Abstract：
BACKGROUND: Pulmonary thromboembolism (PTE) is a cardiovascular emergency that can result in mortality. In the interleukin-33 (IL-33) /soluble suppression of tumorigenicity 2 (sST2) signaling pathway, increased sST2 is a cardiovascular risk factor. This study aimed to investigate the effectiveness of biomarkers in the IL-33/sST2 signaling pathway in determining PTE diagnosis, clinical severity, and mortality.
METHODS: This study was conducted as a single-center, prospective, observational study. Patients admitted to the emergency department and diagnosed with PTE constituted the patient group (n = 112), and healthy volunteers with similar sociodemographic characteristics constituted the control group (n = 62). Biomarkers in the IL-33/sST2 signaling pathway were evaluated for diagnosis, clinical severity, and prognosis.
RESULTS: IL-33 was lower in the patient group than in the control group (275.89 versus 403.35 pg/mL), while sST2 levels were higher in the patient group than in the control group (53.16 versus 11.78 ng/mL) (p < 0.001 and p = 0.001; respectively). The AUC of IL-33 to diagnose PTE was 0.656 (95 % CI: 0.580-0.726). The optimal IL-33 cut-off point to diagnose PTE was ≤304.11 pg/mL (56.2 % sensitivity, 79 % specificity). The AUC of sST2 to diagnose PTE was 0.818 (95 % CI: 0.752-0.872). The optimal sST2 cut-off point to diagnose PTE was >14.48 ng/mL (83 % sensitivity, 71 % specificity). IL-33 levels were lower in patients with mortality (169.85 versus 332.04 pg/mL) compared to patients without mortality, whereas sST2 levels were higher in patients with mortality (118.32 versus 28.07 ng/mL) compared to patients without mortality (p > 0.001 for both). The AUC of IL-33 to predict the mortality of PTE was 0.801 (95 % CI: 0.715-0.870). The optimal IL-33 cut-off point to predict the mortality of PTE was ≤212.05 pg/mL (75 % sensitivity, 79.5 % specificity). The AUC of sST2 to predict the mortality of PTE was 0.824 (95 % CI: 0.740-0.889). The optimal sST2 cut-off point to predict the mortality of PTE was >81 ng/mL (95.8 % sensitivity, 78.4 % specificity).
CONCLUSIONS: In the IL-33/ST2 signaling pathway, decreased IL-33 and increased sST2 are valuable biomarkers for diagnosis and prediction of mortality in patients with PTE.
METHODS: This study was conducted as a single-center, prospective, observational study. Patients admitted to the emergency department and diagnosed with PTE constituted the patient group (n = 112), and healthy volunteers with similar sociodemographic characteristics constituted the control group (n = 62). Biomarkers in the IL-33/sST2 signaling pathway were evaluated for diagnosis, clinical severity, and prognosis.
RESULTS: IL-33 was lower in the patient group than in the control group (275.89 versus 403.35 pg/mL), while sST2 levels were higher in the patient group than in the control group (53.16 versus 11.78 ng/mL) (p < 0.001 and p = 0.001; respectively). The AUC of IL-33 to diagnose PTE was 0.656 (95 % CI: 0.580-0.726). The optimal IL-33 cut-off point to diagnose PTE was ≤304.11 pg/mL (56.2 % sensitivity, 79 % specificity). The AUC of sST2 to diagnose PTE was 0.818 (95 % CI: 0.752-0.872). The optimal sST2 cut-off point to diagnose PTE was >14.48 ng/mL (83 % sensitivity, 71 % specificity). IL-33 levels were lower in patients with mortality (169.85 versus 332.04 pg/mL) compared to patients without mortality, whereas sST2 levels were higher in patients with mortality (118.32 versus 28.07 ng/mL) compared to patients without mortality (p > 0.001 for both). The AUC of IL-33 to predict the mortality of PTE was 0.801 (95 % CI: 0.715-0.870). The optimal IL-33 cut-off point to predict the mortality of PTE was ≤212.05 pg/mL (75 % sensitivity, 79.5 % specificity). The AUC of sST2 to predict the mortality of PTE was 0.824 (95 % CI: 0.740-0.889). The optimal sST2 cut-off point to predict the mortality of PTE was >81 ng/mL (95.8 % sensitivity, 78.4 % specificity).
