寻常性银屑病患者表皮p16INK4a基因启动子高甲基化与临床资料的相关性研究

目的：探讨斑块状银屑病患者表皮p16^INK4a基因启动子甲基化状态，并分析与其临床资料的相关性。方法：按银屑病皮损面积和严重度指数（PASI）评分评估患者病情严重程度。采用甲基化特异PCR（MAP）方法检测p16^INK4a甲基化状态。结果：①银屑病患者皮损和非皮损表皮p16^INK4a基因的甲基化率分别为32．14％（9／28）和7．14％（2／28），皮损处明显高于非皮损处（P〈0．05），正常对照组中无表皮p16^INK4a基因甲基化（0/38）；②进行期皮损表皮p16^INK4a基因的甲基化率明显高于稳定期皮损（P〈0．05）；③皮损表皮p16^INK4a基因甲基化阳性患者的PASI评分明显高于甲基化阴性患者（P〈0．05）。结论：斑块状银屑病患者皮损表皮p16^INK4a基因启动子甲基化率明显增高，并与皮损严重程度和活动性有关，提示p16^INK4a基因启动子高甲基化在银屑病的发病中可能起作用。

Study on the relationship between p16INK4a promoter hypermethylation of epidermis and clinical status in psoriasis

Objective: To investigate the status of promoter methylation of p16INK4a gene from plaque psoriatic epidermis and the correlation between methylation and clinical conditions. Methods: The severity of psoriasis was evaluated by PASI scores. The methylation of p16INK4a gene was detected by methylation specific PCR (MSP). Results: The p16INK4a methylation rate of psoriatic lesions was significantly higher than that of non-lesional skin. Methylation of p16INK4a was not found in normal skins. The frequency of methylation of p16INK4a was markedly increased in progressive phase compared with that in stationary phase. PASI score in methylation patients was higher than that in unmethylation patients. Conclusions: The promotor hypermethylation of p16INK4a is observed significantly in the lesions from plaque psoriatic epidermis, and is related to the severity and of psoriasis. It suggests that the promotor hypermethylation of p16INK4a may play a role in the development of psoriasis.