(Figure 1). Comparing gastrointestinal symptoms, significant differences were observed for the presence of abdominal pain (= 0.012) between SpA (54.3%) and IBD (27.5%), with a higher frequency in the SpA patients. BASDAI 4 and gastrointestinal symptoms ( 0.05) and IgA (= 0.007). The association for abdominal bloating was maintained (OR: 3.93, CI-95%, 1.14C13.56; = 0.030). Conclusions Gastrointestinal symptoms, ASCA, ANAS, and IgA levels were Bax-activator-106 associated with high disease activity in SpA compared with IBD and HS. 1. Introduction Spondyloarthritis (SpA) comprises a group of rheumatic Bax-activator-106 inflammatory chronic diseases that share clinical, radiographic, and immunogenic characteristics [1, 2]. This condition mainly affects males under 45 years of age and includes the following subtypes: ankylosing spondylitis (AS), reactive arthritis (ReA), psoriatic arthritis (PsA), inflammatory bowel disease associated with arthropathy, and undifferentiated spondyloarthritis (uSpA) [3]. The frequency of gastrointestinal manifestations in SpA ranges between 21 and 30% with a wide clinical spectrum. Approximately 5 to 10% of these manifestations are associated with inflammatory bowel disease (IBD). A substantial percentage of patients with unspecific gastrointestinal symptoms may have subclinical gut inflammation that may be confirmed only by endoscopy and histology [4, 5]. The association between gut and musculoskeletal system has been described previously. Wright and Watkinson in 1959 [6] and Wrigth and Watkinson in 1965 [7] described the clinical, radiologic, and serologic characteristics of a distinctive form of arthritis associated with IBD. They further proposed that SpA is not a disease without gastrointestinal involvement. In contrast, SpA may represent a spectrum of extraintestinal manifestations of inflammatory gastrointestinal diseases [8]. The immune dysfunction associated with the role of the microbiota of the gut mucosa is contributing factor to local morbidity [9]. An increase in bacterial growth, absorption of immune complexes, immune mediators (especially IL-6 and TNF-alpha), and gut permeability may be pathogenic determinants. The increase in gut permeability and abnormal levels of colonizing bacteria in active lesions of IBD may lead to absorption of proinflammatory bacterial components that stimulate a pathological immune response [10]. A similar pathogenesis has been discussed and proposed for SpA [11, 12]. It is interesting to consider the relationship between SpA, infection, and gut inflammation. Case reports have reported the clinical association of joint inflammation with the presence ofShigellasp.,Yersiniasp.,Campylobactersp., orSalmonellasp. in the gut [11, 12]. Several studies have evidence of the involvement of gut mucosa and the development of SpA. However, there is scarce evidence about studies assessing gastrointestinal symptoms in patients with SpA without IBD [13]. Having this tool in daily practice would enable an earlier and more focused approach to modulate and influence joint manifestations. Therefore, the main objective of this study is PPP3CC to determine the frequency of gastrointestinal symptoms and the association with the presence of gastrointestinal autoantibodies in a group of patients with SpA and compare them with both patients with IBD and healthy subjects. 2. Materials and Methods 2.1. Study Population A cross-sectional study was designed. The study population was divided into three groups: 103 patients with SpA according to the European Spondyloarthropathy Study Group (ESSG) [14], 29 patients with histological diagnosis of IBD according to the European Classification Consensus and the Montreal Classification for IBD [15, 16], and 117 healthy subjects. Those patients were enrolled from those attending regular rheumatology and proctology appointments at the Hospital from June 2012 to May 2014. Individuals with malignancies, autoinflammatory, or autoimmune diseases and antibiotic treatment in the past 3 months were excluded from the SpA group. Patients with irritable bowel syndrome Bax-activator-106 with histopathology that ruled out IBD or other colitis with specific etiology (ischemic, infectious, or eosinophilic) were excluded from the IBD group. SpA patients with concomitant IBD were excluded. Unmatched 117 controls were included if they had no family history of SpA or IBD. The subjects were enrolled from either the same hospital or the patients’ neighborhood. All patients and controls were between 18 and 65 years of age. The patients were asked about the presence of clinical symptoms and the medical history was retrieved to find information of Bax-activator-106 gastrointestinal symptoms: diarrhea (defined as more than three depositions per day), stools.
