Trimaille Antonin, Thachil Jecko, Marchandot Benjamin, Curtiaud Anaïs, Leonard-Lorant Ian, Carmona Adrien, Matsushita Kensuke, Sato Chisato, Sattler Laurent, Grunebaum Lelia, Hansmann Yves, Fafi-Kremer Samira, Jesel Laurence, Ohana Mickaël, Morel Olivier
Division of Cardiovascular Medicine, Nouvel Hôpital Civil, Strasbourg University Hospital, 67000 Strasbourg, France.
INSERM (French National Institute of Health and Medical Research), UMR 1260, Regenerative Nanomedicine, FMTS, 67000 Strasbourg, France.
J Clin Med. 2020 Dec 24;10(1):39. doi: 10.3390/jcm10010039.
Host defence mechanisms to counter virus infection include the activation of the broncho-alveolar haemostasis. Fibrin degradation products secondary to extravascular fibrin breakdown could contribute to the marked increase in D-Dimers during COVID-19. We sought to examine the prognostic value on lung injury of D-Dimers in non-critically ill COVID-19 patients without thrombotic events.
This study retrospectively analysed hospitalized COVID-19 patients classified according to a D-Dimers threshold following the COVID-19 associated haemostatic abnormalities (CAHA) classification at baseline and at peak (Stage 1: D-Dimers less than three-fold above normal; Stage 2: D-Dimers three- to six-fold above normal; Stage 3: D-Dimers six-fold above normal). The primary endpoint was the occurrence of critical lung injuries on chest computed tomography. The secondary outcome was the composite of in-hospital death or transfer to the intensive care unit (ICU).
Among the 123 patients included, critical lung injuries were evidenced in 8 (11.9%) patients in Stage 1, 6 (20%) in Stage 2 and 15 (57.7%) in Stage 3 ( = 0.001). D-Dimers staging at peak was an independent predictor of critical lung injuries regardless of the inflammatory burden assessed by CRP levels (OR 2.70, 95% CI (1.50-4.86); < 0.001) and was significantly associated with increased in-hospital death or ICU transfer (14.9 % in Stage 1, 50.0% in Stage 2 and 57.7% in Stage 3 ( < 0.001)). D-Dimers staging at peak was an independent predictor of in-hospital death or ICU transfer (OR 2.50, CI 95% (1.27-4.93); = 0.008).
In the absence of overt thrombotic events, D-Dimers quantification is a relevant marker of critical lung injuries and dismal patient outcome.
对抗病毒感染的宿主防御机制包括支气管肺泡止血的激活。血管外纤维蛋白降解产生的纤维蛋白降解产物可能导致COVID-19期间D-二聚体显著升高。我们试图研究在无血栓形成事件的非重症COVID-19患者中，D-二聚体对肺损伤的预后价值。
本研究回顾性分析了根据COVID-19相关止血异常（CAHA）分类在基线和峰值时按D-二聚体阈值分类的住院COVID-19患者（第1阶段：D-二聚体高于正常水平不到三倍；第2阶段：D-二聚体高于正常水平三至六倍；第3阶段：D-二聚体高于正常水平六倍）。主要终点是胸部计算机断层扫描上严重肺损伤的发生情况。次要结局是院内死亡或转入重症监护病房（ICU）的综合情况。
在纳入的123例患者中，第1阶段有8例（11.9%）患者出现严重肺损伤，第2阶段有6例（20%），第3阶段有15例（57.7%）（P = 0.001）。无论通过CRP水平评估的炎症负担如何，峰值时的D-二聚体分期都是严重肺损伤的独立预测因素（OR 2.70，95% CI（1.50 - 4.86）；P < 0.001），并且与院内死亡或转入ICU的增加显著相关（第1阶段为14.9%，第2阶段为50.0%，第3阶段为57.7%（P < 0.001））。峰值时的D-二聚体分期是院内死亡或转入ICU的独立预测因素（OR 2.50，95% CI（1.27 - 4.93）；P = 0.008）。
在没有明显血栓形成事件的情况下，D-二聚体定量是严重肺损伤和患者不良预后的相关标志物。
