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THU0374 A Longitudinal Study of Gut Inflammation and The Development of Inflammatory Bowel Disease in Ankylosing Spondylitis
  1. E. Klingberg1,
  2. H. Strid2,3,
  3. A. Ståhl4,
  4. A. Deminger1,
  5. H. Carlsten1,
  6. L. Öhman4,
  7. H. Forsblad-d'Elia1,5
  1. 1Department of Rheumatology and Inflammation Research, Sahlgrenska Academy at the University of Gothenburg, Göteborg
  2. 2Department of Internal Medicine, Södra Älvsborgs sjukhus, Borås
  3. 3Institute of Medicine, Departments of Internal Medicine and Clinical Nutrition, Sahlgrenska Academy at University of Gothenburg
  4. 4Microbiology and Immunology, Sahlgrenska Academy at the University of Gothenburg, Göteborg
  5. 5Department of Public Health and Clinical Medicine, Rheumatology, Umeå University, Umeå, Sweden

Abstract

Background Patients with ankylosing spondylitis (AS) have an increased risk of developing inflammatory bowel disease (IBD). There is however a lack of knowledge regarding the incidence of IBD in AS and what predicts the development from subclinical gut inflammation to IBD.

Objectives To determine the intra-individual variation in fecal calprotectin (FC) over 5 years in relation to AS disease activity, disease manifestations and medication and to study the 5–year incidence of IBD in AS and identify predictors for its' development.

Methods At baseline FC was assessed in 204 AS patients (NY-criteria) without diagnosed IBD. FC was then reexamined in 164 of the patients at the 5-year follow-up. The patients answered questionnaires regarding gastrointestinal symptoms, medication, physical function and disease activity. Ileocolonoscopy was performed at the 5-year follow-up if FC remained ≥200 mg/kg after 3 weeks NSAID-pause. The medical records were checked for colonoscopies, episodes of gut inflammation or diagnose of IBD during the follow-up period.

Results The characteristics of the 164 AS patients [median (IQR)]: 74♀/90♂, age 54 (46–67) ys, symptom duration 27 (18–39) ys, BASDAI 3.2 (1.8–5.2), ASDASCRP 2.1 (1.3–2.7), BASFI 2.3 (1.0–4.1) and BASMI 3.4 (2.4–4.6).

At the 5-year follow-up FC was elevated (>50 mg/kg) in 63% of the patients, but not associated with gastrointestinal symptoms. In 24% of the patients FC was >200 mg/kg. The intra-individual variation in FC during the 5-year follow-up was less than ±200 mg/mg in 80% (131/164) of the patients. FC was correlated with CRP (rS=0.219; p=0.005), ESR (rS=0.172; p=0.027), ASDASCRP (rS=0.207; p=0.008), hemoglobin (rS=-0.200; p=0.01), BASMI (rS=0.207; p=0.008) and BASFI (rS=0.154; p=0.048).

Users of NSAIDs had higher FC than non-users [93 (44–215) vs. 40 (23–120) mg/kg; p=0.011], whereas DMARD users had lower FC than non-users [45 (29–87) vs. 110 (40–250) mg/kg; p<0.001]. Users of infliximab, adalimumab and golimumab had lower FC than non-users [48 (23–135) vs. 89 (40–210) mg/kg; p=0.022], whereas users of etanercept had higher FC [200 (93–555) mg/kg]. In linear regression DMARD-use (B= -111.6, SE=41.0, p=0.007) and BASMI (B=41.9, SE=10.7, p<0.001) remained independently associated with log-transformed FC.

Totally 1.5% (3/204) had been diagnosed with Crohns disease (CD) and 0.5% with lymphocytic colitis at the five-year follow-up. Furthermore 3% had demonstrated a picture of subclinical CD and 2% a picture of subclinical chronic colitis at ileocolonoscopy. A high FC and presence of mucus in diarrhea were the main predictors of the development of CD.

Conclusions FC was elevated in approximately two-thirds of the patients both at baseline and at the five-year follow-up and positively associated with disease activity at both time points. The results supports a link between gut and joint disease in AS.

Use of NSAIDs and etanercept was associated with a higher FC, whereas use of other TNF-blockers and DMARDs was associated with a lower FC. The five-year incidence of CD was 1.5%, and an elevated FC was a main predictor thereof.

Disclosure of Interest None declared

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