| Objective:Chronic obstructive pulmonary disease(COPD)is a common disease in the respiratory department,and its related pathogenic factors have always been controversial.At present,it is generally believed that external environmental factors and internal genetic factors jointly lead to the occurrence and development of COPD.Smoking is a common external pathogenic factor of COPD,and genetic mutation is a common internal pathogenic factor.With the development of biotechnology,many studies on Single Nucleotide Polymorphism(SNP)are provided.On this basis,we used meta analysis to systematically evaluate the relationship between the gene polymorphism of alveolar surfactant associated protein D(SP-D)and the risk of COPD in order to further study whether the SNP will change the risk of COPD.Methods:A comprehensive search of literatures related to SP-D gene mutation and COPD risk prediction published by domestic and foreign scholars on January 1,1997to December 30,2018 was conducted,and several major medical databases were examined.They include Wangfang Data Knowledge Service Platform,VIP,CNKI,China Dissertation Database,Web of Science,PubMed,EMbase and The Cochrane Library.The two researchers independently screened the literatures in strict accordance with inclusion criteria and exclusion criteria and summarized their opinions.For the articles finally included,the study was graded by the Newburg-Ottawa Scale(NOS).After carefully reading the included literature and extracting the corresponding data,statistical analysis was performed using Stata MP13.0(64-bit)software.After four genetic models(the allele,additive,recessive,and dominant models)were identified,If heterogeneity is not significant(P>0.05,I~2<50%),the mantel-haenszel fixed-effect model is used to calculate the odds ratio(OR)and its 95%confidence interval(CI).If the heterogeneity was significant(P<0.05,I~2>50%),then the mantel-haenszel random effect model was used to randomly calculate OR and its 95%CI.And the Egger method was used to analyze the bias of the articles included.Results:6 qualified literatures were included,including 659patients in case group and 597 patients in control group.For rs2243639,allele model(OR 1.14,95%CI 0.87-1.51,I~2=18.8%,P=0.337),additive model(OR1.36,95%CI 0.69-2.69,I~2=0,P=0.373),recessive model(OR 1.13,95%CI0.76-1.69,I~2=28.1%,P=0.544)dominant model(OR 1.36,95%CI 0.75-2.49,I~2=0,P=0.312)indicated that there was no significant statistical difference between the risk of SNP and COPD.In Caucasian populations,there is only one genetic model,the recessive model(OR 0.37,95%CI 0.14 to 0.96 I~2=0%,P=0.041)suggested an association between SNP and the risk of COPD,while the other three genetic models suggested no association between SNP and the risk of COPD.For the rs721917 gene,for the Asian populations,the allele model(OR 1.44;95%CI 1.20-1.73;I~2=0%,P<0.001),additive model(OR 2.15;95%CI 1.43-3.24;I~2=0%,P=0.001),recessive model(OR 1.47;95%CI1.07-2.01;I~2=0%,P=0.017),dominant model(OR 1.91;95%CI 1.41-2.58;I~2=0%,P<0.001)suggested an association between SNP and COPD risk.In Caucasian populations,all four genotypes suggested no association between SNP and COPD risk.At the same time,there was no obvious publication bias in the Egger test.Conclusions:for rs2243639,SP-D polymorphism does not affect the risk of COPD in Asian populations.In Caucasian populations,the genetic polymorphism of SP-D may be associated with the risk of COPD.For rs721917gene,and only for Asian populations,the polymorphism of SP-D gene may affect the risk of COPD,which is reflected in the increase in the number of T alleles compared with the increase in the number of C alleles may further increase the risk of COPD.Ultimately,we need more large,multicenter clinical trials to confirm these conclusions. |