Introduction 

Patients with ankylosing spondylitis (AS) have a high frequency of asymptomatic acute and chronic gut inflammation resembling inflammatory bowel disease (IBD), with as many as 60% displaying evidence of microscopic gut inflammation in the absence of gastrointestinal (GI) symptoms.1 Further, there is considerable overlap in susceptibility loci between AS and IBD but this pleiotropic phenomenon likely only explains part of the clinical co-occurrence.2 3 Animal model data investigating molecular mechanisms point to a critical relationship between the gut and AS and the potential role of the gut in the pathogenesis of AS.4 5 Several markers are utilised in clinical practice to determine the likelihood that a patient has IBD, the most common of which is the faecal calprotectin which has an estimated sensitivity and specificity of upwards of 80% for identification of patients with IBD and thus serves as a very useful marker of gut inflammation.6 Similarly, various IBD-related antibodies including anti-Saccharomyces cerevisiae antibodies (ASCA), antineutrophil cytoplasmic antibodies (ANCA), anti-I2 (associated with anti-Pseudomonas activity), anti-Escherichia coli outer membrane porin C (anti-OmpC) and antiflagellin antibodies (anti-CBir1) have been shown to have very good utility in distinguishing individuals with IBD from healthy controls, particularly when these tests are used in combination and thus serve as useful serological biomarkers for IBD.7

Using the above biomarkers along with advanced imaging studies, this pilot study investigated if first-degree relatives (FDRs) of patients with AS, who themselves do not carry a diagnosis of AS or IBD, have evidence of mucosal dysregulation, subclinical gut or sacroiliac joint inflammation that could potentially precede the development of overt IBD or AS. We postulate that this group will provide insights into the relationship between the gut and AS.