PDF(Pubmed)
Abstract：
UNASSIGNED: Previous studies have linked genetics to knee osteoarthritis. Angiotensin-converting enzyme (ACE) gene I/D polymorphism may cause OA. However, evidence remains inconsistent. This study examines knee OA risk and ACE gene I/D polymorphism.
UNASSIGNED: We explored Europe PMC, Medline, Scopus, and Cochrane Library using keywords. Three assessment bias factors were assessed using the Newcastle-Ottawa Scale (NOS). Criteria for inclusion: (1) Split the study population into knee OA patients and healthy controls; (2) Analysed the ACE gene I/D polymorphism; (3) Case-control or cross-sectional surveys. Studies with non-knee OA, incomplete data, and no full-text were excluded. The odds ratio (OR) and 95% confidence intervals (95% CI) were calculated using random-effect models.
UNASSIGNED: A total of 6 case-control studies consist of 1,226 patients with knee OA and 1,145 healthy subjects as controls were included. Our pooled analysis revealed that a significant association between ACE gene I/D polymorphism and risk of knee OA was only seen in the dominant (DD + ID vs. II) [OR 1.69 (95% CI 1.14 - 2.50), p = 0.009, I2 = 72%], and ID vs. II [OR 1.37 (95% CI 1.01- 1.86), p = 0.04, I2 = 43%] genotype models. Other genotype models, including recessive (DD vs. ID + II), alleles (D vs. I), DD vs. ID, and DD vs. II models did not show a significant association with knee OA risk. Further regression analysis revealed that ethnicity and sex may influence those relationships in several genotype models.
UNASSIGNED: Dominant and ID vs. II ACE gene I/D polymorphism models increased knee OA risk significantly. More research with larger samples and different ethnic groups is needed to confirm our findings. After ethnicity subgroup analysis, some genetic models in our study showed significant heterogeneities, and most studies are from Asian countries with Asian populations, with little evidence on Arabs.
UNASSIGNED: We explored Europe PMC, Medline, Scopus, and Cochrane Library using keywords. Three assessment bias factors were assessed using the Newcastle-Ottawa Scale (NOS). Criteria for inclusion: (1) Split the study population into knee OA patients and healthy controls; (2) Analysed the ACE gene I/D polymorphism; (3) Case-control or cross-sectional surveys. Studies with non-knee OA, incomplete data, and no full-text were excluded. The odds ratio (OR) and 95% confidence intervals (95% CI) were calculated using random-effect models.
UNASSIGNED: A total of 6 case-control studies consist of 1,226 patients with knee OA and 1,145 healthy subjects as controls were included. Our pooled analysis revealed that a significant association between ACE gene I/D polymorphism and risk of knee OA was only seen in the dominant (DD + ID vs. II) [OR 1.69 (95% CI 1.14 - 2.50), p = 0.009, I2 = 72%], and ID vs. II [OR 1.37 (95% CI 1.01- 1.86), p = 0.04, I2 = 43%] genotype models. Other genotype models, including recessive (DD vs. ID + II), alleles (D vs. I), DD vs. ID, and DD vs. II models did not show a significant association with knee OA risk. Further regression analysis revealed that ethnicity and sex may influence those relationships in several genotype models.
UNASSIGNED: Dominant and ID vs. II ACE gene I/D polymorphism models increased knee OA risk significantly. More research with larger samples and different ethnic groups is needed to confirm our findings. After ethnicity subgroup analysis, some genetic models in our study showed significant heterogeneities, and most studies are from Asian countries with Asian populations, with little evidence on Arabs.
摘要：
■以前的研究已经将遗传学与膝骨关节炎联系起来。血管紧张素转换酶（ACE）基因I/D多态性可能导致OA。然而,证据仍然不一致。这项研究检查了膝关节OA风险和ACE基因I/D多态性。
■我们探索了欧洲PMC，Medline,Scopus,和Cochrane图书馆使用关键字。使用纽卡斯尔-渥太华量表（NOS）评估了三个评估偏倚因素。纳入标准：（1）将研究人群分为膝关节OA患者和健康对照；（2）分析ACE基因I/D多态性；（3）病例对照或横断面调查。非膝关节OA的研究，数据不完整,没有全文被排除在外。使用随机效应模型计算比值比(OR)和95%置信区间(95%CI)。
■总共6项病例对照研究包括1,226名膝关节OA患者和1,145名健康受试者作为对照。我们的汇总分析显示，ACE基因I/D多态性与膝关节OA风险之间的显着关联仅在显性（DDID与II）[OR1.69（95%CI1.14-2.50），p=0.009,I2=72%],和IDvs.II[OR1.37（95%CI1.01-1.86），p=0.04，I2=43%]基因型模型。其他基因型模型，包括隐性（DD与ID+II),等位基因(Dvs.I),DDvs.ID,和DD与II模型未显示与膝关节OA风险显著相关。进一步的回归分析显示，种族和性别可能会影响几种基因型模型中的这些关系。
■显性和ID与ⅡACE基因I/D多态性模子显著增长膝关节OA风险。需要对更大样本和不同种族群体进行更多研究来证实我们的发现。种族亚组分析后，我们研究中的一些遗传模型显示出显著的异质性，大多数研究来自亚洲人口的亚洲国家，几乎没有阿拉伯人的证据。
■我们探索了欧洲PMC，Medline,Scopus,和Cochrane图书馆使用关键字。使用纽卡斯尔-渥太华量表（NOS）评估了三个评估偏倚因素。纳入标准：（1）将研究人群分为膝关节OA患者和健康对照；（2）分析ACE基因I/D多态性；（3）病例对照或横断面调查。非膝关节OA的研究，数据不完整,没有全文被排除在外。使用随机效应模型计算比值比(OR)和95%置信区间(95%CI)。
■总共6项病例对照研究包括1,226名膝关节OA患者和1,145名健康受试者作为对照。我们的汇总分析显示，ACE基因I/D多态性与膝关节OA风险之间的显着关联仅在显性（DDID与II）[OR1.69（95%CI1.14-2.50），p=0.009,I2=72%],和IDvs.II[OR1.37（95%CI1.01-1.86），p=0.04，I2=43%]基因型模型。其他基因型模型，包括隐性（DD与ID+II),等位基因(Dvs.I),DDvs.ID,和DD与II模型未显示与膝关节OA风险显著相关。进一步的回归分析显示，种族和性别可能会影响几种基因型模型中的这些关系。
■显性和ID与ⅡACE基因I/D多态性模子显著增长膝关节OA风险。需要对更大样本和不同种族群体进行更多研究来证实我们的发现。种族亚组分析后，我们研究中的一些遗传模型显示出显著的异质性，大多数研究来自亚洲人口的亚洲国家，几乎没有阿拉伯人的证据。
