Department of Cardiovascular Medicine and Jiangxi Key Laboratory of Molecular Medicine, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi, China.
Department of Hematology Medicine, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
BMC Pulm Med. 2021 Jan 6;21(1):3. doi: 10.1186/s12890-020-01381-7.
Recent basic studies demonstrate that the lung is a primary organ of platelet biogenesis. However, whether the pathophysiological state of the lung affect the platelets is little known. We aim to investigate the incidence of thrombocytopenia in patients with pulmonary infection (PIN) and risk factors associated with pulmonary thrombocytopenia.
In total, 11,941 patients with pulmonary infection (PIN) were enrolled, and patients with other three infectious diseases were collected as controls. The incidence of thrombocytopenia was compared, and the risk factors associated with thrombocytopenia in PIN patients were investigated by multivariate analysis. To explore the mechanism of thrombocytopenia, hypoxic model was constructed. Blood platelet counts from the angular vein (PLTs), left ventricle (PLT) and right ventricle (PLT) were determined. Megakaryocytes identified by anti-CD41 antibody were detected through flow cytometry and immunofluorescence.
The incidence of thrombocytopenia in PIN was higher than that in other three infectious diseases (9.8% vs. 6.4% ~ 5.0%, P < 0.001). Low arterial oxygen partial pressure (PaO) was an important risk factor for thrombocytopenia (OR = 0.88; P < 0.001). In a hypoxic mouse model, PLTs decreased (518.38 ± 127.92 vs 840.75 ± 77.30, P < 0.05), which showed that low PaO induced thrombocytopenia. The difference between the PLT and PLT (∆PLT), representing the production of platelets in the lungs, was significantly attenuated in hypoxic mice when compared with normoxic mice (F = 25.47, P < 0.05). Additionally, proportions of CD41-positive megakaryocytes in the lungs, marrow, spleen all decreased in hypoxic mice.
There is a high incidence for thrombocytopenia in PIN patients. Low PaO-induced thrombocytopenia is associated with impaired generation of platelet in the lungs.
最近的基础研究表明，肺是血小板生成的主要器官。然而，肺部的病理生理状态是否会影响血小板尚不清楚。我们旨在研究肺部感染（PIN）患者血小板减少症的发生率和与肺部血小板减少症相关的危险因素。
共纳入 11941 例肺部感染（PIN）患者，并收集其他三种传染病患者作为对照。比较血小板减少症的发生率，并通过多因素分析探讨 PIN 患者血小板减少症的相关危险因素。为了探讨血小板减少症的机制，构建了缺氧模型。通过流式细胞术和免疫荧光法检测抗 CD41 抗体鉴定的巨核细胞。
PIN 患者血小板减少症的发生率高于其他三种传染病（9.8%比 6.4%~5.0%，P<0.001）。低动脉血氧分压（PaO）是血小板减少症的重要危险因素（OR=0.88；P<0.001）。在缺氧小鼠模型中，血小板减少（518.38±127.92 比 840.75±77.30，P<0.05），表明低 PaO 可引起血小板减少症。与常氧小鼠相比，缺氧小鼠中代表肺部血小板生成的 PLT 和 PLT（∆PLT）之间的差异明显减弱（F=25.47，P<0.05）。此外，缺氧小鼠肺部、骨髓、脾脏中 CD41 阳性巨核细胞的比例均降低。
PIN 患者血小板减少症的发生率较高。低 PaO 诱导的血小板减少症与肺部血小板生成受损有关。
