Patients With a History of Idiopathic Deep Venous Thrombosis Have Long-Term Increased Levels of Inflammatory Markers and Markers of Endothelial Damage.
BACKGROUND
Although the role of inflammation in DVT has been investigated in different studies, there is no definite answer as to whether increased systemic inflammation is the cause or the consequence of DVT.


OBJECTIVE
To follow inflammatory parameters in a cohort of patients with idiopathic DVT.


METHODS
Out of 49 patients with an acute idiopathic DVT, which were investigated four months after an acute episode (DEVTA 1), 43 patients were included in the follow-up study investigating inflammatory markers and hemostatic markers of endothelial damage five years after an acute DVT (DEVTA 2). A control group consisted of 43 sex and age matched healthy subjects (CONTROLS).


RESULTS
The levels of inflammatory markers were significantly higher in DEVTA 2 in comparison to CONTROLS: tumor necrosis factor alpha 2.0 pg/mL (1.1-2.3) vs 1.3 pg/mL (0.8-1.9), p < .001, high sensitivity C-reactive protein 3.2 mg/L (1.5-5.2) vs 1.7 mg/L (0.9-3.0), p = .008, interleukin-6 (IL-6) 2.7 pg/mL (2.0-3.5) vs 2.1 pg/mL (1.5-2.6), p = .025, IL-8 5.0 pg/mL (3.6-7.3) vs 2.4 pg/mL (1.8-2.8), p < .001. IL-10 was significantly decreased (0.9 pg/mL (0.7-1.8) vs 1.8 (1.5-2.2), p < .001. Most of the proinflammatory markers remained elevated in the DEVTA 2 in comparison to DEVTA 1. Markers of endothelial damage were higher in DEVTA 2 in comparison to CONTROLS and higher than in DEVTA 1.


CONCLUSIONS
Patients with idiopathic DVT have long-term increased inflammatory markers and markers of endothelial damage. These findings favor the hypothesis that inflammation is a cause and not merely a consequence of acute DVT.
1 University of Texas Health Science Center at Houston, Houston, TX, USA.
Mateja Kaja
MK
Jezovnik
2 Hemostasis and Thrombosis Research Laboratories, Loyola University Medical Center, Maywood, IL, USA.
Jawed
J
Fareed
3 Department of Vascular Disease, University Medical Center Ljubljana, Ljubljana, Slovenia.
Pavel
P
Poredos
D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D015331:Cohort Studies; D004730:Endothelium, Vascular / Q000293:injuries* / Q000473:pathology; D005260:Female; D005500:Follow-Up Studies; D006487:Hemostasis; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000150:complications*; D018836:Inflammation Mediators / Q000097:blood; D008297:Male; D008875:Middle Aged; D013997:Time Factors; D020246:Venous Thrombosis / Q000097:blood / Q000209:etiology*
D015415:Biomarkers; D018836:Inflammation Mediators
endothelial dysfunction; fibrinolytic activity; inflammation; lipids; risk