“…Thrombosis is a common complication in severely ill COVID-19 patients, as proinflammatory and procoagulant activation pathways coexist [ 1 , 4 , 7 , 30 , 44 ]. The prior presence of APLA or “de novo” APLA positivity could play a role in the pathogenesis of these thrombotic events [ 18 , 23 , 24 , 45 ]. Some APLA antibodies have been detected in patients with COVID-19, but their relationship with thrombosis and mortality is still a matter of debate [ 23 , 37 , 46 , 47 , 48 ].…”
Section: Discussionmentioning
confidence: 99%
“…These signalling molecules not only recruit immune cells to the site of injury but also activate the complement and clotting pathways [ 12 , 13 ]. Inflammatory cells, particularly neutrophils and monocytes, release procoagulant substances, for instance interleukin-1 or tissue factor, and serine proteases such as elastase and cathepsin G, that enhance clot formation [ 16 , 17 , 18 ]. Furthermore, inflammatory molecules can activate platelets and promote their aggregation [ 19 , 20 ].…”
Antiphospholipid antibodies (APLA) are strongly associated with thrombosis seen in patients with antiphospholipid syndrome. In COVID-19, thrombosis has been observed as one of the main comorbidities. In patients hospitalised for COVID-19, we want to check whether APLA positivity is associated with COVID-19-related thrombosis, inflammation, severity of disease, or long COVID-19. We enrolled 92 hospitalised patients with COVID-19 between March and April 2020 who were tested for 18 different APLAs (IgG and IgM) with a single line-immunoassay test. A total of 30 healthy blood donors were used to set the cut-off for each APLA positivity. Of the 92 COVID-19 inpatients, 30 (32.61%; 95% CI [23.41–43.29]) tested positive for APLA, of whom 10 (33.3%; 95% CI [17.94–52.86]) had more than one APLA positivity. Anti-phosphatidylserine IgM positivity was described in 5.4% of inpatients (n = 5) and was associated with the occurrence of COVID-19-related thrombosis (p = 0.046). Anti-cardiolipin IgM positivity was the most prevalent among the inpatients (n = 12, 13.0%) and was associated with a recorded thrombosis in their clinical history (p = 0.044); however, its positivity was not associated with the occurrence of thrombosis during their hospitalisation for COVID-19. Anti-phosphatidylinositol IgM positivity, with a prevalence of 5.4% (n = 5), was associated with higher levels of interleukin (IL)-6 (p = 0.007) and ferritin (p = 0.034). Neither of these APLA positivities was a risk factor for COVID-19 severity or a predictive marker for long COVID-19. In conclusion, almost a third of COVID-19 inpatients tested positive for at least one APLA. Anti-phosphatidylserine positivity in IgM class was associated with thrombosis, and anti-phosphatidylinositol positivity in IgM class was associated with inflammation, as noticed by elevated levels of IL-6. Thus, testing for non-criteria APLA to assess the risk of clinical complications in hospitalised COVID-19 patients might be beneficial. However, they were not related to disease severity or long COVID-19.
“…Thrombosis is a common complication in severely ill COVID-19 patients, as proinflammatory and procoagulant activation pathways coexist [ 1 , 4 , 7 , 30 , 44 ]. The prior presence of APLA or “de novo” APLA positivity could play a role in the pathogenesis of these thrombotic events [ 18 , 23 , 24 , 45 ]. Some APLA antibodies have been detected in patients with COVID-19, but their relationship with thrombosis and mortality is still a matter of debate [ 23 , 37 , 46 , 47 , 48 ].…”
Section: Discussionmentioning
confidence: 99%
“…These signalling molecules not only recruit immune cells to the site of injury but also activate the complement and clotting pathways [ 12 , 13 ]. Inflammatory cells, particularly neutrophils and monocytes, release procoagulant substances, for instance interleukin-1 or tissue factor, and serine proteases such as elastase and cathepsin G, that enhance clot formation [ 16 , 17 , 18 ]. Furthermore, inflammatory molecules can activate platelets and promote their aggregation [ 19 , 20 ].…”
Antiphospholipid antibodies (APLA) are strongly associated with thrombosis seen in patients with antiphospholipid syndrome. In COVID-19, thrombosis has been observed as one of the main comorbidities. In patients hospitalised for COVID-19, we want to check whether APLA positivity is associated with COVID-19-related thrombosis, inflammation, severity of disease, or long COVID-19. We enrolled 92 hospitalised patients with COVID-19 between March and April 2020 who were tested for 18 different APLAs (IgG and IgM) with a single line-immunoassay test. A total of 30 healthy blood donors were used to set the cut-off for each APLA positivity. Of the 92 COVID-19 inpatients, 30 (32.61%; 95% CI [23.41–43.29]) tested positive for APLA, of whom 10 (33.3%; 95% CI [17.94–52.86]) had more than one APLA positivity. Anti-phosphatidylserine IgM positivity was described in 5.4% of inpatients (n = 5) and was associated with the occurrence of