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J Rheumatol. 2010 Nov;37(11):2340-4. doi: 10.3899/jrheum.100269. Epub 2010 Sep 1.

pANCA, ASCA, and OmpC antibodies in patients with ankylosing spondylitis without inflammatory bowel disease.

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Department of Rheumatology, VU University Medical Centre, Room 3A-64, PO Box 7057, 1007 MB Amsterdam, The Netherlands.

Erratum in

  • J Rheumatol. 2010 Dec;37(12):2639. von Blomberg, Mary [corrected to von Blomberg, B Mary E].



Patients with ankylosing spondylitis (AS) can suffer concurrently from inflammatory bowel disease (IBD), as ulcerative colitis (UC) or Crohn's disease (CD). Serological markers have been described to diagnose IBD. We investigated IBD serological markers in AS patients without IBD and whether these antibodies enable differentiating patients with AS and IBD from those without IBD.


Frequencies of perinuclear antineutrophil cytoplasmic antibodies (pANCA), antibodies to the cell-wall mannan of Saccharomyces cerevisiae (ASCA), and antibodies to porin protein C of Escherichia coli (OmpC) were evaluated in 179 patients: 52 with AS, 50 with UC, 51 with CD, and 26 with IBD and AS. Patient groups were matched for age and sex. All AS patients fulfilled the 1984 modified New York criteria. IBD was ascertained by clinical, endoscopic, and microscopic findings.


In 55% of the AS patients without manifest IBD at least one antibody associated with IBD was observed. pANCA, ASCA (IgA and/or IgG), and OmpC antibodies were found in 21%, 30%, and 19% of the AS patients, respectively. pANCA was more frequently present in AS with concurrent UC than in AS alone (OR 8.2, 95% CI 1.2-55.6), thus being an indicator for UC in AS patients.


Antibodies associated with IBD are detectable in more than half of AS patients without symptoms or signs of IBD. A relatively recent marker in this setting, OmpC antibodies, does not contribute to the differentiation between AS and type of IBD. Presence of pANCA, however, is significantly increased in AS patients who also have UC, and is an indicator to perform endoscopy. These results corroborate a pathophysiological link between AS and IBD.

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