RESUMEN
Background: 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. Methods: 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. Results: 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. Conclusion: 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.
RESUMEN
The aim of the study was to evaluate the significance of hypomagnesemia in patients with coronavirus disease 2019 (COVID-19) and clarify its possible pathogenesis. A retrospective cohort study was conducted by reviewing 83 patients hospitalized in Guanggu district, Wuhan Third Hospital, China. Clinical histories, laboratory findings and outcome data were collected. Eighteen patients had hypomagnesemia during hospitalization. Fourteen patients were in the critical group and six died. In the critical group, serum magnesium (0.72 ± 0.15 mmol/L) was much lower than that in the moderate and severe groups. At the same time, we also found that several indicators are correlated with the level of magnesium. The level of magnesium was positively associated with the lymphocyte count (r = 0.203, P = 0.004) and platelet count (r = 0.217, P = 0.002) but negatively related to the levels of CRP (r = -0.277, P = 0.000), LDH (r = -0.185, P = 0.011) and α-hydroxybutyrate dehydrogenase (r = -0.198, P = 0.008) in the critical group. Hypomagnesemia might increase symptoms and may be associated with mortality in COVID-19 by affecting enzyme activity and activating the inflammatory response. Thus, magnesium might play a key role in the pathogenesis of COVID-19.