Thrombotic Complications in Patients With Coronavirus Disease 2019 (COVID-19): Two Contrasting Clinical Presentations Viewed Through the Concept of Thromboinflammation
- 1Department of Intensive Care Medicine, Health Sciences University (HSU) Dr. Suat Seren Chest Diseases and Chest Surgery Training and Research Hospital, Izmir, TUR
Abstract
Thrombotic complications are well-recognized extrapulmonary manifestations of coronavirus disease 2019 (COVID-19). 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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BibTeX
@article{colakoglu2026thrombotic,
title = {{Thrombotic Complications in Patients With Coronavirus Disease 2019 (COVID-19): Two Contrasting Clinical Presentations Viewed Through the Concept of Thromboinflammation}},
author = {Can Colakoglu},
journal = {Cureus},
year = {2026},
month = oct,
doi = {10.7759/cureus.117525},
url = {https://doi.org/10.7759/cureus.117525},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Thrombotic Complications in Patients With Coronavirus Disease 2019 (COVID-19): Two Contrasting Clinical Presentations Viewed Through the Concept of Thromboinflammation
AU - Can Colakoglu
PY - 2026
DA - 2026/10/06
JO - Cureus
DO - 10.7759/cureus.117525
UR - https://doi.org/10.7759/cureus.117525
AB - Thrombotic complications are well-recognized extrapulmonary manifestations of coronavirus disease 2019 (COVID-19). 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.
SN - 2168-8184
ER -