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目的:观察肺气肿合并肺纤维化(CPFE)淋巴细胞亚型的分布和III型前胶原氨基端肽(PIIINP)水平及纤维化程度,探讨其炎症反应、免疫状态与肺纤维化(PF)的关系。方法:对2005-03/2007-03西安交通大学第一附属医院收治的21例CPFE、25例特发性肺纤维化(IPF)19例对照进行如下检测:光镜下观察肺活检标本的病理改变;对支气管肺泡灌洗液(BALF)进行炎细胞计数和分类;流式细胞术(FCM)检测BALF中T淋巴细胞亚型;放射免疫法检测BALF和血清PⅢNP水平。结果:活检病理结果发现,IPF组纤维化率高于CPFE组(P<0.01),但两组纤维化率与是否吸烟均不相关(P>0.05);BALF炎细胞分类结果显示CPFE组细胞总数和淋巴细胞比例均高于IPF组和对照组(P<0.05,P<0.01);FCM检测BALF发现CPFE组CD8+T淋巴细胞百分比高于IPF组和对照组(P<0.05);CPFE组和IPF组CD4+/CD8+比值均明显低于对照组(P<0.01);三组之间CD4+的百分率无统计学差异;CPFE组与IPF组血清PIIINP检测值均高于对照组(P<0.01),其中CPFE组血清PIIINP检测值显著低于IPF组(P<0.01)。BALF与血清PIIINP水平呈正相关(γ=0.82)。结论:CPFE的PF病变具有自身特点和发展规律,香烟烟雾刺激可能并非其直接或主要致纤维化因素;CPFE肺组织局部具有较IPF和对照明显且以CD8+T淋巴细胞增高为主的炎性反应,抗淋巴细胞炎症和免疫调节治疗可能有助于改善病情;血清PⅢNP可用作早期发现CPFE和监测PF治疗的指标。
OBJECTIVE: To observe the distribution of lymphocyte subtypes and pulmonary fibrosis (PFE) in pulmonary emphysema complicated with pulmonary fibrosis (CPFE), the level of PIII and the degree of fibrosis, and to explore the relationship between inflammatory reaction, immune status and pulmonary fibrosis (PF) Relationship. Methods: 21 cases of CPFE and 25 cases of idiopathic pulmonary fibrosis (IPF) treated in the First Affiliated Hospital of Xi’an Jiaotong University from March 2005 to March 2007 were tested as follows: The pathological changes of lung biopsy specimens were observed under light microscope (BALF) were counted and classified. Inflammatory cytokines (BALF) and serum PⅢNP levels were detected by radioimmunoassay (FCM). Results: The results of biopsy showed that the fibrosis rate in IPF group was higher than that in CPFE group (P <0.01), but the fibrosis rate in both groups was not related to smoking (P> 0.05). The results of BALF inflammatory cells showed that the total number of cells in CPFE group (P <0.05, P <0.01). The percentage of CD8 + T lymphocytes in the CPFE group was higher than that in the IPF group and the control group by FCM (P <0.05) The percentage of CD4 + / CD8 + in IPF group was significantly lower than that in control group (P <0.01). There was no significant difference in the percentage of CD4 + between the three groups (P <0.01) The serum PIIINP in CPFE group was significantly lower than that in IPF group (P <0.01). BALF was positively correlated with serum PIIINP level (γ = 0.82). CONCLUSION: The PF lesion of CPFE has its own characteristics and developmental rules. Cigarette smoke stimulation may not be the direct or major cause of fibrosis. CPFE lung tissue has more inflammation than IPF and control and predominately increased CD8 + T lymphocyte Response, anti-lymphocyte inflammation and immunomodulatory therapy may help to improve the condition; serum PⅢNP can be used as an indicator of early detection of CPFE and monitoring of PF treatment.