PDF(Pubmed)
Abstract：
UNASSIGNED: Blood counts and biochemical markers are among the most common tests performed in hospitals and most readily accepted by patients, and are widely regarded as reliable biomarkers in the literature. The aim of this study was to assess the causal relationship between blood counts, biochemical indicators and pulmonary arterial hypertension (PAH).
UNASSIGNED: A two-sample Mendelian randomization (MR) analysis was performed to assess the causal relationship between blood counts and biochemical indicators with PAH. The genome-wide association study (GWAS) for blood counts and biochemical indicators were obtained from the UK Biobank (UKBB), while the GWAS for PAH were sourced from the FinnGen Biobank. Inverse variance weighting (IVW) was used as the primary analysis method, supplemented by three sensitivity analyses to assess the robustness of the results. And we conducted an observational study using data from National Health and Nutrition Examination Survey (NHANES) 2003-2018 to verify the relationship.
UNASSIGNED: The MR analysis primarily using the IVW method revealed genetic variants of platelet count (OR=2.51, 95% CI 1.56-4.22, P<0.001), platelet crit(OR=1.87, 95% CI1.17-7.65, P=0.022), direct bilirubin (DBIL)(OR=1.71, 95%CI 1.18-2.47,P=0.004), insulin-like growth factor (IGF-1)(OR=0.51, 95% CI 0.27-0.96, P=0.038), Lipoprotein A (Lp(a))(OR=0.66, 95% CI 0.45-0.98, P=0.037) and total bilirubin (TBIL)(OR=0.51, 95% CI 0.27-0.96, P=0.038) were significantly associated with PAH. In NHANES, multivariate logistic regression analyses revealed a significant positive correlation between platelet count and volume and the risk of PAH, and a significant negative correlation between total bilirubin and PAH.
UNASSIGNED: Our study reveals a causal relationship between blood counts, biochemical indicators and pulmonary arterial hypertension. These findings offer novel insights into the etiology and pathological mechanisms of PAH, and emphasizes the important value of these markers as potential targets for the prevention and treatment of PAH.
UNASSIGNED: A two-sample Mendelian randomization (MR) analysis was performed to assess the causal relationship between blood counts and biochemical indicators with PAH. The genome-wide association study (GWAS) for blood counts and biochemical indicators were obtained from the UK Biobank (UKBB), while the GWAS for PAH were sourced from the FinnGen Biobank. Inverse variance weighting (IVW) was used as the primary analysis method, supplemented by three sensitivity analyses to assess the robustness of the results. And we conducted an observational study using data from National Health and Nutrition Examination Survey (NHANES) 2003-2018 to verify the relationship.
UNASSIGNED: The MR analysis primarily using the IVW method revealed genetic variants of platelet count (OR=2.51, 95% CI 1.56-4.22, P<0.001), platelet crit(OR=1.87, 95% CI1.17-7.65, P=0.022), direct bilirubin (DBIL)(OR=1.71, 95%CI 1.18-2.47,P=0.004), insulin-like growth factor (IGF-1)(OR=0.51, 95% CI 0.27-0.96, P=0.038), Lipoprotein A (Lp(a))(OR=0.66, 95% CI 0.45-0.98, P=0.037) and total bilirubin (TBIL)(OR=0.51, 95% CI 0.27-0.96, P=0.038) were significantly associated with PAH. In NHANES, multivariate logistic regression analyses revealed a significant positive correlation between platelet count and volume and the risk of PAH, and a significant negative correlation between total bilirubin and PAH.
UNASSIGNED: Our study reveals a causal relationship between blood counts, biochemical indicators and pulmonary arterial hypertension. These findings offer novel insights into the etiology and pathological mechanisms of PAH, and emphasizes the important value of these markers as potential targets for the prevention and treatment of PAH.
摘要：
血细胞计数和生化标志物是医院中最常见的检查，也是患者最容易接受的检查。在文献中被广泛认为是可靠的生物标志物。这项研究的目的是评估血细胞计数之间的因果关系，生化指标和肺动脉高压(PAH)。
■进行了双样本孟德尔随机化（MR）分析，以评估血细胞计数和生化指标与PAH的因果关系。全基因组关联研究（GWAS）的血细胞计数和生化指标是从英国生物银行（UKBB）获得的，而PAH的GWAS来自FinnGen生物库。采用方差反加权(IVW)作为主要分析方法，辅以三项敏感性分析，以评估结果的稳健性。我们使用2003-2018年国家健康和营养调查（NHANES）的数据进行了一项观察性研究，以验证这种关系。
■主要使用IVW方法的MR分析显示血小板计数的遗传变异（OR=2.51，95％CI1.56-4.22，P<0.001），血小板暴动(OR=1.87,95%CI1.17-7.65,P=0.022),直接胆红素（DBIL）（OR=1.71，95CI1.18-2.47，P=0.004），胰岛素样生长因子-1(OR=0.51,95%CI0.27～0.96,P=0.038),脂蛋白A（Lp（a））（OR=0.66，95％CI0.45-0.98，P=0.037）和总胆红素（TBIL）（OR=0.51，95％CI0.27-0.96，P=0.038）与PAH显著相关。在NHANES，多因素logistic回归分析显示血小板计数和体积与PAH风险之间存在显著正相关,总胆红素与PAH呈显著负相关。
■我们的研究揭示了血细胞计数之间的因果关系，生化指标与肺动脉高压。这些发现为PAH的病因和病理机制提供了新的见解，并强调了这些标志物作为预防和治疗PAH的潜在靶标的重要价值。
■进行了双样本孟德尔随机化（MR）分析，以评估血细胞计数和生化指标与PAH的因果关系。全基因组关联研究（GWAS）的血细胞计数和生化指标是从英国生物银行（UKBB）获得的，而PAH的GWAS来自FinnGen生物库。采用方差反加权(IVW)作为主要分析方法，辅以三项敏感性分析，以评估结果的稳健性。我们使用2003-2018年国家健康和营养调查（NHANES）的数据进行了一项观察性研究，以验证这种关系。
■主要使用IVW方法的MR分析显示血小板计数的遗传变异（OR=2.51，95％CI1.56-4.22，P<0.001），血小板暴动(OR=1.87,95%CI1.17-7.65,P=0.022),直接胆红素（DBIL）（OR=1.71，95CI1.18-2.47，P=0.004），胰岛素样生长因子-1(OR=0.51,95%CI0.27～0.96,P=0.038),脂蛋白A（Lp（a））（OR=0.66，95％CI0.45-0.98，P=0.037）和总胆红素（TBIL）（OR=0.51，95％CI0.27-0.96，P=0.038）与PAH显著相关。在NHANES，多因素logistic回归分析显示血小板计数和体积与PAH风险之间存在显著正相关,总胆红素与PAH呈显著负相关。
■我们的研究揭示了血细胞计数之间的因果关系，生化指标与肺动脉高压。这些发现为PAH的病因和病理机制提供了新的见解，并强调了这些标志物作为预防和治疗PAH的潜在靶标的重要价值。
