Shan Cuiting, Yu Feng, Deng Xuemei, Ni Li, Luo Xuming, Li Jialin, Cai Si, Huang Mian, Wang Xiongbiao
Department of Respiratory Medicine, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Shanghai Putuo District People's Hospital, Shanghai, China.
Front Physiol. 2023 Mar 20;14:1100997. doi: 10.3389/fphys.2023.1100997. eCollection 2023.
The pathogenesis of COVID-19, including thrombocytopenia, has not been fully clarified. The lungs are a major organ of platelet production and thrombocytopenia induced by severe COVID-19 was proposed. the change of platelet level was analysed with clinical parameters in 95 hospitalized COVID-19 patients in Wuhan Third Hospital. The production of platelets in the lungs was explored in an ARDS rat model. The level of platelets was negatively correlated with disease severity and was recovered with disease improvement. The non-survivors were accompanied by lower levels of platelet. The odds ratio (OR) of the valley level of the platelet count (PLTlow) was greater than 1, suggesting that PLTlow could be a death exposure factor. The platelet/lymphocyte ratio (PLR) was positively associated with severity of COVID-19, and the platelet/lymphocyte ratio threshold of 248.5 was best correlated with death risk (sensitivity 0.641 and specificity 0.815). To demonstrate the possible biogenesis aberration of platelet in lungs, an LPS-induced ARDS rat model was applied. Lower level of platelet in peripheral and less production of platelet from lungs in ARDS were demonstrated. Though megakaryocyte (MK) number in ARDS lungs is higher than controls, the immature platelet fraction (IPF) in postpulmonary blood is still at the same level as prepulmonary in ARDS rat, indicating that ARDS rats generated fewer platelets in lungs. Our data suggested that COVID-19-induced severe lung inflammation may impair platelet production in the lung. Thrombocytopenia may be mainly caused by platelet consumption for multiorgan thrombosis; however, biogenesis aberration of platelet in the lung induced by diffuse interstitial pulmonary damage cannot be ruled out.
包括血小板减少症在内的新型冠状病毒肺炎（COVID-19）发病机制尚未完全阐明。肺是血小板生成的主要器官，有人提出严重COVID-19可导致血小板减少症。对武汉第三医院95例住院COVID-19患者的血小板水平变化与临床参数进行了分析。在急性呼吸窘迫综合征（ARDS）大鼠模型中探究了肺内血小板的生成情况。血小板水平与疾病严重程度呈负相关，并随疾病好转而恢复。非幸存者的血小板水平较低。血小板计数谷值水平（PLTlow）的比值比（OR）大于1，提示PLTlow可能是死亡暴露因素。血小板/淋巴细胞比值（PLR）与COVID-19的严重程度呈正相关，血小板/淋巴细胞比值阈值248.5与死亡风险的相关性最佳（敏感性0.641，特异性0.815）。为了证明肺内血小板可能存在的生物发生异常，应用了脂多糖诱导的ARDS大鼠模型。结果显示ARDS大鼠外周血小板水平较低，肺内血小板生成减少。尽管ARDS肺内巨核细胞（MK）数量高于对照组，但ARDS大鼠肺后血液中的未成熟血小板分数（IPF）仍与肺前处于同一水平，表明ARDS大鼠肺内生成的血小板较少。我们的数据表明，COVID-19引起的严重肺部炎症可能损害肺内血小板的生成。血小板减少症可能主要是由于多器官血栓形成导致血小板消耗所致；然而，弥漫性间质性肺损伤引起的肺内血小板生物发生异常也不能排除。
