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Increased number of pulmonary megakaryocytes in COVID-19 patients with diffuse alveolar damage: an autopsy study with clinical correlation and review of the literature.
Virchows Archiv ( IF 3.4 ) Pub Date : 2020-09-11 , DOI: 10.1007/s00428-020-02926-1
Mariel F Valdivia-Mazeyra 1 , Clara Salas 2 , Jesús M Nieves-Alonso 3 , Luz Martín-Fragueiro 2 , Carmen Bárcena 4 , Patricia Muñoz-Hernández 1 , Karen Villar-Zarra 5 , Javier Martín-López 2 , Fernando Ramasco-Rueda 3 , Javier Fraga 1 , José A Jiménez-Heffernan 1
Affiliation  

Pulmonary megakaryocytes participate in the pathogenesis of lung damage, particularly in acute lung injury. Although megakaryocytes are not mentioned as a characteristic histologic finding associated to pulmonary injury, a few studies reveal that their number is increased in diffuse alveolar damage (DAD). In this autopsy study, we have observed a relevant number of pulmonary megakaryocytes in COVID-19 patients dying with acute lung injury (7.61 ± 5.59 megakaryocytes per 25 high-power fields vs. 1.14 ± 0.86 for the control group, p < 0.05). We analyzed samples of 18 patients, most of whom died after prolonged disease and use of mechanical ventilation. Most patients showed advanced DAD and abnormal coagulation parameters with high levels of fibrinogen, D-dimers, and variable thrombocytopenia. For comparison, pulmonary samples from a group of 14 non-COVID-19 patients dying with DAD were reviewed. They showed similar pulmonary histopathologic findings and an increase in the number of megakaryocytes (4 ± 4.17 vs. 1.14 ± 0.86 for the control group, p < 0.05). Megakaryocyte count in the COVID-19 group was greater but did not reach statistical significance (7.61 ± 5.59 vs. 4 ± 4.17, p = 0.063). Regardless of the cause, pulmonary megakaryocytes are increased in patients with DAD. Their high number seen in COVID-19 patients suggests a relation with the thrombotic events so often seen these patients. Since the lung is considered an active site of megakaryopoiesis, a prothrombotic status leading to platelet activation, aggregation and consumption may trigger a compensatory pulmonary response.



中文翻译:

弥漫性肺泡损伤的 COVID-19 患者肺巨核细胞数量增加:具有临床相关性和文献回顾的尸检研究。

肺巨核细胞参与肺损伤的发病机制,特别是在急性肺损伤中。尽管巨核细胞并未作为与肺损伤相关的特征性组织学发现被提及,但一些研究表明它们的数量在弥漫性肺泡损伤 (DAD) 中增加。在这项尸检研究中,我们在死于急性肺损伤的 COVID-19 患者中观察到相关数量的肺巨核细胞(每 25 个高倍视野中有 7.61 ± 5.59 个巨核细胞,而对照组为 1.14 ± 0.86 个,p< 0.05)。我们分析了 18 名患者的样本,其中大多数患者在长期患病和使用机械通气后死亡。大多数患者表现出晚期 DAD 和凝血参数异常,伴有高水平的纤维蛋白原、D-二聚体和可变的血小板减少症。为了比较,我们回顾了一组 14 名死于 DAD 的非 COVID-19 患者的肺部样本。他们表现出相似的肺组织病理学发现和巨核细胞数量的增加(对照组为 4 ± 4.17 对 1.14 ± 0.86,p < 0.05)。COVID-19 组的巨核细胞计数更高,但未达到统计学意义(7.61 ± 5.59 对 4 ± 4.17,p= 0.063)。无论原因如何,DAD 患者的肺巨核细胞均增加。在 COVID-19 患者中看到的高数量表明与这些患者经常看到的血栓形成事件有关。由于肺被认为是巨核细胞生成的活跃部位,导致血小板活化、聚集和消耗的血栓前状态可能引发代偿性肺反应。

更新日期:2020-09-11
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