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目的:探讨鼻内翻性乳头状瘤组织中COX-2、p21、Ki-67的表达及HPV感染的临床意义。方法:应用免疫组织化学二步法检测30例鼻内翻性乳头状瘤(NIP)和20例鼻息肉(NP)及10例正常鼻腔黏膜组织(NM)中COX-2、p21、Ki-67表达情况,并用导流杂交方法检测HPV感染的情况。结果:NIP组、NP组和NM组中COX-2、Ki-67的阳性表达率呈依次降低的趋势;COX-2在3组间比较差异有统计学意义(χ2=30.00,P<0.05);Ki-67在NIP和NM组间比较差异有统计学意义(χ2=8.533,P<0.05)。经Spearman秩相关分析,COX-2与Ki-67的表达呈正相关(r=0.78,P<0.05)。p21在NIP组中未见表达。NIP组HPV病毒检出率为26.67%,均为HPV16型。结论:COX-2、Ki-67和HPV感染与NIP的发生、发展有一定相关性。COX-2介导的炎症反应,可能作为NIP发病的危险因素。Ki-67能较好地反映肿瘤细胞增殖活性,可作为衡量鼻内翻性乳头状瘤的增殖活性的指标。COX-2与Ki-67的表达在NIP的发病中具有协同作用。p21与NIP发病无明显相关。HPV感染与NIP的发病有关,但不能作为NIP发病的主要因素。
Objective: To investigate the expression of COX-2, p21 and Ki-67 in nasal inverted papilloma and the clinical significance of HPV infection. Methods: The expressions of COX-2, p21 and Ki-67 in 30 cases of nasal inverted papilloma (NIP), 20 cases of nasal polyps (NP) and 10 cases of normal nasal mucosa (NM) were detected by immunohistochemical two- Expression, and use of diversion method to detect HPV infection. Results: The positive expression rates of COX-2 and Ki-67 in NIP group, NP group and NM group showed a decreasing trend in turn. The difference of COX-2 between the three groups was statistically significant (χ2 = 30.00, P <0.05) Ki-67 was significantly different between NIP and NM (χ2 = 8.533, P <0.05). The Spearman rank correlation analysis showed that the expression of COX-2 and Ki-67 were positively correlated (r = 0.78, P <0.05). p21 was not seen in the NIP group. The detection rate of HPV in NIP group was 26.67%, both of which were HPV16 type. Conclusion: There is some correlation between COX-2, Ki-67 and HPV infection and the occurrence and development of NIP. COX-2-mediated inflammation may play a role as a risk factor for the pathogenesis of NIP. Ki-67 can better reflect tumor cell proliferative activity, can be used as a measure of nasal inverted papilloma proliferation activity index. The expression of COX-2 and Ki-67 have a synergistic effect in the pathogenesis of NIP. P21 and NIP incidence was not significantly correlated. HPV infection and the incidence of NIP, but not as a major factor in the pathogenesis of NIP.