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Causal Effects of COVID-19 on the Risk of Thrombosis: A Two-Sample Mendel Randomization Study

Zhengran Li1,2, Minghui Zeng3, Tong Wu4

  • 1The Second Clinical Medicine School, Southern Medical University, Guangzhou, Guangdong, China.

Thrombosis and Haemostasis
|February 7, 2024
PubMed

Insights

This study reveals how COVID-19 impacts thrombosis biomarkers. Lowering tissue factor pathway inhibitor (TFPI) and interleukin-1 receptor type 1 (IL-1R1) suggests a causal link between COVID-19 and increased thrombosis risk.

Area of Science:

  • Biomedical Science
  • Genetics
  • Epidemiology

Background:

  • The link between Coronavirus disease 2019 (COVID-19) and thrombosis is established, yet the underlying biomolecular mechanisms remain largely unknown.
  • Investigating the causal relationship between COVID-19 and thrombotic biomarkers is crucial for understanding disease pathogenesis and developing targeted therapies.

Purpose of the Study:

  • To investigate the causal relationship between COVID-19 and 20 key thrombotic biomarkers using Mendelian randomization.
  • To elucidate the biomolecular mechanisms linking COVID-19 infection to thrombotic events.

Main Methods:

  • Two-sample Mendelian randomization (MR) was employed to assess the effect of COVID-19 on thrombotic biomarkers.
  • Causality was estimated using inverse variance weighting, with sensitivity analyses performed using weighted median, MR-Egger regression, and MR-PRESSO methods.
  • Results were corrected for multiple testing using the false discovery rate (FDR) with the Benjamin and Hochberg method.

Main Results:

  • COVID-19 was associated with significantly lower levels of tissue factor pathway inhibitor (TFPI) and interleukin-1 receptor type 1 (IL-1R1), nearly doubling the odds of thrombosis.
  • Hospitalized cases showed reduced levels of plasminogen activator, tissue type (tPA) and P-selectin glycoprotein ligand 1 (PSGL-1), while severe cases exhibited higher mean platelet volume (MPV) and lower platelet count.
  • These biomarker changes, particularly in TFPI, tPA, IL-1R1, MPV, and platelet count, suggest an elevated risk of thrombosis in COVID-19 patients.

Conclusions:

  • TFPI, IL-1R1, and seven other indicators provide causal insights into the pathogenesis of COVID-19 and thrombosis.
  • This study provides robust evidence that COVID-19 causally influences thrombosis at the biomolecular level.
  • Findings highlight potential therapeutic targets for managing thrombotic complications in COVID-19.
Abstract

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