Increased faecal calprotectin signals worse disease activity in axial spondyloarthritis
Gut inflammation, as indicated by elevated faecal calprotectin levels, may be a marker of more severe disease in patients with axial spondyloarthritis (axSpA), according to data from the SPARTAKUS cohort. Specifically, increased calprotectin levels are associated with worse disease activity and physical function.
Researchers analysed the association of faecal calprotectin levels and the presence of anti-Saccharomyces cerevisiae antibodies (ASCA) in serum with disease subtype and current status in consecutive patients with a clinical axSpA diagnosis, which was classified as nonradiographic (nr-axSpA; n=40) or ankylosing spondylitis (AS; n=90), and in healthy controls (n=35).
Faecal calprotectin levels were elevated (≥50 mg/kg) in 27 percent of nr-axSpA patients, 38 percent of AS patients and 6 percent of controls. Of note, the levels were significantly higher in AS vs nr-axSpA patients (geometric mean, 41 vs 24 mg/kg; p=0.037) and in each axSpA subtype vs controls.
Overall, axSpA patients with elevated vs normal F-calprotectin levels showed worse disease activity and physical function scores, with marked differences in the visual analogue scale for global health, Ankylosing Spondylitis Disease Activity Score using C-reactive protein, and the Bath AS Functional.
Meanwhile, ASCA titres and seropositivity (≥10 U/ml) were similar in the nr-axSpA (IgA/IgG-seropositivity: 8 percent and 26 percent, respectively) and AS (IgA/IgG-seropositivity: 7 percent and 28 percent, respectively) cohorts. Clinical outcome measures did not significantly differ between patients with elevated vs normal ASCA IgA or IgG.
Compared with controls, patients in both axSpA subtypes had significantly greater ASCA IgA, while those in the AS group had markedly increased ACSA IgG.
The present data are in line with previous observations of more pronounced sacroiliitis in patients with microscopic gut inflammation, thus providing further evidence of an important interplay between gastrointestinal and musculoskeletal manifestations of axSpA, as researchers pointed out.