IL-2 Levels, Smoking, and Number of Injuries Correlate with Platelet Procoagulant Potential in Veterans with Mild TBI - Supporting a Link Between Prior Injury and Long-term Risk of Stroke
Zalan Kaposzta1, Philion Gatchoff1, Andrea Vincent2, Eleanor Mathews1, Leslie Guthery1, Andriy Yabluchanskiy1, Angelia Kirkpatrick3, George Dale1, Calin Prodan3
1University of Oklahoma Health Sciences Center, 2University of Oklahoma, 3University of Oklahoma Health Sciences Center/Oklahoma City VA Medical Center
Objective:
To explore mechanisms associated with increased platelet procoagulant potential in patients with mild traumatic brain injury (mTBI).
Background:
Coated-platelets are a subset of highly procoagulant platelets, observed upon dual-agonist stimulation with collagen and thrombin. While in healthy controls they represent ~32% of all platelets, elevated coated-platelet levels are present in patients with ischemic stroke and are associated with increased risk for infarct recurrence. Prior work, prompted by the recognition of stroke as a long-term complication of TBI, showed elevated coated-platelet levels in mTBI patients several years after the injury. Furthermore, a relationship between increased number of injuries and increased coated-platelet potential was observed.
Design/Methods:
Coated-platelet levels (expressed as percentage of platelets) were assayed as previously described in veterans with combat related mTBI. Subjects with moderate/severe TBI, prior stroke/TIA, intracerebral hemorrhage, dementia, bleeding diatheses or recent blood transfusions were excluded. An array of 27 inflammatory markers was assessed with a multiplex assay system for each patient. Demographics, medications, number and timing of injuries, and comorbidities were recorded for each participant. Regression analysis was conducted to assess factors associated with coated-platelet levels.
Results:
We enrolled 39 randomly selected veterans with mTBI (>14 months from the last injury), with a mean age of 38 years (range 27-54), and mean coated-platelet levels of 37.2% (SD 13.3%). The following inflammatory markers and clinical variables showing associations with coated-platelet levels at P≤0.15 were included as predictors in a multiple regression analysis: IL-2, IL-10, IL-15, GM-CSF, injury type, smoking status, and number of injuries. The model accounted for 51.8% of the variance in coated-platelet levels. Only IL-2, number of injuries and smoking retained significance in the full model.
Conclusions:
These results support the existence of a possible molecular link between TBI and the long-term risk of stroke through thrombotic and inflammatory mechanisms. Further examination of the mechanisms involved is warranted.
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