肝硬化患者肝、颈静脉炎性细胞因子水平的比较

IF 4.4 3区 医学 Q2 CELL BIOLOGY Mediators of Inflammation Pub Date : 2023-11-29 DOI:10.1155/2023/9930902
Leonard Kaps, Carolina Medina-Montano, Matthias Bros, Stephan Grabbe, Simon Johannes Gairing, Eva M. Schleicher, Stephan Gehring, Jörn M. Schattenberg, Peter R. Galle, Marcus-Alexander Wörns, Michael Nagel, Christian Labenz
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Serum levels of 13 inflammatory cytokines (IL-1<i>β</i>, Int-<i>α</i>2, Int-<i>γ</i>, TNF-<i>α</i>, MCP-1, IL-6, IL-8, IL-10, IL-12p70, IL-17A, IL-18, IL-23, and IL-33) were quantified by cytometric bead array. <i>Results</i>. Cytokine levels of IFN-<i>α</i>2, IFN-<i>γ</i>, TNF-<i>α</i>, IL-6, IL-8, IL-10, IL-17A, IL-18, IL-23, and IL-33 were significantly elevated in patients with decompensated cirrhosis compared to patients with compensated cirrhosis. When comparing patients with clinically significant portal hypertension (CSPH, HVPG ≥ 10 mmHg) to patients without CSPH, there were significantly enhanced serum levels of IL-6 and IL-18 in the former group. There was no significant difference between cytokine serum levels between blood obtained from the jugular versus hepatic veins. Even in subgroup analyses stratified for an early cirrhosis stage (Child-Pugh (CP) A) or more decompensated stages (CP B/C), cytokine levels were similar. <i>Conclusion</i>. 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引用次数: 0

摘要

背景。炎症细胞因子升高的全身性炎症是肝硬化患者的标志,也是代偿失代偿的主要驱动因素。关于肝静脉和颈静脉之间炎症细胞因子水平是否不同的数据不足,这可能对进一步的免疫学研究有影响。方法。采集40例肝硬化患者的肝静脉和颈静脉血液,测量肝静脉压梯度(HVPG)。采用细胞头阵列法测定血清中13种炎症因子(IL-1β、Int-α2、Int-γ、TNF-α、MCP-1、IL-6、IL-8、IL-10、IL-12p70、IL-17A、IL-18、IL-23、IL-33)的水平。结果。与代偿性肝硬化患者相比,失代偿性肝硬化患者的IFN-α2、IFN-γ、TNF-α、IL-6、IL-8、IL-10、IL-17A、IL-18、IL-23和IL-33的细胞因子水平显著升高。将有临床意义的门脉高压(CSPH, HVPG≥10 mmHg)患者与无CSPH患者进行比较,前者血清IL-6、IL-18水平显著升高。颈静脉与肝静脉的血清细胞因子水平无显著差异。即使在早期肝硬化阶段(Child-Pugh (CP) A)或更多失代偿期(CP B/C)的亚组分析中,细胞因子水平也相似。结论。细胞因子水平随着肝硬化患者失代偿和门静脉高压的增加而升高。肝硬化患者肝血和颈血细胞因子水平无相关差异。
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Comparison of Inflammatory Cytokine Levels in Hepatic and Jugular Veins of Patients with Cirrhosis
Background. Systemic inflammation with elevated inflammatory cytokines is a hallmark in patients with cirrhosis and the main driver of decompensation. There is insufficient data on whether inflammatory cytokine levels differ between hepatic and jugular veins, which may have implications for further immunological studies. Methods. Blood from the hepatic and jugular veins of 40 patients with cirrhosis was collected during hepatic venous pressure gradient (HVPG) measurements. Serum levels of 13 inflammatory cytokines (IL-1β, Int-α2, Int-γ, TNF-α, MCP-1, IL-6, IL-8, IL-10, IL-12p70, IL-17A, IL-18, IL-23, and IL-33) were quantified by cytometric bead array. Results. Cytokine levels of IFN-α2, IFN-γ, TNF-α, IL-6, IL-8, IL-10, IL-17A, IL-18, IL-23, and IL-33 were significantly elevated in patients with decompensated cirrhosis compared to patients with compensated cirrhosis. When comparing patients with clinically significant portal hypertension (CSPH, HVPG ≥ 10 mmHg) to patients without CSPH, there were significantly enhanced serum levels of IL-6 and IL-18 in the former group. There was no significant difference between cytokine serum levels between blood obtained from the jugular versus hepatic veins. Even in subgroup analyses stratified for an early cirrhosis stage (Child-Pugh (CP) A) or more decompensated stages (CP B/C), cytokine levels were similar. Conclusion. Cytokine levels increase with decompensation and increasing portal hypertension in patients with cirrhosis. There is no relevant difference in cytokine levels between hepatic and jugular blood in patients with cirrhosis.
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来源期刊
Mediators of Inflammation
Mediators of Inflammation 医学-免疫学
CiteScore
8.70
自引率
0.00%
发文量
202
审稿时长
4 months
期刊介绍: Mediators of Inflammation is a peer-reviewed, Open Access journal that publishes original research and review articles on all types of inflammatory mediators, including cytokines, histamine, bradykinin, prostaglandins, leukotrienes, PAF, biological response modifiers and the family of cell adhesion-promoting molecules.
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