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

• Published in: Journal of translational medicine 2017-12, Vol.15 (1), p.255-5, Article 255
• Main Authors: Omarjee, Loukman, Jaquinandi, Vincent, Mahe, Guillaume
• Format: Article
• Language: English
• Subjects: Antimitotic agents; Antineoplastic agents; Atherosclerosis; Blood Vessels - drug effects; Cardiovascular Diseases - chemically induced; Complications and side effects; Drug therapy; Humans; Inflammation; Inflammation - complications; Inflammation - drug therapy; Life Sciences; Major adverse cardiovascular events; Mortality; Nilotinib; Peripheral artery disease; Phenols; Protein Kinase Inhibitors - adverse effects; Protein Kinase Inhibitors - pharmacology; Protein Kinase Inhibitors - therapeutic use; Pyrimidines - adverse effects; Pyrimidines - pharmacology; Pyrimidines - therapeutic use; Review; Spondylarthritis - complications; Spondylarthritis - drug therapy; Spondyloarthritis; Tyrosine; Tyrosine kinase inhibitor; Vascular toxicity
• ISSN: 1479-5876; 1479-5876
• DOI: 10.1186/s12967-017-1334-1

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.