Health research has high value to society. It can provide important information about disease trends and risk factors, outcomes of treatment, functional abilities, patterns of care, and health care costs and use. The different approaches to research provide complementary insights. Clinical trials can provide important information about the efficacy and adverse effects of medical interventions by controlling the variables that could impact the results of the study, but feedback from real-world clinical experience is also crucial for comparing and improving the use of drugs, vaccines, medical devices, and diagnostics.
Below you will find links to some of the studies that have contributed to our increased understanding of spondyloarthritis.
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Ankylosing spondylitis (AS), psoriasis and inflammatory bowel disease (IBD) often coexist in the same patient and in their families. In AS, genes within the MHC region, in particular HLA‑B27, account for nearly 25% of disease hereditability, with additional small contributions from genes outside of the MHC locus, including those involved in intracellular antigen processing (that is, ERAP1, which interacts with HLA‑B27) and cytokine genes such as those involved in the IL‑17–IL‑23 pathway. Similar to AS, the strongest genetic signal of susceptibility to psoriasis and psoriatic arthritis also emanates from the MHC region (attributable mostly to HLA‑C*06:02 although other genes have been implicated), and gene–gene interaction of HLA‑C with ERAP1. The remaining hereditary load is from genes involved in cytokine production, specifically genes in the IL‑17–IL‑23 pathway, the NFκB pathway and the type 2 T‑helper pathway. In IBD, similar genetic influences are operative. Indeed, genes important in the regulation of the IL‑17–IL‑23 pathway and, in Crohn’s disease, genes important for autophagy (that is, NOD2 and ATG16L1 and IRGM) have a role in conferring susceptibility of individuals to these diseases. Thus, AS, psoriasis and IBD seem to share similar pathogenic mechanisms of aberrant intracellular antigen processing or elimination of intracellular bacteria and cytokine production, especially in the IL‑17–IL‑23 pathway.
The following is an announcement from SAA about a third party study. SAA is not affiliated with this study.
Juvenile spondyloarthritis (SpA) is a distinct disease to adult SpA, and usually manifests as peripheral arthritis and enthesitis. Importantly, many patients with juvenile SpA continue to be at risk of developing ankylosing spondylitis during their disease course. In this Review, the classification and diagnostic criteria, clinical manifestations and treatment guidelines for juvenile SpA will be discussed. Advances in the diagnosis of and management strategies for juvenile SpA will lead to earlier recognition, appropriate treatmen
A new rate of prevalence of axial spondyloarthritis (SpA) has been published in the journal, "Arthritis Care & Research". The data...
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