Medical Intensive Care Unit, Groupe Hospitalier Broca Cochin Hotel-Dieu, AP-HP, 27 rue du Faubourg Saint Jacques, 75679 Paris Cedex 14, France.
Resuscitation. 2013 Jan;84(1):60-5. doi: 10.1016/j.resuscitation.2012.06.010. Epub 2012 Jun 26.
Gut dysfunction is suspected to play a major role in the pathophysiology of post-resuscitation disease through an increase in intestinal permeability and endotoxin release. However this dysfunction often remains occult and is poorly investigated. The aim of this pilot study was to explore intestinal failure biomarkers in post-cardiac arrest patients and to correlate them with endotoxemia.
Following resuscitation after cardiac arrest, 21 patients were prospectively studied. Urinary intestinal fatty acid-binding protein (IFABP), which marks intestinal permeability, plasma citrulline, which reflects the functional enterocyte mass, and whole blood endotoxin were measured at admission, days 1-3 and 6. We explored the kinetics of release and the relationship between IFABP, citrulline and endotoxin values.
IFABP was extremely high at admission and normalized at D3 (6668 pg/mL vs 39 pg/mL, p=0.01). Lowest median of citrulline (N=20-40 μmol/L) was attained at D2 (11 μmol/L at D2 vs 24 μmol/L at admission, p=0.01) and tended to normalize at D6 (21 μmol/L). During ICU stay, 86% of patients presented a detectable endotoxemia. Highest endotoxin level was positively correlated with highest IFABP level (R(2)=0.31, p=0.01) and was inversely correlated with lowest plasma citrulline levels (R(2)=0.55, p<0.001). Endotoxin levels increased between admission and D2 in patients with post-resuscitation shock, whereas it decreases in patients with no shock (median +0.33 EU vs -0.19 EU, p=0.03). Highest endotoxin level was positively correlated with D3 SOFA score (R(2)=0.45, p=0.004).
Biomarkers of intestinal injury are altered after cardiac arrest and are associated with endotoxemia. This could worsen post-resuscitation shock and organ failure.
肠道功能障碍通过增加肠通透性和内毒素释放，被怀疑在心脏骤停后疾病的病理生理学中起主要作用。然而，这种功能障碍通常仍然是隐匿的，且研究不足。本研究旨在探索心脏骤停后患者的肠道衰竭生物标志物，并将其与内毒素血症相关联。
心脏骤停复苏后，前瞻性研究了 21 例患者。尿肠脂肪酸结合蛋白（IFABP）标记肠通透性，血浆瓜氨酸反映功能性肠细胞群，全血内毒素在入院时、第 1-3 天和第 6 天进行测量。我们探讨了释放动力学以及 IFABP、瓜氨酸和内毒素值之间的关系。
IFABP 在入院时极高，并在 D3 时正常化（6668 pg/mL 比 39 pg/mL，p=0.01）。瓜氨酸的最低中位数（N=20-40 μmol/L）在 D2 时达到（11 μmol/L 在 D2 比入院时的 24 μmol/L，p=0.01），并在 D6 时趋于正常（21 μmol/L）。在 ICU 期间，86%的患者存在可检测的内毒素血症。最高内毒素水平与最高 IFABP 水平呈正相关（R(2)=0.31，p=0.01），与最低血浆瓜氨酸水平呈负相关（R(2)=0.55，p<0.001）。在复苏后休克的患者中，内毒素水平在入院和 D2 之间增加，而在无休克的患者中则降低（中位数+0.33 EU 比-0.19 EU，p=0.03）。最高内毒素水平与 D3 SOFA 评分呈正相关（R(2)=0.45，p=0.004）。
心脏骤停后肠道损伤的生物标志物发生改变，并与内毒素血症相关。这可能会使复苏后休克和器官衰竭恶化。
