Seminars in arthritis and rheumatism最新文献

{"title":"Using patient reported outcomes measurement information system (PROMIS®) measures in rheumatoid arthritis clinical care, research, and trials","authors":"Clifton O. Bingham , Susan J. Bartlett","doi":"10.1016/j.semarthrit.2024.152576","DOIUrl":"10.1016/j.semarthrit.2024.152576","url":null,"abstract":"","PeriodicalId":21715,"journal":{"name":"Seminars in arthritis and rheumatism","volume":"70 ","pages":"Article 152576"},"PeriodicalIF":4.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142644773","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unraveling the role of neutrophil extracellular traps in rheumatoid arthritis: From triggers to therapeutic targets","authors":"Carmelo Carmona-Rivera, Shuichiro Nakabo, Mariana J. Kaplan","doi":"10.1016/j.semarthrit.2024.152585","DOIUrl":"10.1016/j.semarthrit.2024.152585","url":null,"abstract":"","PeriodicalId":21715,"journal":{"name":"Seminars in arthritis and rheumatism","volume":"70 ","pages":"Article 152585"},"PeriodicalIF":4.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142648636","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Defining immune cell phenotypes that distinguish treatment responders and non-responders in RA","authors":"Kathryne E. Marks ,&nbsp;Alice Horisberger ,&nbsp;Daniel H. Solomon ,&nbsp;Deepak A. Rao","doi":"10.1016/j.semarthrit.2024.152581","DOIUrl":"10.1016/j.semarthrit.2024.152581","url":null,"abstract":"<div><div></div></div>","PeriodicalId":21715,"journal":{"name":"Seminars in arthritis and rheumatism","volume":"70 ","pages":"Article 152581"},"PeriodicalIF":4.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142676472","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comments on the article by Goldman et al.","authors":"Emre Bilgin ,&nbsp;Sedat Kiraz","doi":"10.1016/j.semarthrit.2024.152595","DOIUrl":"10.1016/j.semarthrit.2024.152595","url":null,"abstract":"","PeriodicalId":21715,"journal":{"name":"Seminars in arthritis and rheumatism","volume":"70 ","pages":"Article 152595"},"PeriodicalIF":4.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142732481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comments on the article by Bilgin et al.","authors":"Adam Goldman ,&nbsp;Ilan Ben-Zvi","doi":"10.1016/j.semarthrit.2024.152600","DOIUrl":"10.1016/j.semarthrit.2024.152600","url":null,"abstract":"","PeriodicalId":21715,"journal":{"name":"Seminars in arthritis and rheumatism","volume":"70 ","pages":"Article 152600"},"PeriodicalIF":4.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142819234","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of the gastrointestinal microbiome on rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis and reactive arthritis: A systematic review","authors":"Beverly Cheok Kuan Ng ,&nbsp;Marissa Lassere","doi":"10.1016/j.semarthrit.2024.152574","DOIUrl":"10.1016/j.semarthrit.2024.152574","url":null,"abstract":"<div><h3>Background</h3><div>There is an increasing body of literature observing a state of dysbiosis in the gut microbiome in different autoimmune conditions including inflammatory arthritis. It is unknown whether the microbiome can be a biomarker for prognostication purposes or for stratification of treatment strategies. This review aims to evaluate the existing evidence on the association between the microbiome and inflammatory arthritis, including rheumatoid arthritis (RA), psoriatic arthritis (PsA) and ankylosing spondylitis (AS) and reactive arthritis (ReA) population groups.</div></div><div><h3>Methods</h3><div>This systematic review was performed based on methods from the Cochrane guidelines and reported based on PRISMA criteria. Studies exploring the microbiome of patients with RA, AS, PsA or ReA compared with controls via 16s rRNA or shotgun sequencing were evaluated. The outcomes of interest include alpha and beta diversity, abundance or depletion of organisms and functional analysis. Literature up to August 2024 was retrieved searching the databases PubMed, Medline, ScienceDirect, Scopus, Web of Science, Cochrane, EMBASE and CINAHL. All references were systematically evaluated by two reviewers. Quality of the studies were evaluated by the Newcastle-Ottawa Scale.