Artur Słomka1, Gennaro Martucci2, Giuseppe Maria Raffa3, Pietro Giorgio Malvindi4, Ewa Żekanowska1, Roberto Lorusso5,6, Piotr Suwalski7, Mariusz Kowalewski8,9,10. 1. Department of Pathophysiology, Nicolaus Copernicus University in Toruń, Ludwik Rydygier Collegium Medicum in Bydgoszcz, Bydgoszcz, Poland. 2. Department of Anesthesia and Intensive Care, IRCCS-ISMETT, Palermo, Italy. 3. Cardiac Surgery Unit, IRCCS-ISMETT, Palermo, Italy. 4. Wessex Cardiothoracic Centre, University Hospital Southampton, Southampton, UK. 5. Cardiovascular Research Institute Maastricht (CARIM), Maastricht, The Netherlands. 6. Cardio-Thoracic Surgery Department, Heart and Vascular Centre, Maastricht University Medical Centre, Maastricht, The Netherlands. 7. Department of Cardiac Surgery, Central Clinical Hospital of the Ministry of Interior, Centre of Postgraduate Medical Education, Warsaw, Poland. 8. Cardio-Thoracic Surgery Department, Heart and Vascular Centre, Maastricht University Medical Centre, Maastricht, The Netherlands. kowalewskimariusz@gazeta.pl. 9. Department of Cardiac Surgery, Central Clinical Hospital of the Ministry of Interior, Centre of Postgraduate Medical Education, Warsaw, Poland. kowalewskimariusz@gazeta.pl. 10. Thoracic Research Centre, Collegium Medicum, Nicolaus Copernicus University, Innovative Medical Forum, Bydgoszcz, Poland. kowalewskimariusz@gazeta.pl.
Abstract
INTRODUCTION: Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has recently and rapidly emerged and developed into a global pandemic. Through the renin-angiotensin system, the virus may impact the lung circulation, but the expression on endothelium may conduct to its activation and further systemic damage. While precise mechanisms underlying these phenomena remain to be further clarified, the understanding of the disease, its clinical course, as well as its immunological and hematological implications is of paramount importance in this phase of the pandemic. METHODS: This review summarizes the evidence gathered until 12 June; electronic databases were screened for pertinent reports on coronavirus and inflammatory and hematological changes. Search was conducted by two independent investigators; keywords used were "SARS-CoV-2," "COVID-19," "inflammation," "immunological," and "therapy." RESULTS: The viral infection is able to trigger an excessive immune response in predisposed individuals, which can result in a "cytokine storm" that presents an hyperinflammation state able to determine tissue damage and vascular damage. An explosive production of proinflammatory cytokines such as TNF-α IL-1β and others occurs, greatly exaggerating the generation of molecule-damaging reactive oxygen species. These changes are often followed by alterations in hematological parameters. Elucidating those changes in SARS-CoV-2-infected patients could help to understand the pathophysiology of disease and may provide early clues to diagnosis. Several studies have shown that hematological parameters are markers of disease severity and suggest that they mediate disease progression. According to the available literature, the primary hematological symptoms-associated COVID-19, and which distinguish patients with severe disease from patients with nonsevere disease, are lymphocytopenia, thrombocytopenia, and a significant increase in D-dimer levels. CONCLUSIONS: SARS-CoV-2 infection triggers a complex response altering inflammatory, hematological, and coagulation parameters. Measuring these alterations at certain time points may help identify patients at high risk of disease progression and monitor the disease severity.
INTRODUCTION: Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has recently and rapidly emerged and developed into a global pandemic. Through the renin-angiotensin system, the virus may impact the lung circulation, but the expression on endothelium may conduct to its activation and further systemic damage. While precise mechanisms underlying these phenomena remain to be further clarified, the understanding of the disease, its clinical course, as well as its immunological and hematological implications is of paramount importance in this phase of the pandemic. METHODS: This review summarizes the evidence gathered until 12 June; electronic databases were screened for pertinent reports on coronavirus and inflammatory and hematological changes. Search was conducted by two independent investigators; keywords used were "SARS-CoV-2," "COVID-19," "inflammation," "immunological," and "therapy." RESULTS: The viral infection is able to trigger an excessive immune response in predisposed individuals, which can result in a "cytokine storm" that presents an hyperinflammation state able to determine tissue damage and vascular damage. An explosive production of proinflammatory cytokines such as TNF-α IL-1β and others occurs, greatly exaggerating the generation of molecule-damaging reactive oxygen species. These changes are often followed by alterations in hematological parameters. Elucidating those changes in SARS-CoV-2-infected patients could help to understand the pathophysiology of disease and may provide early clues to diagnosis. Several studies have shown that hematological parameters are markers of disease severity and suggest that they mediate disease progression. According to the available literature, the primary hematological symptoms-associated COVID-19, and which distinguish patients with severe disease from patients with nonsevere disease, are lymphocytopenia, thrombocytopenia, and a significant increase in D-dimer levels. CONCLUSIONS: SARS-CoV-2 infection triggers a complex response altering inflammatory, hematological, and coagulation parameters. Measuring these alterations at certain time points may help identify patients at high risk of disease progression and monitor the disease severity.
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