GIScaSpA-study of subclinical gut involvement in axial spondyloarthritis

Background Axial spondyloarthritis (axSpA) had a predilection for the axial skeleton and belong to the group of Spondyloarthritis, a set of inflammatory rheumatic diseases with common clinical, radiologic, and serologic features in which extraarticular manifestations are frequent, including inflammatory bowel disease (IBD). The link between SpA and IBD has been recognized for decades, with 5-10% of axial SpA patients suffering from concurrent IBD. [2] But, emerging evidence suggests that subclinical gut inflammation in patients with SpA is an important pathophysiological event that plays a role in disease pathogenesis. However, it is difficult to detect subclinical gut inflammation since it is largely asymptomatic. Faecal calprotectin (FC) is a very sensitive marker for inflammation in the gastrointestinal tract. The role of FC in patients with SpA is not clearly defined, but some studies suggest that FC levels may predict the onset of IBD and may be related to disease activity. Objectives To test the validity of FC as a marker of intestinal inflammation in patients with axSpA and to investigate factors associated with increased FC levels in patients with axSpA. Methods Patients involved fulfilled ASAS classification criteria for axSpA and were divided into two groups - ankylosing spondylitis (AS) or non-radiographic axSpA (nr-axSpA); a control group without rheumatologic diseases or IBD was also included. All patients and controls answered a structured questionnaire about the presence of gastrointestinal symptoms - Red Flags Questionnaire for IBD and underwent FC measurement with enzyme-linked immunosorbent assay (≥50 mg/g was considered positive). Patients treated with oral NSAIDs should undergo adequate washout (at least 3 weeks). In patients, BASDAI, BASFI, ASDAS-PCR and BASMI were recorded. A general analysis was performed; p-value ≤0.05 was statistically significant. Results We included 64 patients (34 with AS and 30 with nr-axSpA) and 25 controls. Demographic, clinical data is represented in table 1. In AS group, 2.9% had nocturnal diarrhoea, first-degree relative with confirmed IBD and rectal urgency; in nr-axSpA, 6.7% had abdominal pain 30-45 minutes after meals and 3.3% chronic abdominal pain; all controls were asymptomatic. Elevated FC was observed in 32.4% of AS patients (129.2±404.0), 23.3% of nr-axSpA patients (70.9±114.4) and 4.2% of controls (21.9±18.4). FC was significantly higher in each axSpA subtype vs controls (p=0.03). There were no statistically significant differences in ASDAS, BASDAI, BASFI or BASMI scores between axSpA patients with normal vs high FC levels. Table 1. Characteristics of the population according to axSpA groups and controls. AS (n=34) axSpA (n=30) Controls (n=25) P* Age (years), mean±SD 55.5±14.7 44.9±13.3 40.2±14.0 0.004 Sex (F/M) 15/19 18/12 13/11 0.205 Age at disease onset (years), mean±SD 11.8±7.7 5.4±3.3 - <0.001 Comorbidities, n (%) Arterial Hypertension 13(38.2) 10(33.3) 1(4) 0.166 Dyslipidemia 8(23.5) 7(23.3) 2(8) 0.985 Diabetes Mellitus 3(8.8) 2(6.7) 0 0.748 Obesity 1(2.9) 1(3.3) 0 Smoking status, n (%) 4(11.8) 1(3.3) 1(4) 0.850 Peripheral involvement, n (%) 9(26.5) 5(16.7) - 0.344 Dactylitis (ever), n (%) 0 1(3.3) - 0.283 Enthesitis (ever), n (%) 1(2.9) 2(6.7) - 0.482 Uveitis (ever), n (%) 9(26.5) 4(13.3) - 0.192 Positivity HLA-B27, n (%) 25(73.5) 13(43.3) - 0.014 BASDAI, mean±SD 3.4±2.5 3.8±2.4 - 0.589 BASFI, mean±SD 3.3±2.5 3.3±2.1 - 0.981 ASDAS-PCR, mean±SD 2.3±1.0 2.4±1.1 - 0.070 BASMI, mean±SD 4.2±1.8 3.1±1.7 - 0.226 Therapeutic, n (%) - AINEs ** 16 (47.1) 14 (46.7) 0.124 cDMARDs 2 (5.9) 2 (6.7) 0.897 bDMARDs 9 (26.5) 11 (36.7) 0.408 *Comparison between nr-axSpA and AS groups. ** washout before collecting stool. Conclusion In patients with axSpA, gut inflammation measured by FC was higher than among controls and it was also higher in patients with AS than in nr-axSpA. We also found that high FC values were not associated with more pronounced gastrointestinal symptoms. Thus, studies with a larger population and invasive studies are needed to assess the impact that this marker may have on the management of this pathology. REFERENCES: NIL. Acknowledgements: NIL. Disclosure of Interests None Declared.