Immature platelets as a biomarker for disease severity and mortality in COVID‐19 patients

Abstract

COVID-19, caused by SARS-CoV-2, is a contagious life-threatening viral disease that has killed more than three million people worldwide to date. Attempts have been made to identify biomarker(s) to stratify disease severity and improve treatment and resource allocation. Patients with SARS-COV-2 infection manifest with a higher inflammatory response and platelet hyperreactivity; this raises the question of the role of thrombopoiesis in COVID-19 infection. Immature platelet fraction (IPF, %) and immature platelet counts (IPC, 910 9 /l) can be used to assess thrombopoiesis. This study investigates whether the level of thrombopoiesis correlates with COVID-19 severity. A large cohort of 678 well-characterized COVID-19 patients was analyzed, including 658 (97%) hospitalized and 139 (21%) admitted to the intensive care unit (ICU). Elevated percentage IPF at presentation was predictive of length of hospitalization (P < 0Á01) and ICU admission (P < 0Á05). Additionally, percentage IPF at the peak was significantly higher among ICU patients than non-ICU patients (6Á9 AE 5Á1 vs 5Á3 AE 8Á4, P < 0Á01) and among deceased patients than recovered patients (7Á9 AE 6Á3 vs 5Á4 AE 7Á8, P < 0Á01). Furthermore, IPC at the peak was significantly higher among ICU patients than non-ICU patients (18Á5 AE 16Á2 vs. 13Á2 AE 8Á3, P < 0Á05) and among patients on a ventilator than those not (22Á1 AE 20Á1 vs.13Á4 AE 8Á4, P < 0Á05). Our study demonstrated that elevated initial and peak values of percentage IPF and IPC might serve as prognostic biomarkers for COVID-19 progression to severe conditions.

Impact of asthma on COVID-19 mortality in the United States: Evidence based on a meta-analysis

“…After evaluating and assessing as much as 257 potential studies, 201 studies were removed due to outcome of interest being not available. In the end, what underlay this meta-analysis were eligible fifty-six articles with 426,261 COVID-19 patients [5] , [6] , [7] , [8] , [9] , [16] , [17] , [18] , [19] , [20] , [21] , [22] , [23] , [24] , [25] , [26] , [27] , [28] , [29] , [30] , [31] , [32] , [33] , [34] , [35] , [36] , [37] , [38] , [39] , [40] , [41] , [42] , [43] , [44] , [45] , [46] , [47] , [48] , [49] , [50] , [51] , [52] , [53] , [54] , [55] , [56] , [57] , [58] , [59] , [60] , [61] , [62] , [63] , [64] , [65] , [66] . The detail of selection process is shown by a chart flow in Figure 1 .…”

Plasma Fibrinogen Independently Predicts Hypofibrinolysis in Severe COVID-19

“…Despite the small number of included patients, an elevated level of H-IPF (%) was found to be predictive of the fatal outcome here. Welder et al found that elevated percentages of IPF at presentation was predictive of the length of hospitalization, the need of ICU admission, and mechanical ventilation [15]. Importantly, a higher H-IPF level was associated with lower plasminogen levels in those COVID-19 patients who died.…”

“…IPF represents young cells that have recently been released into the circulation and contain a higher concentration of ribonucleic acid than mature platelets [14]. Recently, IPF was reported as a novel early predictive marker for disease severity in patients with COVID-19 [15]. Critically ill COVID-19 patients have impaired fibrinolysis.…”

Autoimmune anti-DNA and anti-phosphatidylserine antibodies predict development of severe COVID-19

“…Anti-PS antibodies correlated with high levels of platelets. Although a low platelet count is associated with increased risk of severe disease and mortality in patients with COVID-19 ( Lippi et al, 2020 ), it has also been observed that platelets are hyperactivated during the disease ( Zaid et al, 2020 ) and that immature platelets ( Welder et al, 2021 ) and coated-platelet levels ( Khattab et al, 2021 ) correlate with severity and death in COVID-19 patients, suggesting that they may be involved in thrombo-inflammation and contribute to disease severity.…”