Lung damage may induce thrombocytopenia

Abstract

Thrombocytopenia is common in patients with lung diseases. Lung injury is associated with deranged platelet homeostasis. The potential mechanisms underlying this association were investigated in this study. The number and morphology of circulating megakaryocytes (MK) were investigated in vivo during cardiopulmonary bypass (CPB) in patients undergoing elective cardiac surgery for heart disease. The association between lung injury and thrombocytopenia was further investigated in vitro in rats with lung injury. MK and platelet counts, and platelet activation between the prepulmonary (right atrial) and postpulmonary (left atrial) blood were also compared. In human, the total number of MK in central venous was higher than those of peripheral arteries during normal circulation. During CPB, the total MK and Type-4 MK of central venous and peripheral arteries were significant increased when compared with that in normal circulation. In healthy rats, the postpulmonary blood had lower MK count, higher platelet count, and similar P-selectin expression. However, the lung-damaged animals showed no such differences in either MK or platelet count, but P-selectin expression was greater in the postpulmonary blood. Peripheral platelets in the lung-injured rats were significantly lower than those in their respective controls. The lungs may play an active role in the regulation of MK levels and the lung damage may reduce circulating platelets.

Thrombopoietin levels increased in patients with severe acute respiratory syndrome

“…Specifically, the lungs of SARS patients showed diffused alveolar damage [4]. The damaged lung tissue and pulmonary endothelial cells may cause the activation and entrapment of platelets in the lungs, along with the thrombi formation at the sites of the injury, may lead to the consumption of platelets subsequently [20,21]. In addition, the lungs may also be the sites of platelet release from mature megakayocytes.…”

“…In addition, the lungs may also be the sites of platelet release from mature megakayocytes. In this case, the damaged lungs may result in pulmonary fibrosis and pathological changes, affecting the lung megakaryocyte fragmentation and platelet pro-duction [20,21]. Taken together, the increased consumption of platelet or/and the decreased production of platelet may lead to thrombocytopenia.…”

Lung as a Niche for Hematopoietic Progenitors

“…Data supporting this includes the observation that megakaryocytes are also found in pulmonary vascular beds and a higher platelet counts in postpulmonary vessels as compared to pulmonary arteries [20, 21]. In addition, more recent study shows that lung damage reduces circulating platelets, suggesting that lungs may play an active role in the regulation of platelet formation [22]. These studies suggested the presence of a pool of newly formed platelets in the pulmonary circulation.…”

The incredible journey: From megakaryocyte development to platelet formation

“…A study of higher platelet counts in postpulmonary vessels suggests that the lung may be a site of terminal platelet formation (Howell and Donahue, 1937). In addition, a study using rat models reveals that lung damage may reduce circulating platelets, suggesting that the lungs play an active role in the regulation of platelet formation (Xiao et al, 2006). Megakaryocyte development and platelet formation • Machlus and Italiano…”