Comorbidities and clinical complications associated with SARS-CoV-2 infection: an overview

Gupta, Anamika; Marzook, Hezlin; Ahmad, Firdos

doi:10.1007/s10238-022-00821-4

Cited by 31 publications

(26 citation statements)

References 209 publications

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“…Hypoxic condition induces VEGF expression that disrupts vascular permeability in lung tissues causing pulmonary inflammation and congestion [16] , [17] . Since a severe infection of SARS-CoV-2 often leads to endothelial dysfunction, acute respiratory distress syndrome (ARDS), and dyspnea with systemic hypoxia [18] , VEGF may play a critical role in the COVID-19 pathogenesis.…”

Section: Introductionmentioning

confidence: 99%

SARS-CoV-2 infection- induced growth factors play differential roles in COVID-19 pathogenesis

et al. 2022

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Section: Introductionmentioning

confidence: 99%

SARS-CoV-2 infection- induced growth factors play differential roles in COVID-19 pathogenesis

et al. 2022

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“…SARS-CoV-2 infected patients, mostly elderly people and patients with existing comorbidity factor present severe clinical complications. 1 One of these complications includes coagulation dysfunction and impaired fibrinolysis leading to thromboembolism, multi-organ damage, and death. 2 D-dimer is an endogenous fibrin clot degradation (fibrinolysis) product and is expected in patients with venous thromboembolism (VTE).…”

Section: Introductionmentioning

confidence: 99%

TFPI and FXIII negatively and S100A8/A9 and Cystatin C positively correlate with D-dimer in COVID-19

Gupta

Qaisar

Halwani

et al. 2022

Exp Biol Med (Maywood)

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D-dimer is an established biomarker of thromboembolism and severity in COVID-19. We and others have recently reported the dysregulation of tissue factor pathway inhibitor (TFPI), FXIII, fibrinolytic pathway, inflammatory markers, and tissue injury markers, particularly in severe COVID-19. However, association of these markers with thromboembolism in COVID-19 remains elusive. The correlation analyses between these markers in patients with moderate (non-ICU) and severe COVID-19 (ICU) were performed to delineate the potential pathomechanisms and impact of thromboembolism. We observe a negative correlation of plasma TFPI ( r2 = 0.148, P = 0.035), FXIII ( r2 = 0.242, P = 0.006), and plasminogen ( r2 = 0.27, P = 0.003) with D-dimer, a biomarker of thromboembolism, levels in these patients. Further analysis revealed a strong positive correlation between fibrinolytic markers tissue plasminogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1) ( r2 = 0.584, P < 0.0001). Interestingly, a significant positive correlation of PAI-1, but not tPA, was observed with platelets and endothelial cells dysfunction markers P-selectin ( r2 = 0.184, P = 0.01) and soluble CD40 ligand (sCD40 L) ( r2 = 0.163, P = 0.02). Moreover, calprotectin (S100A8/A9) and cystatin C (CST3), previously linked with thromboembolism, exhibited positive correlations with each other ( r2 = 0.339, P = 0.0007) and with the level of D-dimer independently in COVID-19. Finally, the tissue injury marker myoglobin demonstrated a strong positive correlation with D-dimer ( r2 = 0.408, P = 0.0001). Taken together, inverse correlations of TFPI and FXIII with D-dimer suggest the TF pathway activation and aberrant fibrin polymerization in COVID-19 patients. The elevated level of PAI-1 is potentially contributed by activated platelets and endothelial cells. S100A8/A9 may also play roles in impaired fibrinolysis and thromboembolism, in part, through regulating the CST3. These findings strengthen the understanding of thromboembolism and tissue injury and may help in better management of thromboembolic complications in COVID-19 patients.

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“…Pathogenesis of COVID-19 infection involves a complex interplay between coagulopathy and endotheliopathy due to viral infection and replication in the target cells with consequent immune and coagulation systems dysregulation [5], leading to uncontrolled inflammatory responses and eventually resulting in the cytokine storm [6]. The fibrinogen level in COVID-19 patients increases by 2-3 folds due to cytokine storm, causing thrombus formation, particularly in severe cases [7]. Moreover, the cytokine storm can damage both epithelial cells and endothelial cells, vascular leakage and finally result in ARDS and death [8].…”

Section: Introductionmentioning

confidence: 99%

Serum interleukin 1β and sP-selectin as biomarkers of inflammation and thrombosis, could they be predictors of disease severity in COVID 19 Egyptian patients? (a cross-sectional study)

et al. 2022

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Background Thromboembolism was a chief cause of mortality in 70% of patients with COVID-19. Our objective was to see if serum interleukins 1 beta (IL-1β) and soluble platelets selectin (sP-selectin) could serve as novel markers of thromboembolism in COVID-19 patients. Methods This cross sectional study involved 89 COVID-19 patients who were recruited from 1st of February to 1st of May 2021. Clinical and laboratory data were collected, and chest imaging was performed. The levels of IL-1β and sP-selectin were assessed in all cases through ELISA kits. Comparisons between groups were done using an unpaired t-test in normally distributed quantitative variables. In contrast, a non-parametric Mann-Whitney test was used for non-normally distributed quantitative variables. Results Severe COVID-19 infection was associated with higher serum levels of CRP, Ferritin, LDH, D dimer, IL-1β and sP-selectin (P < 0.001) with significant correlation between levels of IL-1β and sP-selectin (r 0.37, P < 0.001), D-dimer (r 0.29, P 0.006) and Ferritin (r 0.5, p < 0.001). Likewise, a positive correlation was also found between levels of sP-selectin, D-dimer and Ferritin (r 0.52, P < 0.001) (r 0.59, P < 0.001). Imaging studies revealed that 9 (10.1%) patients developed venous and 14 (15.7%) developed arterial thrombosis despite receiving anticoagulant therapy. Patients with thrombotic events had significantly higher levels of IL-1β, sP-selectin and LDH serum levels. Meanwhile, there was no statistical significance between CRP, D-dimer or Ferritin levels and the development of thrombotic events. Conclusion IL-1β and sP-selectin levels can be promising predictors for severe COVID-19 infection and predictable thrombosis.

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Comorbidities and clinical complications associated with SARS-CoV-2 infection: an overview

Cited by 31 publications

References 209 publications

SARS-CoV-2 infection- induced growth factors play differential roles in COVID-19 pathogenesis

SARS-CoV-2 infection- induced growth factors play differential roles in COVID-19 pathogenesis

TFPI and FXIII negatively and S100A8/A9 and Cystatin C positively correlate with D-dimer in COVID-19

Serum interleukin 1β and sP-selectin as biomarkers of inflammation and thrombosis, could they be predictors of disease severity in COVID 19 Egyptian patients? (a cross-sectional study)

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