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| http://dx.doi.org/10.5152/AnatolJCardiol.2021.9 | DOI Listing |
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Unravelling the impact of SARS-CoV-2 on hemostatic and complement systems: a systems immunology perspective.
Front Immunol
January 2025
School of Interdisciplinary Engineering and Sciences (SINES), Department of Sciences, National University of Sciences and Technology (NUST), Islamabad, Pakistan.
The hemostatic system prevents and stops bleeding, maintaining circulatory integrity after injury. It directly interacts with the complement system, which is key to innate immunity. In coronavirus disease 2019 (COVID-19), dysregulation of the hemostatic and complement systems has been associated with several complications.
View Article and Find Full Text PDFAnti-platelet factor 4 antibody-mediated disorders: an updated narrative review.
Semin Thromb Hemost
January 2025
of Medicine, Universita degli Studi di Padova Scuola di Medicina e Chirurgia, Padova, Italy.
Anti-platelet factor 4 (PF4) antibody-mediated disorders are a heterogenous group of diseases characterized by the presence of highly pathogenic immunoglobulins G directed against PF4 and/or PF4/heparin complexes. These antibodies are able to activate platelets, neutrophils and monocytes, thus resulting in thrombocytopenia and a hypercoagulable state. Five different forms of anti-PF4 antibody-mediated disorders have been identified: i) classic heparin-induced thrombocytopenia (cHIT) mediated by heparin and certain polyanionic drugs; ii) autoimmune HIT (aHIT) characterized by the presence of anti-PFA/polyanion antibodies that can strongly activate platelets even in the absence of heparin; iii) spontaneous HIT (spHIT) characterized by thrombocytopenia and thrombosis without proximate exposure to heparin, with two subtypes: (a) post-total knee arthroplasty, and cardiac surgery using cardiopulmonary bypass or extracorporeal membrane oxygenation, and (b) post-infections; iv) vaccine-induced immune thrombotic thrombocytopenia (VITT) characterized by thrombocytopenia, arterial and venous thrombosis, or secondary hemorrhage after receiving adenoviral vector vaccines for COVID-19; v) VITT-like disorders triggered by adenoviral infections.
View Article and Find Full Text PDFComplex Lower Extremity Salvage Using Composite Flap Grafting in COVID-19-Induced Arterial Thrombosis: A Case Report.
JBJS Case Connect
January 2025
Department of Orthopedic Surgery, Texas Tech University Health Sciences, Center; Lubbock, Texas.
Case: We present a 42-year-old man who developed extensive left lower extremity arterial thrombosis following COVID-19 pneumonia. Despite multiple revascularization attempts and a below-knee amputation, he faced wound necrosis and insufficient soft tissue coverage. An innovative approach using a pedicled flap and sequential flow-through free flaps was used for limb salvage.
View Article and Find Full Text PDFCaspase-1 activation, IL-1/IL-6 signature and IFNγ-induced chemokines in lungs of COVID-19 patients.
Front Immunol
January 2025
Aix-Marseille Université, INSERM, INRAE, C2VN, Marseille, France.
Rationale: COVID-19-associated acute-respiratory distress syndrome (C-ARDS) results from a direct viral injury associated with host excessive innate immune response mainly affecting the lungs. However, cytokine profile in the lung compartment of C-ARDS patients has not been widely studied, nor compared to non-COVID related ARDS (NC-ARDS).
Objectives: To evaluate caspase-1 activation, IL-1 signature, and other inflammatory cytokine pathways associated with tissue damage using post-mortem lung tissues, bronchoalveolar lavage fluids (BALF), and serum across the spectrum of COVID-19 severity.
Peculiarities of in-Stent Thrombosis and Restenosis in Coronary Arteries Post-COVID-19: A Systematic Review of Clinical Cases and Case Series.
Open Access Emerg Med
January 2025
Nuclear Medicine Department, Center of Nuclear Medicine and Oncology, Semey, Abay Region, Kazakhstan.
Background: One of the most serious complications of coronary artery stenting is restenosis and in-stent thrombosis; their prevalence can reach 20-25%. Stent thrombosis can be acute (up to 24 hours), subacute (24 hours to 30 days), late (30 days to 1 year), and very late (> 1 year after previous stenting). In the patients with COVID-19 in intensive care units, the proportion of those with elevated troponin levels reached 25%.
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