The use of the tyrosine kinase inhibitor Nilotinib in Spondyloarthritis: does targeting inflammatory pathways with a treatment lead to vascular toxicity?

Abstract

Spondylarthritis (SpA) is an inflammatory rheumatic disease associated with increased incidence of major adverse cardiovascular events (MACEs). Recently, Paramarta et al. proposed the use of the tyrosine kinase inhibitor Nilotinib in Spondyloarthritis to target certain inflammatory pathways. However, Nilotinib, which is highly effective for the treatment of patients with chronic myeloid leukaemia (CML), is also associated with an increased risk of MACEs. The authors suggest that Nilotinib may be effective in peripheral SpA by modulating inflammation, but not in axial SpA. Considering the vascular toxicity of Nilotinib and the acceleration of atherosclerosis in SpA patients, we suggest taking MACEs as an end-point in future trials.

Nilotinib related acute myocardial infarction with nonobstructive coronary arteries: a case report and literature review

“…The mechanism of nilotinib related cardiovascular disease is still unclear. Lipid metabolism disorder [ 14 ], endothelial dysfunction [ 9 ] and inflammation overactivation [ 15 ] are several suggested mechanisms, which can accelerate atherosclerotic process and cause vascular spasm [ 16 ]. To the best of our knowledge, there have been only three cases reported of nilotinib related coronary spasm [ 17 , 18 ].…”