Ina Isabella Høiland‘s PhD thesis suggests that complement activation is involved in the pathogenesis of venous thromboembolism.
- Classical complement activation and mannose-binding lectin are linked to venous thromboembolism.
- A high degree of overall complement activation is linked to increased risk of venous thromboembolism.
- Short-Chained PolyPs might initiate coagulation without affecting complement activation.
Thesis: Role of the Complement System in the Pathogenesis of Venous Thromboembolism
Candidate: Ina Isabella Høiland
Time: April 2, 2019 at 12:15
Place: UiT The Arctic University of Norway, MH-Vest: Auditorium Cortex
Link to university website
(1) The 20 % with the highest activity in the classical complement pathway seem to have more than four-fold increased risk of venous thromboembolism. Low levels of mannose-binding lectin was also linked to 3.5 times increased risk. Tissue-factor induced thrombin generation does not impact these associations.
The study compared 24 individuals with unprovoked venous thromboembolism and 24 healthy control of the same age and sex.
(2) Individuals with a high degree of complement activation have higher risk of venous thromboembolism, according to a currently unpublished article.
(3) The third paper of the thesis shows that Short-Chained-PolyPs can activate the coagulation system through the pathway associated with thrombus formation. However, Short-Chained-PolyPs does not inhibit the complement system.
(1) Høiland, I. I., Liang, R. A., Hindberg, K., Latysheva, N., Brekke, O. L., Mollnes, T. E., & Hansen, J. B. (2018). Associations between complement pathways activity, mannose-binding lectin, and odds of unprovoked venous thromboembolism. Thrombosis research, 169, 50-56.