Gastroenterology Department, The James Cook University Hospital, Middlesbrough, UK.
Aliment Pharmacol Ther. 2013 Dec;38(11-12):1395-404. doi: 10.1111/apt.12530. Epub 2013 Oct 20.
Macrophage activation is implicated in the pathogenesis of the systemic inflammatory response syndrome (SIRS) following paracetamol (acetaminophen) overdose (POD). Neopterin is synthesised from macrophages and reflects the intensity of monocyte/macrophage activation. Soluble CD163 (sCD163) is a marker of alternatively activated M2 macrophages.
To examine neopterin and sCD163 levels in a cohort of acute liver injury patients.
Consecutive patients (n = 41, (18 (43.9%) male) with acute liver injury were enrolled. Neopterin and sCD163 levels were measured by ELISA.
A total of 24/33 (72.7%) POD patients developed hepatic encephalopathy (HE), and therefore acute liver failure. Both neopterin and sCD163 levels were significantly higher in PODs compared with chronic liver disease (neopterin P < 0.001, sCD163 P = 0.038) and healthy (both P < 0.001) controls. Admission neopterin levels were significantly higher in PODs: with HE (P = 0.001); with the SIRS (P = 0.005); who required renal replacement therapy (P = 0.003); who died or required liver transplantation (P = 0.006; AUROC 78.6% (95% CI 62.2-94.9%). Serum sCD163 levels were significantly higher in those PODs with the SIRS (P = 0.033) on admission, and were higher in those PODs who died or required OLT (P = 0.024). Both admission neopterin and sCD163 levels in PODs correlated with organ failure scores but not with serum ALT. There was no significant correlation between neopterin and sCD163 values.
Both serum neopterin and sCD163 levels are significantly elevated following paracetamol overdose, and reflect the degree of macrophage activation in this condition. Serum neopterin in particular may have value as an early proxy marker of macrophage activation following paracetamol overdose.
在对乙酰氨基酚（扑热息痛）过量（POD）后全身炎症反应综合征（SIRS）的发病机制中，巨噬细胞激活被认为是其发病机制之一。新蝶呤由巨噬细胞合成，反映单核细胞/巨噬细胞激活的强度。可溶性 CD163（sCD163）是 M2 巨噬细胞替代激活的标志物。
检查急性肝损伤患者队列中的新蝶呤和 sCD163 水平。
连续入组 41 例（18 例（43.9%）男性）急性肝损伤患者。通过 ELISA 测定新蝶呤和 sCD163 水平。
24/33（72.7%）POD 患者发生肝性脑病（HE），因此发生急性肝衰竭。与慢性肝病（新蝶呤 P < 0.001，sCD163 P = 0.038）和健康对照（均 P < 0.001）相比，POD 患者的新蝶呤和 sCD163 水平均显著升高。POD 患者入院时的新蝶呤水平明显升高：有 HE（P = 0.001）；有 SIRS（P = 0.005）；需要肾脏替代治疗（P = 0.003）；死亡或需要肝移植（P = 0.006；AUROC 为 78.6%（95%CI 62.2-94.9%））。入院时 POD 患者 SIRS（P = 0.033）时血清 sCD163 水平显著升高，且死亡或需要 OLT 的 POD 患者 sCD163 水平更高（P = 0.024）。POD 患者入院时新蝶呤和 sCD163 水平与器官衰竭评分相关，但与血清 ALT 无关。新蝶呤和 sCD163 值之间无显著相关性。
扑热息痛过量后，血清新蝶呤和 sCD163 水平均显著升高，反映了该情况下巨噬细胞激活的程度。血清新蝶呤尤其可能作为扑热息痛过量后巨噬细胞激活的早期替代标志物。
