Elevated platelet expression of CD36 may contribute to increased risk of thrombo-embolism in active inflammatory bowel disease

• Published in: Archives of physiology and biochemistry Vol. 119; no. 5; pp. 202 - 208
• Main Authors: Wilhelmsen, Peter, Kjær, Jens, Thomsen, Karen Louise, Nielsen, Christoffer Tandrup, Dige, Anders, Maniecki, Maciej Bogdan, Heegaard, Niels, Grønbæk, Henning, Dahlerup, Jens, Handberg, Aase
• Format: Journal Article
• Language: English
• Published: England Informa UK Ltd 01.12.2013; Taylor & Francis
• Subjects: Adult; Anti-Inflammatory Agents - pharmacology; Blood Platelets - drug effects; Blood Platelets - metabolism; CD36 antigen; CD36 Antigens - blood; CD36 Antigens - chemistry; Cell-derived microparticles; Colitis, Ulcerative - complications; Crohn Disease - complications; Female; flow cytometry; Gene Expression Regulation - drug effects; Glucose - metabolism; Humans; inflammation; Male; platelets; Risk; Solubility; Thromboembolism - blood; Thromboembolism - complications
• DOI: 10.3109/13813455.2013.808671
• ISSN: 1381-3455

Abstract 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.