Inflammatory Bowel Disease and Ankylosing Spondylitis: Differences Tested

They are similar chronic inflammatory diseases with causes unknown, and recent clinical and genetic evidence supports an intertwined pathogenic relationship.

Inflammatory bowel disease (IBD) and ankylosing spondylitis (AS) are similar chronic inflammatory diseases with causes unknown, and recent clinical and genetic evidence supports an intertwined pathogenic relationship, according to authors at the Cedars-Sinai Medical Center, University of California, Los Angeles, School of Medicine. Therefore, they conducted a pilot study1 to measure fecal calprotectin (fCal) levels and IBD-related serologies in patients with AS.

With the manufacturer’s recommended cutoff for positivity at 50 μg/g, fCal levels were elevated in 41% of patients with AS. Medians of most IBD-specific antibodies were higher in fCal-positive patients with AS than in healthy controls and fCal-negative patients with AS.

Matzkies and colleagues1 recruited consecutive patients with AS from a long-term prospectively collected longitudinal cohort; 81 patients were included for analysis (76% of them were HLA-B27–positive). They tested sera by enzyme-linked immunosorbent assay (ELISA) for IBD-associated serologies (antineutrophil cytoplasmic antibodies [ANCAs], anti-Saccharomyces cerevisiae antibody IgG and IgA, Anti-I2, Anti-OmpC, and Anti-CBir1). They also completed the Bath Ankylosing Spondylitis Disease Activity Index, Bath Ankylosing Spondylitis Functional Index, and Bath Ankylosing Spondylitis Radiology Index for patients with AS.

The AS group and controls showed median fCAL levels of 42 μg/g and 17 μg/g, respectively. Stool samples of 41% of patients with AS and 10% of controls were positive for fCal. There were no significant differences in antibody levels between patients and controls, except for ANCAs. Median ANCA ELISA units were 6.9 and 4.3 in patients with AS and controls, respectively. Among patients with AS stratified by fCal level, statistically significant differences were seen between patients and controls for multiple IBD-associated antibodies.

The authors noted that further studies are needed to determine whether fCal may be used to identify and characterize a subgroup of patients with AS whose disease might be driven by subclinical bowel inflammation.

A study coauthor, Dermot McGovern, MD, PhD, is presenting at 2012 Advances in Inflammatory Bowel Diseases, the Crohn’s & Colitis Foundation’s Clinical & Research Conference, to be held December 13-15 in Hollywood, Florida. His topics include a discussion of genetic regulation of IBD pathogenesis.

For information on a possible link between IBD and obesity, listen to the podcast “The Changing Shape of Inflammatory Bowel Disease.”

Reference
1. Matzkies FG, Targan S, Berel D, et al. Markers of intestinal inflammation in patients with ankylosing spondylitis: a pilot study. Arthritis Res Ther. 2012;14:R261. [Epub ahead of print.]