Hisamune Ryo, Yamakawa Kazuma, Ushio Noritaka, Mochizuki Katsunori, Matsuoka Tadashi, Umemura Yutaka, Hayakawa Mineji, Mori Hirotaka, Endo Akira, Ogura Takayuki, Hirayama Atsushi, Yasunaga Hideo, Tagami Takashi, Okamoto Kohji, Takasu Akira
Department of Emergency and Critical Care Medicine, Osaka Medical and Pharmaceutical University, 2-7 Daigakumachi, Takatsuki, Osaka, 569-8686, Japan.
LOCOMOCO (Landmark Of Clinical Observations in MicrOcirculation and Coagulation Outcomes) Study Group, Tokyo, Japan.
Thromb J. 2025 Jun 10;23(1):61. doi: 10.1186/s12959-025-00747-3.
Severe acute respiratory syndrome coronavirus 2 infection causes systemic immune overresponse (cytokine storm), which can lead to microthrombi and dysfunction of coagulation such as disseminated intravascular coagulation (DIC) of sepsis. Coronavirus disease 2019 (COVID-19) coagulopathy is known to occur mainly in the pulmonary microcirculation. We aimed to investigate hematological differences in coagulopathy between COVID-19 pneumonia and bacterial pneumonia.
We performed an observational cohort study using the Japanese REsearch of COVID-19 by assEmbling Real-world data (J-RECOVER) study database for COVID-19 patients and the Japan Medical Data Center (JMDC) database for bacterial pneumonia patients. The J-RECOVER database includes data from patients discharged between January 1 and September 31, 2020. The JMDC database covers patients emergently hospitalized from 2014 to 2022. We analyzed the association between hematological coagulopathy, systematic inflammation, and organ dysfunction in both groups after one-to-one propensity score matching.
We enrolled 572 COVID-19 patients and 2,413 bacterial pneumonia patients who required mechanical ventilation. The COVID-19 group was younger, had higher intensive care unit admission rates, and lower mortality in comparison to the bacterial group (p < 0.05). On day 1, the two groups showed no significant differences in JAAM-2 and sepsis-induced coagulopathy criteria. After matching, platelet counts, antithrombin activity, and prothrombin time-international normalized ratio were consistently maintained within normal ranges in the COVID-19 group. However, trends in D-dimer and fibrin degradation products in the COVID-19 group were similar to those in the bacterial pneumonia group.
COVID-19 coagulopathy differs from bacterial septic DIC by exhibiting lower platelet consumption and minimal vascular hyperpermeability. Consequently, management strategies for COVID-19 coagulopathy should be distinct from those for septic DIC.
严重急性呼吸综合征冠状病毒2感染会引发全身免疫过度反应(细胞因子风暴),这可能导致微血栓形成以及凝血功能障碍,如脓毒症的弥散性血管内凝血(DIC)。2019冠状病毒病(COVID-19)凝血病主要发生在肺微循环中。我们旨在研究COVID-19肺炎和细菌性肺炎在凝血病方面的血液学差异。
我们进行了一项观察性队列研究,使用日本通过汇总真实世界数据研究COVID-19(J-RECOVER)研究数据库中的COVID-19患者数据以及日本医学数据中心(JMDC)数据库中的细菌性肺炎患者数据。J-RECOVER数据库包含2020年1月1日至9月31日出院患者的数据。JMDC数据库涵盖2014年至2022年紧急住院的患者。在进行一对一倾向评分匹配后,我们分析了两组血液学凝血病、全身炎症和器官功能障碍之间的关联。
我们纳入了572例需要机械通气的COVID-19患者和2413例细菌性肺炎患者。与细菌组相比,COVID-19组患者更年轻,重症监护病房入住率更高,死亡率更低(p<0.05)。在第1天,两组在JAAM-2和脓毒症诱导的凝血病标准方面无显著差异。匹配后,COVID-19组的血小板计数、抗凝血酶活性和凝血酶原时间-国际标准化比值始终维持在正常范围内。然而,COVID-19组的D-二聚体和纤维蛋白降解产物的变化趋势与细菌性肺炎组相似。
COVID-19凝血病与细菌性脓毒症DIC不同,其血小板消耗较低且血管通透性增加最小。因此,COVID-19凝血病的管理策略应与脓毒症DIC不同。