Background Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), which causes novel coronavirus disease 2019 (COVID‐19), is spreading rapidly around the world. Thrombocytopenia in patients with COVID‐19 has not been fully studied. Objective To describe thrombocytopenia in patients with COVID‐19. Methods For each of 1476 consecutive patients with COVID‐19 from Jinyintan Hospital, Wuhan, China, nadir platelet count during hospitalization was retrospectively collected and categorized into (0, 50], (50, 100], (100‐150], or (150‐) groups after taking the unit (×109/L) away from the report of nadir platelet count. Nadir platelet counts and in‐hospital mortality were analyzed. Results Among all patients, 238 (16.1%) patients were deceased and 306 (20.7%) had thrombocytopenia. Compared with survivors, non‐survivors were older, were more likely to have thrombocytopenia, and had lower nadir platelet counts. The in‐hospital mortality was 92.1%, 61.2%, 17.5%, and 4.7% for (0, 50], (50, 100], (100‐150], and (150‐) groups, respectively. With (150‐) as the reference, nadir platelet counts of (100‐150], (50, 100], and (0, 50] groups had a relative risk of 3.42 (95% confidence interval [CI] 2.36‐4.96), 9.99 (95% CI 7.16‐13.94), and 13.68 (95% CI 9.89‐18.92), respectively. Conclusions Thrombocytopenia is common in patients with COVID‐19, and it is associated with increased risk of in‐hospital mortality. The lower the platelet count, the higher the mortality becomes.

The pandemic of the coronavirus disease 2019 has become a global public health crisis. The symptoms of COVID-19 range from mild to severe conditions. However, the physiological changes associated with COVID-19 are barely understood. In this study, we performed targeted metabolomic and lipidomic analyses of plasma from a cohort of COVID-19 patients who had experienced different symptoms. We found the metabolite and lipid alterations exhibit apparent correlation with the course of disease in these COVID-19 patients, indicating that the development of COVID-19 affected whole-body metabolism of the patients. In particular, malic acid of the TCA cycle and carbamoyl phosphate of urea cycle reveal the altered energy metabolism and hepatic dysfunction, respectively. It should be noted that carbamoyl phosphate is profoundly down-regulated in fatal patients compared with mild patients. And more importantly, guanosine monophosphate (GMP), which is mediated by not only GMP synthase but also CD39 and CD73, is significantly changed between healthy subjects and COVID-19 patients, as well as between the mild and fatal groups. In addition, the dyslipidaemia was observed in COVID-19 patients. Overall, the disturbed metabolic patterns have been found to align with the progress and severity of COVID-19. This work provides valuable knowledge about plasma biomarkers associated with COVID-19 and potential therapeutic targets, as well as important resource for further studies of COVID-19 pathogenesis.

The COVID-19 pandemic is a global public health crisis. However, little is known about the pathogenesis and biomarkers of COVID-19. Herein, we profiled host responses to COVID-19 by performing plasma proteomics of a cohort of COVID-19 patients including non-survivors and survivors recovered from mild or severe symptoms, and uncovered numerous COVID-19-associated alterations of plasma proteins. We developed a machine learning-based pipeline to identify 11 proteins as biomarkers and a set of biomarker combinations, which were validated by an independent cohort and accurately distinguished and predicted COVID-19 outcomes. Some of the biomarkers were further validated by ELISA using a larger cohort. These markedly altered proteins, including the biomarkers mediate pathophysiological pathways such as immune or inflammatory responses, platelet degranulation and coagulation, and metabolism, that likely contribute to the pathogenesis. Our findings provide valuable knowledge about COVID-19 biomarkers, and shed light on the pathogenesis and potential therapeutic targets of COVID-19.