In her PhD thesis, Gro Grimnes has looked at aspects of the association between infection, inflammation and venous thromboembolism.
- There is no association between neutrophil to lymphocyte ratio and risk of future venous thromboembolism.
- Acute infection is a strong trigger for venous thromboembolism in hospitalized patients.
- Acute inflammation is also a trigger for venous thromboembolism.
Thesis: Infection, inflammation, and risk of venous thromboembolism
Candidate: Gro Grimnes
Time: June 18, 2018 at 12:15
Place: UiT The Arctic University of Norway, Farmasibygget: Tabletten
Link to university website (in Norwegian)
(1) The risk of venous thromboembolism was not affected by the neutrophil to lymphocyte ratio, a biomarker of low-grade inflammation. However, high neutrophil to lymphocyte ratio was associated with increased risk of mortality among those who experienced venous thromboembolism.
The study includes 25,107 subjects from the fourth survey of the Tromsø Study in 1994–95, followed until 2012. After multivariable adjustment neutrophil to lymphocyte ratio showed no significant association with either provoked or unprovoked venous thromboembolism, deep vein thrombosis or pulmonary embolism.
(2) Immobilization does not explain the strong association between acute infection and venous thromboembolism in hospitalized patients. The risk of venous thromboembolism was 24-fold higher within three months after an acute infection. Adjustment for immobilization reduced the increase to 15-fold. Infection and immobilization had a synergistic effect on the risk.
707 Tromsø study participants who later suffered from venous thromboembolism were included in the study.
(3) Acute inflammation was also a trigger for venous thromboembolism in the same 707 patients. The level of C-reactive protein was 58% higher in the hazard period than in the control periods, and the association was only slightly attenuated after adjustment for immobilization and infection.
(4) The antibiotic Vancomyosin changes the gut microbiome, and the changes are accompanied by increased inflammation (C-reactive protein) and levels of coagulation factor VIII:C. These findings are the result of a currently unpublished randomized controlled trial.
(1) Grimnes, G., Horvei, L. D., Tichelaar, V., Brækkan, S. K., & Hansen, J. B. (2016). Neutrophil to lymphocyte ratio and future risk of venous thromboembolism and mortality: the Tromsø Study. Haematologica, 101(10), e401-e404.
(2) Grimnes, G., Isaksen, T., Tichelaar, Y. V., Brækkan, S. K., & Hansen, J. B. (2018). Acute infection as a trigger for incident venous thromboembolism: Results from a population‐based case‐crossover study. Research and Practice in Thrombosis and Haemostasis, 2(1), 85-92.
(3) Grimnes, G., Isaksen, T., Tichelaar, Y. I. G. V., Brox, J., Brækkan, S. K., & Hansen, J. B. (2018). C-reactive protein and risk of venous thromboembolism: Results from a population-based case-crossover study. Haematologica, haematol-2017.