■一些研究已经检查了COVID-19血栓形成性增加的参数,但很少有研究检查这些参数与COVID-19住院患者的长期预后和抗病毒药物的潜在影响。
为了评估住院期间血浆止血蛋白水平与疾病严重程度的关系,治疗方式,3个月后持续肺部病理。
■在纳入NOR-团结试验(NCT04321616)并随机接受羟氯喹治疗的165例COVID-19患者中,remdesivir,或护理标准,我们通过酶免疫测定分析了住院前10天(n=160)和随访3个月时(n=100)的血浆止血蛋白水平.
■我们的主要发现如下:(i)严重疾病患者的组织纤溶酶原激活物(tPA)和组织因子途径抑制物(TFPI)升高(即,呼吸衰竭的综合终点[Po2与FiO2比值,<26.6kPa]或需要在重症监护病房治疗)住院期间。与没有严重疾病的患者相比,tPA水平中位数为42%(P<.001),29%(P=0.002),基线时高36%(P=0.015),3到5天,7到10天,分别。对于TFPI,中位数水平为37%(P=0.003),25%(P<.001),在这些时间点,患有严重疾病的患者高出10%(P=0.13),分别。凝血酶-抗凝血酶复合物无变化;α2-抗纤溶酶;具有血小板反应蛋白1型基序的解整合素和金属蛋白酶,成员13;或观察到抗凝血酶与严重疾病有关。(ii)用瑞德西韦治疗的患者的TFPI水平低于单独用标准治疗的患者。(iii)住院期间的TFPI水平,但不是在3个月的随访中,入院后3个月,在胸部计算机断层扫描成像中具有持续性病理的患者高于没有此类病理的患者。凝血酶-抗凝血酶复合物无一致变化,α2-抗纤溶酶,ADAMTS-13,tPA,在随访3个月时,观察到抗凝血酶与肺部病理有关。
■TFPI和tPA与COVID-19住院患者的严重疾病相关。对于TFPI,即使在入院后3个月内,在住院前10天测量到的高水平也与持续性肺部病理相关.
UNASSIGNED: Several studies have examined parameters of increased thrombogenicity in COVID-19, but studies examining their association with long-term outcome and potential effects of antiviral agents in hospitalized patients with COVID-19 are scarce.
UNASSIGNED: To evaluate plasma levels of hemostatic proteins during hospitalization in relation to disease severity, treatment modalities, and persistent pulmonary pathology after 3 months.
UNASSIGNED: In 165 patients with COVID-19 recruited into the NOR-Solidarity trial (NCT04321616) and randomized to treatment with hydroxychloroquine, remdesivir, or standard of care, we analyzed plasma levels of hemostatic proteins during the first 10 days of hospitalization (n = 160) and at 3 months of follow-up (n = 100) by enzyme immunoassay.
UNASSIGNED: Our main findings were as follows: (i) tissue plasminogen activator (tPA) and tissue factor pathway inhibitor (TFPI) were increased in patients with severe disease (ie, the combined endpoint of respiratory failure [Po2-to-FiO2 ratio, <26.6 kPa] or need for treatment at an intensive care unit) during hospitalization. Compared to patients without severe disease, tPA levels were a median of 42% (P < .001), 29% (P = .002), and 36% (P = .015) higher at baseline, 3 to 5 days, and 7 to 10 days, respectively. For TFPI, median levels were 37% (P = .003), 25% (P < .001), and 10% (P = .13) higher in patients with severe disease at these time points, respectively. No changes in thrombin-antithrombin complex; alpha 2-antiplasmin; a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13; or antithrombin were observed in relation to severe disease. (ii) Patients treated with remdesivir had lower levels of TFPI than those in patients treated with standard of care alone. (iii) TFPI levels during hospitalization, but not at 3 months of follow-up, were higher in those with persistent pathology on chest computed tomography imaging 3 months after hospital admission than in those without such pathology. No consistent changes in thrombin-antithrombin complex, alpha 2-antiplasmin, ADAMTS-13, tPA, or antithrombin were observed in relation to pulmonary pathology at 3 months of follow-up.
UNASSIGNED: TFPI and tPA are associated with severe disease in hospitalized patients with COVID-19. For TFPI, high levels measured during the first 10 days of hospitalization were also associated with persistent pulmonary pathology even 3 months after hospital admittance.