No Evidence for Classic Thrombotic Microangiopathy in COVID-19

Tanja Falter1, Heidi Rossmann1, Philipp Menge2

  • 1Institute of Clinical Chemistry and Laboratory medicine, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany.

Insights

Disseminated intravascular coagulation (DIC) occurred in some COVID-19 patients, but fibrinogen and platelet consumption were mostly compensated. Thrombotic microangiopathy (TMA) hallmarks were absent, suggesting localized alveolar microcirculation issues.

Area of Science:

  • Hematology
  • Infectious Diseases
  • Critical Care Medicine

Background:

  • Coronavirus disease-2019 (COVID-19) is a systemic infection impacting the respiratory tract.
  • Some patients develop hemostatic abnormalities, increasing mortality risk.

Purpose of the Study:

  • To investigate the occurrence and characteristics of disseminated intravascular coagulation (DIC) and thrombotic microangiopathy (TMA) in COVID-19 patients.
  • To analyze laboratory parameters and clinical features associated with these hemostatic disorders in COVID-19.

Main Methods:

  • Retrospective analysis of 65 COVID-19 patients (SARS-CoV-2 infection) from March to May 2020.
  • Assessment of disseminated intravascular coagulation (DIC) and thrombotic microangiopathy (TMA) using ISTH criteria and laboratory data.
  • Analysis of fibrinogen levels, platelet counts, and ADAMTS13 activity.

Main Results:

  • Seven out of 65 COVID-19 patients (10.8%) showed overt DIC.
  • Fibrinogen levels dropped significantly in DIC patients but remained above 100 mg/dl.
  • Hallmarks of TMA, including thrombocytopenia and microangiopathic hemolytic anemia, were absent. ADAMTS13 activity was mildly reduced in some patients with elevated procalcitonin.

Conclusions:

  • DIC occurred in a subset of COVID-19 patients, but consumption of fibrinogen and platelets was largely compensated.
  • Classic TMA and TTP were excluded by ADAMTS13 assays and absence of key TMA markers.
  • A hypothesis suggests COVID-19-associated microangiopathy is localized to alveolar microcirculation, explaining limited erythrocyte fragmentation and platelet consumption.
Abstract

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