Department of Pharmacology, Toxicology & Therapeutics, USA.
Department of Internal Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, University of Kansas Medical Center, Kansas City, Kansas, USA.
Toxicol Lett. 2022 Aug 15;367:59-66. doi: 10.1016/j.toxlet.2022.07.813. Epub 2022 Jul 26.
Acetaminophen (APAP) overdose causes liver injury in animals and humans. Although well-studied in animals, limited longitudinal data exist on cytokine release after APAP overdose in patients. The purpose of this study was to quantify concentrations of cytokines in APAP overdose patients to determine if early cytokine or complement measurements can distinguish between surviving and non-surviving patients. Plasma was obtained from healthy controls, APAP overdose patients with no increase in liver transaminases, and surviving and non-surviving APAP overdose patients with severe liver injury. Interleukin-10 (IL-10), and CC chemokine ligand-2 (CCL2, MCP-1) were substantially elevated in surviving and non-surviving patients, whereas IL-6 and CXC chemokine ligand-8 (CXCL8, IL-8) had early elevations in a subset of patients only with liver injury. Day 1 IL-10 and IL-6 levels, and Day 2 CCL2, levels correlated positively with survival. There was no significant increase in IL-1α, IL-1β or TNF-α in any patient during the first week after APAP. Monitoring cytokines such as CCL2 may be a good indicator of patient prognosis; furthermore, these data indicate the inflammatory response after APAP overdose in patients is not mediated by a second phase of inflammation driven by the inflammasome.
对乙酰氨基酚(APAP)过量会导致动物和人类的肝损伤。尽管在动物中进行了充分的研究,但关于 APAP 过量后细胞因子释放的纵向数据在患者中非常有限。本研究的目的是定量测定 APAP 过量患者的细胞因子浓度,以确定早期细胞因子或补体测量是否可以区分存活和非存活患者。从健康对照、肝转氨酶无升高的 APAP 过量患者以及存活和非存活的严重肝损伤 APAP 过量患者中获得血浆。白细胞介素 10(IL-10)和 C 趋化因子配体 2(CCL2,MCP-1)在存活和非存活患者中明显升高,而白细胞介素 6(IL-6)和 CXC 趋化因子配体 8(CXCL8,IL-8)仅在部分肝损伤患者中早期升高。第 1 天的 IL-10 和 IL-6 水平以及第 2 天的 CCL2 水平与存活呈正相关。在 APAP 后第一周,任何患者的 IL-1α、IL-1β 或 TNF-α均无明显增加。监测 CCL2 等细胞因子可能是患者预后的良好指标;此外,这些数据表明,患者 APAP 过量后的炎症反应不是由炎症小体驱动的第二阶段炎症引起的。