</div></div><div><h3>Findings</h3><div>The review yielded 25,794 search results, of which 53 studies were included for the RA group, 34 studies for the AS group, 6 studies for the PsA group and 2 studies for the ReA group. Reduced diversity has been observed in disease groups and in patients with higher disease activity.</div></div><div><h3>Interpretation</h3><div>There are limited longitudinal studies on the role of the microbiome in inflammatory arthritis, in particular PsA. Existing cross-sectional studies suggest altered microbiome in disease states compared with controls. Further studies are required to understand the utility of the microbiome as a biomarker to better understand prognosis and tailor treatments.</div></div>","PeriodicalId":21715,"journal":{"name":"Seminars in arthritis and rheumatism","volume":"70 ","pages":"Article 152574"},"PeriodicalIF":4.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142792429","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The overlooked epidemic: Fibromyalgia in the shadows of long COVID","authors":"Mariangela Salvato,&nbsp;Andrea Doria,&nbsp;Alessandro Giollo","doi":"10.1016/j.semarthrit.2024.152596","DOIUrl":"10.1016/j.semarthrit.2024.152596","url":null,"abstract":"","PeriodicalId":21715,"journal":{"name":"Seminars in arthritis and rheumatism","volume":"70 ","pages":"Article 152596"},"PeriodicalIF":4.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142695908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic checkpoints in rheumatoid arthritis","authors":"Cornelia M. Weyand ,&nbsp;Jörg J. Goronzy","doi":"10.1016/j.semarthrit.2024.152586","DOIUrl":"10.1016/j.semarthrit.2024.152586","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Rheumatoid Arthritis is a systemic autoimmune disease affecting 0.5–1 % of the population. Despite a growing therapeutic armamentarium, RA remains incurable, and many patients suffer significant morbidity over time. The strongest genetic risk derives from HLA class II polymorphisms, implicating T cells as pathogenic drivers. Innate immune cells, e.g. monocytes and macrophages (Mⱷ) contribute to chronic tissue inflammation through an array of pro-inflammatory functions but also present antigen to autoreactive T cells. Differentiation, survival, and effector functions of both T cells and Mⱷ are ultimately controlled by their bioenergetic and biosynthetic programs, identifying cellular metabolism as a critical disease mechanism in RA.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Objectives&lt;/h3&gt;&lt;div&gt;Summarize current knowledge about metabolic conditions in the RA joint and disease-relevant metabolic circuits shaping the effector repertoire of RA T cells and Mⱷ.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;The rheumatoid joint is a glucose deplete tissue environment, selecting for invading immune cells that can survive on non-glucose fuel sources. Inflamed synovium instead offers the amino acid glutamine and RA CD4&lt;sup&gt;+&lt;/sup&gt; T cells and RA Mⱷ rely on glutamine and glutamate to support their pathogenic functions. The metabolic hallmark of RA T cells is their low mitochondrial performance, resulting in low ATP production, low generation of reactive oxygen species (ROS) and low availability of tricarboxylic acid (TCA) cycle intermediates, all shifting RA T cells towards autoreactivity. The underlying defect stems from insufficient repair of mitochondrial DNA (mtDNA). Functional consequences include reversal of the TCA cycle, accumulation of citrate and lack of malate production. Excessive citrate promotes cytoskeletal hyperacetylation, creating hypermigratory and tissue-invasive T cells. Surplus acetyl-CoA supports lipid droplet formation and lipotoxicity. Lack of malate production disrupts the malate-aspartate shuttle, restricts recovery of cytosolic NAD and drives the endoplasmic reticulum (ER) into expansion. The bioenergetically stressed ER accumulates &lt;em&gt;TNF&lt;/em&gt; mRNA and turns RA T cells into TNF superproducers. ATP low production