What proportion of clinically diagnosed AS patients (initially without XRay evidence of sacroiliitis) progress to showing XRay damage, and how fast?
What's the fuss? Well, all the expensive treatments approved for treating AS were "proven" in patients with sacroiliitis seen on XRays. So, there is no justification for using such costly and potentially hazardous biologics in "non-radiographic" patients. However, a case can be made for "pre-radiographic" patients, since increasing evidence suggests that disease progression to damage in at-risk patients occurs early, and early intervention may prevent progression to ankylosis (disabling joint and spine fusion). As in RA, the difficulty lies in identifying those "destined" to do badly, so as to better target such targeted therapies. Based on this and the 2011 study referenced in this article, MRI features of inflammation at the sacroiliac joints (even before XRay changes become visible) and a high CRP (indicating systemic inflammation) can help to identify this group for biologic treatment. But in a clinical setting, it's a no-brainer: in a clinically diagnosed "non-radiographic" AS patient suffering disabling pain inadequately relieved by NSAIDs, wouldn't we treat with a biologic, finances permitting? So, what's the fuss?
Cosentyx (Secukinumab) gets European Commission nod for treating Ankylosing Spondylitis and Psoriatic Arthritis.
A puzzling aspect of AS, distinct from RA, is how damage (as characterised by new bone formation and ankylosis) can progress inexorably despite arresting inflammation.
My cursory read of this article highlighted 2 salient explanations: 1) arresting inflammation early before irreversible damage has occurred can prevent new bone formation, but the suppression of inflammation has to be constant and prolonged; 2) damage begets damage, with fatty replacement of bone oedema (as seen on MRI) possibly inciting osteoneogenesis. If true, this must make the pharmas very happy: AS patients may have to keep at their biologics for 2 years perhaps, without tapering or "on-demand" treatment (treat on clinical flare). But ongoing studies on whether NSAIDs can inhibit new bone formation (not just suppressing AS inflammation weakly), thereby behaving as a true disease-modifying drug (DMARD) in AS, can position it as a synergistic combination drug with biologics for remission induction, or even replacing the biologics in maintenance of remission.
This post by my Orthopaedic friend lighted a bulb on the role of NSAID in new bone formation and the link in AS: