Mannose-Binding Lectin is Associated with Thrombosis and Coagulopathy in Critically Ill COVID-19 Patients

Oskar Eriksson1, Michael Hultström2,3, Barbro Persson1

  • 1Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.

Thrombosis and Haemostasis
|September 2, 2020
PubMed

Insights

Mannose-binding lectin (MBL) may amplify blood clotting in critically ill COVID-19 patients, increasing the risk of dangerous thromboembolic events. Measuring MBL levels could identify patients needing targeted therapies for COVID-19 thrombosis.

Area of Science:

  • Immunology
  • Hematology
  • Critical Care Medicine

Background:

  • COVID-19 is associated with severe morbidity, mortality, and a high risk of thromboembolic (TE) complications.
  • The precise mechanisms driving COVID-19-associated coagulopathy, even with thromboprophylaxis, remain incompletely understood.
  • Mannose-binding lectin (MBL), a key initiator of the lectin complement pathway, is implicated in amplifying coagulation during thromboinflammation.

Purpose of the Study:

  • To investigate the role of MBL in the coagulopathy of critically ill COVID-19 patients.
  • To determine if MBL levels correlate with the development of symptomatic thromboembolic events.
  • To explore MBL as a potential biomarker and therapeutic target for COVID-19-related thrombosis.

Main Methods:

  • Analysis of a cohort of 65 critically ill COVID-19 patients admitted to an intensive care unit (ICU).
  • Measurement of plasma MBL levels and activity upon ICU admission.
  • Correlation analysis of MBL levels with clinical outcomes, including symptomatic TE, D-dimer levels, inflammation markers, and organ dysfunction.

Main Results:

  • A subset of patients exhibited significantly elevated MBL plasma levels and activity.
  • Patients who developed symptomatic TE (14%) had markedly higher MBL levels compared to those without TE.
  • MBL levels showed a strong correlation with D-dimer, a marker of coagulopathy, but not with inflammation or organ dysfunction.

Conclusions:

  • Complement activation via the MBL pathway represents a novel mechanism amplifying pathological thrombosis in critically ill COVID-19 patients.
  • Targeting the MBL pathway presents a potential therapeutic strategy for managing thrombosis in COVID-19.
  • Assessing MBL levels may aid in identifying COVID-19 patients at elevated risk for TE events.