renders RA T cells susceptible to cell death, depositing highly inflammatory mtDNA in the tissue. Mitochondrial deficiency leads to a slowdown in glycolysis and pyruvate processing, such that RA CD4&lt;sup&gt;+&lt;/sup&gt; T cells shunt glucose towards the pentose phosphate pathway to support nucleotide synthesis and clonal proliferation. Metabolically deprived CD4&lt;sup&gt;+&lt;/sup&gt; T cells partner with Mⱷ that have highly functional mitochondria. A hallmark of RA Mⱷ is the high expression of the DNA binding protein RFX5, which co-ordinates adaptations to metabolic needs with function. RFX5 upregulates HLA-DR expression and induces the glutaminolytic enzyme glutamate dehydrogenase 1 (GLUD1), providing bioenergetic resources for antigen pres","PeriodicalId":21715,"journal":{"name":"Seminars in arthritis and rheumatism","volume":"70 ","pages":"Article 152586"},"PeriodicalIF":4.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142644771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Promises and pitfalls of artificial intelligence models in forecasting rheumatoid arthritis treatment response and outcomes","authors":"Augusto Garcia-Agundez,&nbsp;Gabriela Schmajuk,&nbsp;Jinoos Yazdany","doi":"10.1016/j.semarthrit.2024.152584","DOIUrl":"10.1016/j.semarthrit.2024.152584","url":null,"abstract":"<div><div>None.</div></div>","PeriodicalId":21715,"journal":{"name":"Seminars in arthritis and rheumatism","volume":"70 ","pages":"Article 152584"},"PeriodicalIF":4.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142644772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between Kawasaki disease and subsequent autoimmune disease: National cohort study of adolescents with 12-year follow-up from birth","authors":"Ji Hee Kwak ,&nbsp;Ju Hee Kim ,&nbsp;Eun Kyo Ha ,&nbsp;Gi Chun Lee ,&nbsp;Jeewon Shin ,&nbsp;Man Yong Han","doi":"10.1016/j.semarthrit.2025.152633","DOIUrl":"10.1016/j.semarthrit.2025.152633","url":null,"abstract":"<div><h3>Background</h3><div>There is little known about the association of Kawasaki disease with autoimmune diseases. This 12-year follow-up study determined the risk for an autoimmune disease in children who had Kawasaki disease.</div></div><div><h3>Methods</h3><div>All individuals born in South Korea between 2002 and 2005 were identified using the National Health Insurance Service's (NHIS) database. Incidence density sampling was used to identify 16,398 patients in the exposed cohort (diagnosis of Kawasaki disease between 2002 and 2005) and 163,980 matched (1:10) children in the unexposed cohort. Participants were followed from the date of diagnosis of Kawasaki disease (index date) until the first diagnosis of an autoimmune disease, death, or end of the study (December 31, 2017). Diagnoses of autoimmune diseases were according to ICD-10 codes.</div></div><div><h3>Findings</h3><div>The median age at the index date was 2.2 years (interquartile range: 1.1–3.7). During follow-up, 1139 children had newly diagnosed autoimmune diseases in the exposed cohort (incidence rate: 59.3 per 10,000 person-years) and 9752 children had newly diagnosed autoimmune disease in the unexposed cohort (incidence rate: 50.4 per 10,000 person-years), corresponding to an absolute difference of 8.9/10,000 person years (95 % CI: 5.3–12.5). Kawasaki disease was also associated with multiple individual autoimmune diseases: juvenile idiopathic arthritis (HR=1.27), Henoch-Schönlein purpura (HR=1.21), polymyositis/dermatomyositis (HR=2.12), vitiligo (HR=1.17), idiopathic thrombocytopenic purpura (HR=2.30), and acute rheumatic fever and chorea (HR=3.35).</div></div><div><h3>Interpretation</h3><div>Korean children with Kawasaki disease had an increased risk of autoimmune disease during a 12-year follow-up period. These findings suggest a biological relationship between Kawasaki disease and subsequent autoimmune disease.</div></div>","PeriodicalId":21715,"journal":{"name":"Seminars in arthritis and rheumatism","volume":"71 ","pages":"Article 152633"},"PeriodicalIF":4.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143372596","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}