Mucosal Inflammation in Spondylarthritides: Past, Present, and Future

Praet, Liesbet Van; Bosch, Filip Van den; Mielants, Herman; Elewaut, Dirk

doi:10.1007/s11926-011-0198-2

Cited by 31 publications

(18 citation statements)

References 51 publications

(52 reference statements)

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“…115 Inflammation in the gut has been consistently observed in spondyloarthritis. 116 Cigarette smoking has also been implicated in AS susceptibility, underscoring its role in multiple inflammatory and autoimmune diseases. 117 Unlike most other rheumatic diseases, males are more likely than females to develop AS, so male-specific factors such as testosterone may also be involved in the pathogenesis of AS.…”

Section: Introductionmentioning

confidence: 99%

Genetics, Environment, and Gene-Environment Interactions in the Development of Systemic Rheumatic Diseases

Costenbader¹

2014

Rheumatic Disease Clinics of North America

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Understanding disease susceptibility factors and gene-environment interactions may offer valuable insights into the biological mechanisms for the etiology of rheumatic diseases. Defining the contributions of genetic and environmental factors to the pathogenesis of rheumatic diseases such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and ankylosing spondylitis (AS), may have important implications for understanding risk prediction, pathogenic mechanisms, cellular pathways, drug discovery, and prevention strategies. However, rheumatic diseases offer distinct challenges to researchers due to heterogeneity in disease phenotypes, low disease incidence, and geographic variation in both genetic and environmental factors. Emerging research areas, including epigenetics, metabolomics, and the microbiome, may provide additional links between genetic and environmental risk factors in rheumatic disease pathogenesis. This article reviews the methods used to establish genetic and environmental risk factors and to study gene-environment interactions in rheumatic diseases and provides specific examples of successes and challenges for identifying gene-environment interactions in RA, SLE, and AS. Finally, we describe how emerging research strategies may build upon previous discoveries as well as future challenges.

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Section: Introductionmentioning

confidence: 99%

Genetics, Environment, and Gene-Environment Interactions in the Development of Systemic Rheumatic Diseases

Costenbader¹

2014

Rheumatic Disease Clinics of North America

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“…Although both appear to be distinct and well-defined phenotypes, there is increasing clinical and genetic evidence supporting an intertwined pathogenic relationship [1]. Clinically, 5 to 10% of all patients with AS have concurrent IBD [2].…”

Section: Introductionmentioning

confidence: 99%

Markers of intestinal inflammation in patients with ankylosing spondylitis: a pilot study

et al. 2012

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IntroductionInflammatory bowel disease (IBD) and ankylosing spondylitis (AS) are similar chronic inflammatory diseases whose definitive etiology is unknown. Following recent clinical and genetic evidence supporting an intertwined pathogenic relationship, we conducted a pilot study to measure fecal calprotectin (fCAL) and IBD-related serologies in AS patients.MethodsConsecutive AS patients were recruited from a long-term prospectively collected longitudinal AS cohort at Cedars-Sinai Medical Center. Controls were recruited from Cedars-Sinai Medical Center employees or spouses of patients with AS. Sera were tested by ELISA for IBD-associated serologies (antineutrophil cytoplasmic antibodies (ANCA), anti-Saccharomyces cerevisiae antibody IgG and IgA, anti-I2, anti-OmpC, and anti-CBir1). The Bath Ankylosing Spondylitis Disease Activity Index, the Bath Ankylosing Spondylitis Functional Index, and the Bath Ankylosing Spondylitis Radiology Index were completed for AS patients.ResultsA total of 81 subjects (39 AS patients and 42 controls) were included for analysis. The average age of AS patients was 47 years and the average disease duration was 22 years. AS patients were predominantly male; 76% were HLA-B27-positive. Median fCAL levels were 42 μg/g and 17 μg/g in the AS group and controls, respectively (P < 0.001). When using the manufacturer's recommended cutoff value for positivity of 50 μg/g, stool samples of 41% of AS patients and 10% of controls were positive for fCAL (P = 0.0016). With the exception of ANCA, there were no significant differences in antibody levels between patients and controls. Median ANCA was 6.9 ELISA units in AS patients and 4.3 ELISA units in the controls. Among AS patients stratified by fCAL level, there were statistically significant differences between patients and controls for multiple IBD-associated antibodies.ConclusionCalprotectin levels were elevated in 41% of patients with AS with a cutoff value for positivity of 50 μg/g. fCAL-positive AS patients displayed higher medians of most IBD-specific antibodies when compared with healthy controls or fCAL-negative AS patients. Further studies are needed to determine whether fCAL can be used to identify and characterize a subgroup of AS patients whose disease might be driven by subclinical bowel inflammation.

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“…Recently, additional shared associations between SpA and IBD were found at chromosome 1q32 near KIF21B (genome-wide significant), STAT3, IL-12B, CDKAL1, LRRK2/MUC19, and chromosome 13q14 (experiment-wise association). As the genes IL-23R, STAT3, and IL-12B all influence Th17 lymphocyte differentiation/activation, this provides further evidence implicating the Th17 lymphocyte subset in the pathogenesis of SpA [65]. …”

Section: Pathogenesismentioning

confidence: 97%

“…In fact, several common genetic predispositions between SpA and IBD were identified, of which the association with IL-23R polymorphisms is most prominent [64]. The functional role of IL-23 receptor polymorphisms remains unclear, the fact that IL-23 signaling plays a critical role in the Th17-mediated inflammation indicates that Th17 cells may represent a common pathogenetic mechanism in both IBD and SpA [65]. The first susceptibility gene that has been identified for CD is CARD15 (or NOD2).…”

Section: Pathogenesismentioning

confidence: 99%

Enteropathic Spondyloarthritis: From Diagnosis to Treatment

Peluso

Minno

Iervolino

et al. 2013

Clinical and Developmental Immunology

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Enteropathic arthritis (EA) is a spondyloarthritis (SpA) which occurs in patients with inflammatory bowel diseases (IBDs) and other gastrointestinal diseases. Diagnosis is generally established on the medical history and physical examination. It was, generally, made according to the European Spondyloarthropathy Study Group (ESSG) criteria. Rheumatic manifestations are the most frequent extraintestinal findings of IBD with a prevalence between 17% and 39%, and IBD is associated, less frequently, with other rheumatic disease such as rheumatoid arthritis, Sjogren syndrome, Takayasu arteritis, and fibromyalgia. Although the pathogenesis of EA has not been plainly clarified, the most popular theory supposes that joint inflammation occurs in genetically predisposed subjects with bacterial gut infections, provided an important evidence for a possible relationship between inflammation of the gut mucosa and arthritis. The management of patients with EA requires an active cooperation between the gastroenterologist and rheumatologist.

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Mucosal Inflammation in Spondylarthritides: Past, Present, and Future

Cited by 31 publications

References 51 publications

Genetics, Environment, and Gene-Environment Interactions in the Development of Systemic Rheumatic Diseases

Genetics, Environment, and Gene-Environment Interactions in the Development of Systemic Rheumatic Diseases

Markers of intestinal inflammation in patients with ankylosing spondylitis: a pilot study

Enteropathic Spondyloarthritis: From Diagnosis to Treatment

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