IL-33/sST2 signaling pathway in pulmonary thromboembolism: A clinical observational study

IF 3.7 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Cytokine Pub Date : 2024-07-30 DOI:10.1016/j.cyto.2024.156707
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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.

Method

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).

Conclusion

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.

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肺血栓栓塞症中的 IL-33/sST2 信号通路:一项临床观察研究
背景:肺血栓栓塞症(PTE)是一种可导致死亡的心血管急症。在白细胞介素-33(IL-33)/可溶性抑制致瘤性2(sST2)信号通路中,sST2的增加是一个心血管风险因素。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、临床严重程度和死亡率方面的有效性:本研究是一项单中心、前瞻性、观察性研究。急诊科收治并确诊为 PTE 的患者构成患者组(n = 112),具有相似社会人口学特征的健康志愿者构成对照组(n = 62)。通过评估 IL-33/sST2 信号通路中的生物标志物来确定诊断、临床严重程度和预后:患者组的 IL-33 水平低于对照组(275.89 对 403.35 pg/mL),而患者组的 sST2 水平高于对照组(53.16 对 11.78 ng/mL)(p 14.48 ng/mL,敏感性 83%,特异性 71%)。与非死亡患者相比,死亡患者的 IL-33 水平较低(169.85 对 332.04 pg/mL),而与非死亡患者相比,死亡患者的 sST2 水平较高(118.32 对 28.07 ng/mL)(两者的 p > 0.001)。预测 PTE 死亡率的 IL-33 AUC 为 0.801(95 % CI:0.715-0.870)。预测 PTE 死亡率的最佳 IL-33 临界点为≤212.05 pg/mL(灵敏度为 75%,特异度为 79.5%)。预测 PTE 死亡率的 sST2 AUC 为 0.824(95 % CI:0.740-0.889)。预测 PTE 死亡率的最佳 sST2 临界点为 >81 ng/mL(灵敏度 95.8%,特异度 78.4%):结论:在 IL-33/ST2 信号通路中,IL-33 的降低和 sST2 的升高是诊断和预测 PTE 患者死亡率的重要生物标志物。
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来源期刊
Cytokine
Cytokine 医学-免疫学
CiteScore
7.60
自引率
2.60%
发文量
262
审稿时长
48 days
期刊介绍: The journal Cytokine has an open access mirror journal Cytokine: X, sharing the same aims and scope, editorial team, submission system and rigorous peer review. * Devoted exclusively to the study of the molecular biology, genetics, biochemistry, immunology, genome-wide association studies, pathobiology, diagnostic and clinical applications of all known interleukins, hematopoietic factors, growth factors, cytotoxins, interferons, new cytokines, and chemokines, Cytokine provides comprehensive coverage of cytokines and their mechanisms of actions, 12 times a year by publishing original high quality refereed scientific papers from prominent investigators in both the academic and industrial sectors. We will publish 3 major types of manuscripts: 1) Original manuscripts describing research results. 2) Basic and clinical reviews describing cytokine actions and regulation. 3) Short commentaries/perspectives on recently published aspects of cytokines, pathogenesis and clinical results.
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