COVID-19-related thrombosis (p = 0.046). Anti-cardiolipin IgM positivity was the most prevalent among the inpatients (n = 12, 13.0%) and was associated with a recorded thrombosis in their clinical history (p = 0.044); however, its positivity was not associated with the occurrence of thrombosis during their hospitalisation for COVID-19. Anti-phosphatidylinositol IgM positivity, with a prevalence of 5.4% (n = 5), was associated with higher levels of interleukin (IL)-6 (p = 0.007) and ferritin (p = 0.034). Neither of these APLA positivities was a risk factor for COVID-19 severity or a predictive marker for long COVID-19. In conclusion, almost a third of COVID-19 inpatients tested positive for at least one APLA. Anti-phosphatidylserine positivity in IgM class was associated with thrombosis, and anti-phosphatidylinositol positivity in IgM class was associated with inflammation, as noticed by elevated levels of IL-6. Thus, testing for non-criteria APLA to assess the risk of clinical complications in hospitalised COVID-19 patients might be beneficial. However, they were not related to disease severity or long COVID-19.
“…105 Although elements of the pathophysiology of COVID, sepsis, and other diseases characterized by thromboinflammation may overlap with major trauma, the specific mechanisms involved are distinct. 106 Moreover, the link between early changes in platelet behavior during TIC and subsequent postinjury organ dysfunction is still being elucidated.…”
Section: Platelets In Postinjury Inflammation and Organ Dysfunctionmentioning
Trauma currently accounts for 10% of the total global burden of disease and over 5 million deaths per year, making it a leading cause of morbidity and mortality worldwide. Although recent advances in early resuscitation have improved early survival from critical injury, the mortality rate in patients with major hemorrhage approaches 50% even in mature trauma systems. A major determinant of clinical outcomes from a major injury is a complex, dynamic hemostatic landscape. Critically injured patients frequently present to the emergency department with an acute traumatic coagulopathy that increases mortality from bleeding, yet, within 48 to 72 hours after injury will switch from a hypocoagulable to a hypercoagulable state with increased risk of venous thromboembolism and multiple organ dysfunction. This review will focus on the role of platelets in these processes. As effectors of hemostasis and thrombosis, they are central to each phase of recovery from injury, and our understanding of postinjury platelet biology has dramatically advanced over the past decade. This review describes our current knowledge of the changes in platelet behavior that occur following major trauma, the mechanisms by which these changes develop, and the implications for clinical outcomes. Importantly, supported by research in other disease settings, this review also reflects the emerging role of thromboinflammation in trauma including cross talk between platelets, innate immune cells, and coagulation. We also address the unresolved questions and significant knowledge gaps that remain, and finally highlight areas that with the further study will help deliver further improvements in trauma care.
“…These structural changes foster blood cell adhesion and upregulate the crosstalk between inflammatory cells and coagulation. Enhanced interactions between platelets and leukocytes induce the formation of neutrophil extracellular traps (NETs), further increasing endothelial injury and facilitating thromboinflammation [ 20 ]. Fig.…”
Section: Glycocalyx Damage In Sepsismentioning
confidence: 99%
“…Thromboinflammation plays an important role in the progression of tissue injury in sepsis [ 20 ]. Although various trials have been performed to examine the effects of anticoagulant therapy, robust evidence supporting a beneficial role is lacking [ 70 ].…”
Maintaining tissue perfusion in sepsis depends on vascular integrity provided by the endothelial glycocalyx, the critical layer covering the luminal surface of blood vessels. The glycocalyx is composed of proteoglycans, glycosaminoglycans, and functional plasma proteins that are critical for antithrombogenicity, regulating tone, controlling permeability, and reducing endothelial interactions with leukocytes and platelets. Degradation of the glycocalyx in sepsis is substantial due to thromboinflammation, and treatments for sepsis and septic shock may exacerbate endotheliopathy via additional glycocalyx injury. As a result, therapeutic strategies aimed at preserving glycocalyx integrity should be considered, including modifications in fluid volume resuscitation, minimizing catecholamine use, controlling hyperglycemia, and potential use of corticosteroids and anticoagulants. In this review, we explore treatment strategies aligned with the recommendations outlined in the Surviving Sepsis Campaign Guidelines 2021 with a special emphasis on evidence regarding glycocalyx protection.
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