Levels of Inflammatory Markers and the Development of the Post Thrombotic Syndrome.

Background: The post-thrombotic syndrome (PTS) occurs frequently after deep vein thrombosis (DVT) despite appropriate anticoagulant therapy. A close relationship between inflammation and thrombosis exists. While the inflammatory process at the time of DVT appears to improve thrombus resolution, it may promote destruction of venous valves, valvular reflux and subsequent development of PTS.

Objective: We prospectively evaluated the association between levels of four cytokines (IL-6, IL-8, IL-10 and MCP-1), two adhesion molecules (ICAM-1 and VCAM-1) and the development of PTS in a well-defined cohort of patients with DVT.

Methods: The study population consisted of 387 patients with objectively diagnosed symptomatic DVT who participated in the Venous Thrombosis Outcomes (VETO) Study and were followed for two years to determine the incidence of PTS. For this substudy, plasma samples frozen at the 4 month visit in 307 study patients who consented to provide blood samples were thawed and analyzed for the above inflammatory markers using the Luminex beads technology. Associations between marker levels and development of the PTS during follow-up were evaluated.

Results: Mean levels of IL-6 were significantly higher in patients with PTS compared to patients without PTS (7.35 pg/ml ± 14.26 vs. 4.60 pg/ml ± 4.90;p=0.03). Logistic regression analyses showed significant associations between PTS and levels above vs. below the median of IL-6 (OR 1.66; 95% CI 1.05, 2.62 (p=0.03)) and ICAM-1 (OR 1.63; 95% CI 1.03, 2.58 (p=0.04)). None of the other markers showed any association with PTS.

Conclusion: Our study suggests the presence of significant associations between markers of inflammation such as IL-6 and ICAM-1 and the development of PTS. Further work is needed to evaluate this relationship and to analyze other candidate markers that could be implicated etiologically in the association between DVT and PTS. If confirmed, this could lead to identification of new therapeutic targets for preventing PTS after DVT.