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

Journal of Translational Medicine

Review

Vincent Jaquinandi¹  Guillaume Mahe¹  Loukman Omarjee² 

[1] Vascular Medicine Department, CHU de Rennes, 35033, Rennes Cedex 9, France;Univ Rennes, CHU Rennes, INSERM, CIC 1414, 35000, Rennes, France;Vascular Medicine Department, CHU de Rennes, 35033, Rennes Cedex 9, France;Univ Rennes, CHU Rennes, INSERM, CIC 1414, 35000, Rennes, France;Department of Vascular Medicine, Centre Hospitalier de Redon, 35600, Redon, France;Vascular Medicine Department, Pôle imagerie médicale et explorations fonctionnelles, Hôpital Pontchaillou, CHU de Rennes, 2 rue Henri Le Guilloux, 35033, Rennes, France;

关键词: Spondyloarthritis;    Nilotinib;    Tyrosine kinase inhibitor;    Vascular toxicity;    Major adverse cardiovascular events;    Peripheral artery disease;    Inflammation;    Atherosclerosis;    Morbi-mortality;   

DOI  :  10.1186/s12967-017-1334-1

 received in 2016-11-23, accepted in 2017-10-30,  发布年份 2017

来源: Springer

【 摘 要 】

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.

【 授权许可】

CC BY   
© The Author(s) 2017