TNFα Inhibitors Versus Newer Therapies in Spondyloarthritis: Where do we Stand Today?

Abstract

The spondyloarthritides (SpA) are a group of chronic inflammatory diseases that affect the axial skeleton (ax-SpA), peripheral joints and entheses (p-SpA) and are expressed with several clinical phenotypes such as psoriasis, psoriatic arthritis (PsA), inflammatory bowel disease (IBD), and uveitis. The pathogenesis of SpA involves the pivotal role of tumour necrosis factor alpha (TNFα) and the interleukins (IL) IL-17/IL-23. Their distribution and hierarchy in the affected organs and tissues is differently expressed in SpA. TNFα is expressed in all tissues and organs, while IL-17 and IL-12/IL-23 is lacking from the gut and the axial skeleton respectively. This knowledge is a dilemma for physicians when they must choose a biological therapy. Nowadays, the armamentarium of SpA treatment has been expanded comprising biological therapies such as TNFα inhibitors (TNFαi), IL-17 inhibitors (IL-17i), IL-12/IL-23 inhibitors (IL-12/IL-23i), as well as the Janus Kinase inhibitors (JAKi). Several studies have shown that IL-12/IL-23i are very effective to treat psoriasis, PsA and IBD, but are ineffective in treating ax-SpA. IL-17i are very effective in patients with ax-SpA, psoriasis and PsA, but seem ineffective in IBD. Finally, TNFαi have shown to be effective in all SpA phenotypes with an acceptable toxicity profile. On the other hand, JAKi are also effective in almost all SpA phenotypes, but caution is required for elderly patients who may develop Herpes-Zoster infection, thromboembolic events and malignancies. However, the treatment of SpA is individualised according to the clinical phenotype and after shared decision between patients and physicians.