Key result
Active IBD linked to ~34% higher platelet CD36 expression with sCD36 restored by anti-TNF therapy.
Why the study?
Does anti-TNF treatment alter CD36 expression and related biomarkers in patients with active inflammatory bowel disease?
Case-Control (n=26)
Does anti-TNF treatment alter CD36 expression and related biomarkers in patients with active inflammatory bowel disease?
Elevated platelet CD36 expression in active inflammatory bowel disease may contribute to increased thrombo-embolic risk and is partially modulated by anti-TNF therapy.
Active IBD may heighten thromboembolic risk via platelet CD36; leaves open whether anti-TNF modulation of sCD36 affects outcomes.
CONTEXT: Inflammatory bowel disease (IBD) induces increased risk of thrombo-embolism. CD36 is involved in platelet activation, glucose metabolism and inflammation. OBJECTIVE: The relationship between CD36 expression on platelets and monocytes, plasma sCD36, and CD36-positive platelet-derived microparticles (PDMPs) and inflammation in both active IBD and after one week of anti-tumour necrosis alpha antibody (anti-TNF) treatment was investigated. MATERIAL AND METHODS: Patients with exacerbation of Crohn's disease (n = 8) or ulcerative colitis (n = 5) and 13 healthy controls were enrolled. Seven patients underwent anti-TNF treatment for one week. Platelet, monocyte, and PDMP-CD36 were measured by flow-cytometry. RESULTS: Platelet CD36 expression was 34% higher in patients, and correlated with insulin resistance and fasting glucose. sCD36 was 37% lower and restored after anti-TNF treatment. CONCLUSION: Elevated platelet CD36 expression may contribute to increased risk of thrombo-embolism in active IBD. This may not entirely be attributed to inflammation and secondary insulin resistance may play a role.
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Wilhelmsen et al. (2013) conducted a case-control in Active inflammatory bowel disease (n=26). Active inflammatory bowel disease vs. Healthy controls was evaluated on Platelet CD36 expression and plasma sCD36 levels. Active inflammatory bowel disease was associated with 34% higher platelet CD36 expression and 37% lower sCD36 compared to healthy controls, with sCD36 restored after anti-TNF treatment.
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