硬蛋白中的电子密度沉积物代表了抗原抗体复合物的沉积 ,而中性粒细胞的浸润则将导致血管受损。由于受损后的血管将变得脆弱并易于破裂及腹腔内出血 ,因此推测预先存在于血管壁的抗原抗体复合物沉积及血管受损将与肝癌破裂有关。结论 抗原抗体复合物的血管壁沉积及其导致的血管受损与肝癌破裂有关。
The purpose of spontaneous rupture of liver cancer in Asia, a higher incidence, and the pathogenesis is unknown. In our previous study, it was first discovered that the deposition of the antigen-antibody complex on the vascular wall and the impairment of the blood vessel are related to their rupture. In this study, elastin around the arterioles was explored in depth to further verify our previous findings. Methods The specimens of 23 cases of liver cancer rupture and 30 cases of non-ruptured liver cancer were detected by immunohistochemistry and projection electron microscopy. Results In the ruptured liver cancer group, the thickness of elastin around the arterioles was significantly thicker, elastin hyperplasia, elastase abnormality and degradation of collagen fibers were widespread. At the same time, electron density deposits in elastin and Neutrophils are infiltrated by blood into the walls of blood vessels; electron density deposits in elastin represent deposits of antigen-antibody complexes, while neutrophil infiltration causes blood vessel damage. Since damaged blood vessels will become fragile and prone to rupture and intraperitoneal hemorrhage, presumably pre-existing in the walls of the antigen-antibody complex deposition and vascular damage will be related to liver cancer rupture. Conclusion The deposition of the vascular wall of the antigen-antibody complex and the consequent vascular damage are related to the rupture of the liver cancer.