COVID-19可诱发内皮炎，主要并发症之一是凝血功能增强。COVID-19（CPE）中肺栓塞（PE）的发病率有所增加，临床特征仍需进行严格分析。因此，我们评估了CPE的临床特征和发生的免疫浸润。2021年1月1日至12月31日，38名患者受到CPE的影响(9名ICU，19男/19女,459例COVID-19病例中有70.18±11.24年）。对照组是在2015年1月1日至2019年12月31日之间进行PE评估的受试者（92例患者，9ICU,48男/45女,69.55±16.59年）。所有患者都接受了完整的体检，肺计算机断层扫描,实验室测试,D-二聚体,和血气分析.实验室检查或D-二聚体没有差异。在CPE患者中，PO2，肺泡-动脉血氧差（A-aDO2），氧饱和度%,以及动脉氧分压（PaO2）与吸入氧气分数（FiO2）之间的比率，P/F,显着增加。PaCO2没有差异。仅在CPE患者中，血小板计数与P/F呈负相关（r=-0.389，p=0.02），但与A-aDO2呈负相关（r=0.699，p=0.001）。CPE患者的肺活检（7个CPE/7个对照）的组织学显示CD15+细胞增加，HMGB1和细胞外MPO作为NETosis的标志物，虽然在CD3+中没有发现显著差异，CD4+,CD8+,和细胞内MPO。总的来说,数据表明，CPE具有不同的临床设置。CPE患者中描述的氧含量和饱和度降低不应被认为是值得信赖的疾病体征。与经典PE相比,增加的A-aDO2可能表明CPE涉及最小的血管。NETosis的显着差异可能提示与血栓形成有关的机制。
COVID-19 induces endotheliitis and one of the main complications is enhanced coagulation. The incidence of pulmonary embolism (PE) in COVID-19 (CPE) has increased and clinical features for a rigorous analysis still need to be determined. Thus, we evaluated the clinical characteristics in CPE and the immune infiltration that occurred. Between January 1 and December 31, 2021, 38 patients were affected by CPE (9 ICU, 19 males/19 females, 70.18 ± 11.24 years) out of 459 COVID-19 cases. Controls were subjects who were evaluated for PE between January 1 2015, and December 31, 2019 (92 patients, 9 ICU, 48 males/45 females, 69.55 ± 16.59 years). All patients underwent complete physical examination, pulmonary computed tomography, laboratory tests, D-dimer, and blood gas analysis. There were no differences in laboratory tests or D-dimer. In patients with CPE, pO2, alveolar-arterial oxygen difference (A-aDO2), oxygen saturation %, and the ratio between arterial partial pressure of oxygen (PaO2) and fraction of inspired oxygen (FiO2), P/F, were significantly increased. There were no differences in PaCO2. Platelet count was inversely correlated to P/F (r = - 0.389, p = 0.02) but directly to A-aDO2 (r = 0.699, p = 0.001) only in patients with CPE. Histology of lung biopsies (7 CPE/7 controls) of patients with CPE showed an increase in CD15+ cells, HMGB1, and extracellular MPO as a marker of NETosis, while no significant differences were found in CD3+, CD4+, CD8+, and intracellular MPO. Overall, data suggest that CPE has a different clinical setting. Reduced oxygen content and saturation described in Patients with CPE should not be considered a trustworthy sign of disease. Increased A-aDO2 may indicate that CPE involves the smallest vessels as compared to classical PE. The significant difference in NETosis may suggest the mechanism related to thrombi formation.
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