Journal of Medical Council of Iran
Volume 43 - Series of Sessions on Post-Acute COVID-19 Syndrome
jmciri 2025, 43 - Series of Sessions on Post-Acute COVID-19 Syndrome: 37-51 |
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Zolfaghari M, Toogeh G, Ahmadi M, Mehrab Safdari S M, Soleimanifar N, Assadiasl S, et al . Hematological complications of post-acute COVID-19 syndrome (PASC). jmciri 2025; 43 (S1) :37-51
URL: http://jmciri.ir/article-1-3450-en.html
URL: http://jmciri.ir/article-1-3450-en.html
Mohammadali Zolfaghari 
, Gholamreza Toogeh , Maryam Ahmadi , Seyed Mehrab Mehrab Safdari , Narjes Soleimanifar , Sara Assadiasl , Alireza Esteghamati , Abdolrahman Rostamian , Behzad Poopak , Mohammad Hossein Niknam
, Gholamreza Toogeh , Maryam Ahmadi , Seyed Mehrab Mehrab Safdari , Narjes Soleimanifar , Sara Assadiasl , Alireza Esteghamati , Abdolrahman Rostamian , Behzad Poopak , Mohammad Hossein Niknam
Molecular Immunology Research Center, Tehran University of Medical Sciences, Tehran, Iran
Abstract: (192 Views)
Background: Post-Acute Sequelae of COVID-19 (PASC), or Long COVID, poses a major challenge to global healthcare systems with its chronic, multi-system complications. Hematologic and thrombotic disorders are a key and complex aspect of this syndrome, characterized by a pathophysiology of chronic "thromboinflammation." The emergence of the rare but fatal Vaccine-Induced Immune Thrombotic Thrombocytopenia (VITT) adds to this complexity.
Results: The pathophysiology of coagulopathy in PASC is rooted in a vicious cycle of persistent endothelial injury, immune dysregulation (including NETosis), low-grade chronic inflammation, and the formation of fibrinolysis-resistant microthrombi. This process explains common symptoms like fatigue, dyspnea, and brain fog. In contrast, VITT is an acute immunological emergency requiring immediate and distinct management (avoidance of heparin and administration of IVIG). Despite strong pathophysiological evidence, clinical trials do not support the routine use of prophylactic anticoagulants in outpatient PASC, highlighting a critical evidence gap.
Conclusion: The proposed algorithm is based on risk stratification using accessible biomarkers such as D-dimer and the neutrophil-to-lymphocyte ratio (NLR). This approach recommends aggressive treatment for patients with confirmed thrombosis but suggests a conservative strategy based on monitoring and risk factor management for the majority of PASC patients to avoid the risks of unnecessary treatment. Validation of this algorithm requires prospective studies in the Iranian patient population.
Results: The pathophysiology of coagulopathy in PASC is rooted in a vicious cycle of persistent endothelial injury, immune dysregulation (including NETosis), low-grade chronic inflammation, and the formation of fibrinolysis-resistant microthrombi. This process explains common symptoms like fatigue, dyspnea, and brain fog. In contrast, VITT is an acute immunological emergency requiring immediate and distinct management (avoidance of heparin and administration of IVIG). Despite strong pathophysiological evidence, clinical trials do not support the routine use of prophylactic anticoagulants in outpatient PASC, highlighting a critical evidence gap.
Conclusion: The proposed algorithm is based on risk stratification using accessible biomarkers such as D-dimer and the neutrophil-to-lymphocyte ratio (NLR). This approach recommends aggressive treatment for patients with confirmed thrombosis but suggests a conservative strategy based on monitoring and risk factor management for the majority of PASC patients to avoid the risks of unnecessary treatment. Validation of this algorithm requires prospective studies in the Iranian patient population.
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