CONGRESS ABSTRACT

Inflammatory bowel disease (IBD) is a risk factor of thrombotic accidents. This risk is high in the flare and chronic activity phase but low in the remission period. Infliximab is a potent anti-tumor necrosis factor (TNF) antibody, highly effective in inflammatory bowel disease (IBD). Infection and development of malignancy, especially systemic lymphoma, are well-known adverse event of Infliximab (IFX). Furthermore, it seems likely that the administration of IFX to IBD patients further increases the risk of arterial or venous thrombotic complications. The location and timing of the thrombotic complications have been widely inconsistent among these patients. We reported a case of acute and proximal occlusion of the left anterior descending (LAD) coronary artery in a patient with Crohn’s disease, in an endoscopic remission phase, after high-dose IFX administration. A 46-years-old men was sent to our center because of severe chest pain. He had been diagnosed with Crohn’s disease five years earlier. Initially, his disease had been controlled using but later had required the additional use of oral steroid due to deterioration. Despite high-dose steroid administration, Crohn’s disease remained active and refractory to conventional medical therapy. Therefore, steroids were discontinued and IFX was started. The patient was treated using high-dose IFX at 10 mg/kg with a 6 week interval, maintained disease remission. He experienced chest pain 3 day after the last injection of IFX. The ECG showed biphasic T waves in leads V1-V2-V3 and the cardiac enzymes are elevated. The cardiac catheterization with percutaneous coronary intervention (PCI) relieved the trombotic occlusion of the LAD coronary artery, without coronary atherosclerosis. The occlusion was treated with thromboaspiration and secondary reperfusion of the coronary artery. Extensive work-up provided no evidence of predisposing factors for coronary thrombosis. We concluded that coronary artery thrombosis was related  to high-dose IFX infusion. The expression of TNF-a receptors has been proposed as a possible reason for thrombosis occurring in IBD patients after IFX administration. The TNF-a driven procoagulant loop increase the incidence of thrombosis after TNF-a administration. A counter-regolation mechanism might upregulate the expression of TNF-areceptors on the inflammatory cell membrane when IFX administration leads to a reduction in serum TNF-alevels, resulting in thrombus formation.