Abstract
Spondyloarthritis (SpA) is a group of rheumatic diseases whose pathogenesis relies on a complex interplay between genetic and environmental factors. Over the last several years, the importance of the alteration of the gut microbiota, known as dysbiosis, and the interaction of bacterial products with host immunity have been highlighted as intriguing key players in SpA development. The recent advent of the so called “-omics” sciences, that include metabolomics, opened the way to a new approach to SpA through a deeper characterisation of the pathogenetic mechanisms behind the disease. In addition, metabolomics can reveal potential new biomarkers to diagnose and monitor SpA patients. The aim of this review is to highlight the most recent advances concerning the application of metabolomics to SpA, in particular focusing attention on Ankylosing Spondylitis and Psoriatic Arthritis.
Highlights
Spondyloarthritis (SpA) refers to a group of chronic inflammatory diseases sharing heterogeneous clinical features and pathogenic mechanisms
Over the last several years, the importance of the alteration of the gut microbiota, known as dysbiosis, and the interaction of bacterial products with host immunity have been highlighted as intriguing key players in SpA development
The aim of this review is to highlight the most recent advances concerning the application of metabolomics to SpA, in particular focusing attention on Ankylosing Spondylitis and Psoriatic Arthritis
Summary
Spondyloarthritis (SpA) refers to a group of chronic inflammatory diseases sharing heterogeneous clinical features and pathogenic mechanisms It encompasses several distinct diseases; among them, Ankylosing Spondylitis (AS) and Psoriatic Arthritis (PsA) are the most common ones [1]. SpA features consist of inflammatory back pain, arthritis, enthesitis, dactylitis, uveitis, psoriasis, IBD, good response to NSAIDs, family history of spondyloarthropathy, HLA-B27 positive status and elevated C-reactive protein. A growing body of evidence supports the strict correlation between SpA and subclinical gut inflammation, which has been reported in approximately 60% of patients with SpA [6]. In these patients, the progression to IBD has been observed in up to 10% [7]. The metabolic fingerprinting in such diseases could explore even the link between dysbiosis, bacterial metabolites and disease development, representing an intriguing new field of research
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