COVID-19 and metabolic syndrome, though seemingly different disorders, appear to share certain common pathogenic components, especially in the development of COVID-19-associated diabetes mellitus. The similarities include impairment in immunoendothelial, gastrointestinal, pancreatic, adipose and mitochondrial functions, with several critical micronutrients undergirding the intricate interactions among these dysfunctions. This discussion aims to highlight the parallels between COVID-19 and metabolic syndrome and to propose the possibility of SARS-CoV-2 being a prototype of an acquired etiological agent which can eventually lead to the development of classical metabolic syndrome. Based on the proposed model, the discussion will include the implication for early management of COVID-19 and metabolic syndrome.

COVID-19 caused by Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) and other respiratory viral (non-CoV-2-RV) infections are associated with thrombotic complications. The differences in prothrombotic potential between SARS-CoV-2 and non-CoV-2-RV have not been well characterised. We compared the thrombotic rates between these two groups of patients directly and further delved into their coagulation profiles. In this single-center, retrospective cohort study, all consecutive COVID-19 and non-CoV-2-RV patients admitted between January 15^th and April 10^th 2020 were included. Coagulation parameters studied were prothrombin time and activated partial thromboplastin time and its associated clot waveform analysis (CWA) parameter, min1, min2 and max2. In the COVID-19 (n=181) group there were two (1.0 event/1000-hospital-days) thrombotic events while one (1.8 event/1000-hospital-day) was reported in the non-CoV-2-RV (n=165) group. All of these events were myocardial infarction occurring in the intensive care unit. Coagulation parameters did not differ throughout the course of mild COVID-19. However, CWA parameters were significantly higher in severe COVID-19 compared with mild disease, suggesting hypercoagulability (min1: 6.48%/s vs 5.05%/s, P<0.001; min2: 0.92%/s² vs 0.74%/s², P=0.033). In conclusion, the thrombotic rates were low and did not differ between COVID-19 and non-CoV-2-RV patients. The hypercoagulability in COVID-19 is a highly dynamic process with the highest risk occurring when patients were most severely ill. Such changes in haemostasis could be detected by CWA. In our population, a more individualized thromboprophylaxis approach, considering clinical and laboratory factors, is preferred over universal pharmacological thromboprophylaxis for all hospitalized COVID-19 patients and such personalized approach warrants further research.