巨噬细胞吞噬功能受损对肝癌自发性破裂的影响

Dysfunction of macrophage phagocytosis in patients with spontaneous rupture of hepatocellular carcinoma

目的检测巨噬细胞吞噬功能,探讨肝癌自发性破裂的发病机制。方法收集肝癌破裂组和非破裂组患者标本各9例,采用流式细胞术和免疫组织化学的方法。检测两组患者肝脏标本内巨噬细胞吞噬功能。结果自发性破裂组巨噬细胞吞噬免疫复合物能力明显低于非破裂组 [6．35‰(4．05、8．42‰)vs 9．16‰(6．42、10．82‰),P<0．05];自发性破裂组内巨噬细胞表面受体 CD11b、CD18和CD16的表达量百分率明显少于非破裂组[6．19％(4．70、7．02％)VS 10．25％ (8．83、11．95％),P<0．05;4．46％(3．85、5．77％)vs 7．09％(5．55、12．60％),P<0．05;2．64％ (1．74、4．11％vS6．43％(4．83、9．67％),P<0．05]。结论患者肝脏内巨噬细胞吞噬功能下降导致血管壁免疫复合物沉积、血管受损及小动脉脆病弱性变,在稍受外力的情况下极易破裂出血,并可能与肝癌自发性破裂有关。

Objective To study the relationship between the phagocytic function of macrophages and spontaneous rupture of hepatocellular carcinoma （HCC）. Methods The specimens were collected from 9 patients with ruptured HCC and 9 patients with non-ruptured HCC. Flow cytometry and immunohistochemical techniques were used to detect macrophage phagocytosis. Resalts Expression percents of CD11b, CD18 and CD16 of hepatic macrophage surface receptors from groups with spontaneous ruptured HCC were less than those in non-ruptured HCC in liver carcinoma tissues and adjacent non-carcinoma liv- er tissues markedly, with the difference being statistical significant [6.19 % （4.70, 7.02 % ） vs 10.25 % （8.83,11.95%）,P〈0.05;4.46% （3.85, 5.77%） vs 7.09% （5.55,12.60%）,P〈0.05;2.64% （1.74, 4.11%） vs 6.43% （4.83, 9.67%）, P〈 0.05]; Moreover, phagocytic permil of hepatic macrophage from groups with spontaneous ruptured HCC was less in non-raptured HCC markedly, with the difference being statistical significant [6.35%o （4.05, 8.42‰） vs 9.16‰ （6.42, 10.82‰） P 〈 0.05 ]. Conclusion The dysfunction of macrophage, which could result in the cumulating and deposition of immune compound and vascular injury, may be the factors involved in the pathogenesis of spontaneous rupture of HCC.