Thrombotic complications are well-recognized extrapulmonary manifestations of coronavirus disease 2019 .Although initially attributed to virus-specific endothelial injury, increasing evidence suggests that these events are better explained by thromboinflammatory mechanisms involving immunothrombosis.We present two contrasting thrombotic complications observed during acute severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and discuss them within the framework of thromboinflammation and host susceptibility.The first patient was a previously healthy 35-year-old postpartum woman who developed acquired thrombotic thrombocytopenic purpura (TTP) characterized by microangiopathic hemolytic anemia, severe thrombocytopenia, acute kidney injury, neurological deterioration, reduced ADAMTS13 activity, and a favorable response to therapeutic plasma exchange.Despite hematological recovery, distal ischemic injury resulted in digital amputation.The second patient was a 61-year-old man with a heavy smoking history and a radiologically suspicious pulmonary malignancy who developed acute right femoral artery thrombosis during severe COVID-19 pneumonia, requiring emergency thromboembolectomy.Although revascularization was successful, distal tissue necrosis developed, whereas ischemic manifestations in the remaining extremities resolved with combined medical therapy.Both cases demonstrated distinct thrombotic phenotypes despite a common inflammatory trigger.These contrasting cases support the concept that severe systemic inflammation may produce different thrombotic manifestations according to underlying host susceptibility rather than reflecting a unique SARS-CoV-2-specific vasculopathy.The COVID-19 pandemic provided an unprecedented opportunity to observe diverse thromboinflammatory phenotypes, contributing to a broader understanding of thromboinflammation beyond COVID-19 itself.
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Can Çolakoğlu (2026) studied this question.
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