CONCLUSIONS: In the IL-33/ST2 signaling pathway, decreased IL-33 and increased sST2 are valuable biomarkers for diagnosis and prediction of mortality in patients with PTE.
摘要：
背景：肺血栓栓塞症（PTE）是一种心血管急症，可导致死亡。在白细胞介素-33（IL-33）/可溶性肿瘤形成抑制2（sST2）信号通路中，sST2升高是心血管危险因素。本研究旨在探讨IL-33/sST2信号通路中的生物标志物在确定PTE诊断中的有效性。临床严重程度，和死亡率。
方法：本研究以单中心，prospective,观察性研究。进入急诊科并诊断为PTE的患者构成患者组（n=112），和具有相似社会人口统计学特征的健康志愿者组成对照组(n=62)。评估IL-33/sST2信号通路中的生物标志物用于诊断，临床严重程度，和预后。
结果：患者组的IL-33低于对照组（275.89比403.35pg/mL），而患者组的sST2水平高于对照组（53.16对11.78ng/mL）（分别为p<0.001和p=0.001）。IL-33诊断PTE的AUC为0.656（95％CI：0.580-0.726）。诊断PTE的最佳IL-33临界点≤304.11pg/mL(灵敏度56.2%,79%的特异性)。sST2诊断PTE的AUC为0.818（95％CI：0.752-0.872）。诊断PTE的最佳sST2截止点>14.48ng/mL(83%灵敏度，71%的特异性)。与无死亡率患者相比，有死亡率患者的IL-33水平较低（169.85比332.04pg/mL），而与无死亡患者相比,有死亡患者的sST2水平较高(118.32vs28.07ng/mL)(两者p>0.001).IL-33预测PTE死亡率的AUC为0.801(95%CI:0.715-0.870)。预测PTE死亡率的最佳IL-33临界点≤212.05pg/mL(灵敏度为75%,79.5%特异性)。sST2预测PTE死亡率的AUC为0.824（95％CI：0.740-0.889）。预测PTE死亡率的最佳sST2临界点>81ng/mL(灵敏度为95.8%,78.4%的特异性)。
结论：在IL-33/ST2信号通路中，IL-33降低和sST2升高是诊断和预测PTE患者死亡率的有价值的生物标志物.
方法：本研究以单中心，prospective,观察性研究。进入急诊科并诊断为PTE的患者构成患者组（n=112），和具有相似社会人口统计学特征的健康志愿者组成对照组(n=62)。评估IL-33/sST2信号通路中的生物标志物用于诊断，临床严重程度，和预后。
结果：患者组的IL-33低于对照组（275.89比403.35pg/mL），而患者组的sST2水平高于对照组（53.16对11.78ng/mL）（分别为p<0.001和p=0.001）。IL-33诊断PTE的AUC为0.656（95％CI：0.580-0.726）。诊断PTE的最佳IL-33临界点≤304.11pg/mL(灵敏度56.2%,79%的特异性)。sST2诊断PTE的AUC为0.818（95％CI：0.752-0.872）。诊断PTE的最佳sST2截止点>14.48ng/mL(83%灵敏度，71%的特异性)。与无死亡率患者相比，有死亡率患者的IL-33水平较低（169.85比332.04pg/mL），而与无死亡患者相比,有死亡患者的sST2水平较高(118.32vs28.07ng/mL)(两者p>0.001).IL-33预测PTE死亡率的AUC为0.801(95%CI:0.715-0.870)。预测PTE死亡率的最佳IL-33临界点≤212.05pg/mL(灵敏度为75%,79.5%特异性)。sST2预测PTE死亡率的AUC为0.824（95％CI：0.740-0.889）。预测PTE死亡率的最佳sST2临界点>81ng/mL(灵敏度为95.8%,78.4%的特异性)。
结论：在IL-33/ST2信号通路中，IL-33降低和sST2升高是诊断和预测PTE患者死亡率的有价值的生物标志物.
