Oral JAK 1 Inhibitor Eases Spine Inflammation in Ankylosing Spondylitis

Treatment with filgotinib among patients with ankylosing spondylitis was associated with declines in inflammation in the spine, a post-hoc analysis of a multicenter randomized trial found.

“Ankylosing spondylitis is a chronic inflammatory disease affecting the sacroiliac joints and spine and can result in structural damage and disability,” noted Xenofon Baraliakos, MD, of Ruhr University in Bochum, Germany, speaking at the European League Against Rheumatism virtual congress.

In the phase II TORTUGA trial, treatment with the oral JAK 1 inhibitor filgotinib significantly improved MRI scores of bone marrow edema among patients with active ankylosing spondylitis using the criteria of the Spondyloarthritis Research Consortium of Canada (SPARCC).

To further explore the effects of filgotinib on inflammation, Baraliakos and colleagues conducted a post-hoc analysis of data from 88 patients in TORTUGA using the Canada-Denmark (CANDEN) method, which allows more comprehensive semiquantitative assessment than SPARCC of inflammation, fat, erosions, and new bone formation of the spine according to anatomic location.

Patients with ankylosing spondylitis were randomized to filgotinib, 200 mg, or placebo daily for 12 weeks, and magnetic resonance imaging of the total spine was performed at baseline and at week 12. Participants had previously had an inadequate response or intolerance to two or more nonsteroidal anti-inflammatory drugs.

At baseline, patients’ mean age was 41, disease duration was 6.5 years, and mean ankylosing spondylitis disease activity score was 4.2. Three-quarters of the participants were men.

There were some baseline differences between the filgotinib and placebo groups. The total CANDEN spine inflammation score was 18 in the filgotinib group but 11.8 in the placebo group, while the total CANDEN new bone formation score was 17.7 in the filgotinib group but 38.1 in the placebo group.

At week 12, the least squares mean of group difference on the total spine inflammation score was -4.49 (95% CI -6.85 to -2.12, P=0.0003). Differences between the groups were not significant for total spine fat scores, bone erosion scores, and total ankylosis scores, although fat lesions showed a tendency to increase and the lack of change in erosion scores was expected in a 12-week trial, Baraliakos noted.

There also were significant differences from baseline at week 12 on specific CANDEN inflammation subscores, according to least squares means of group differences:

• Posterior elements of the spine, -1.09 (95% CI -1.85 to -0.32, P=0.006)

• Facet joints, -0.35 (95% CI -0.65 to -0.04, P=0.026)

• Vertebral body, -2.84 (95% CI -4.96 to -0.73, P=0.009).

Cumulative probability plots for each of these subscores also favored filgotinib.

The decreased inflammation in the posterior elements and facet joints has not been demonstrated previously, Baraliakos said, adding, however, that because of imbalances in MRI measures at baseline and the post-hoc nature of the analysis, the findings will need to be confirmed in a large trial.