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Best Practice & Research in Clinical Rheumatology最新文献

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The inequity of global healthcare in pediatric rheumatology 儿科风湿病学全球医疗保健的不平等。
IF 4.5 2区 医学
Best Practice & Research in Clinical Rheumatology Pub Date : 2024-09-01 DOI: 10.1016/j.berh.2024.101983
Soamarat Vilaiyuk , Djohra Hadef , Wafa Hamdi , Chris Scott , Waheba Slamang , Helen E. Foster , Laura B. Lewandowski
{"title":"The inequity of global healthcare in pediatric rheumatology","authors":"Soamarat Vilaiyuk ,&nbsp;Djohra Hadef ,&nbsp;Wafa Hamdi ,&nbsp;Chris Scott ,&nbsp;Waheba Slamang ,&nbsp;Helen E. Foster ,&nbsp;Laura B. Lewandowski","doi":"10.1016/j.berh.2024.101983","DOIUrl":"10.1016/j.berh.2024.101983","url":null,"abstract":"<div><div>In pediatric rheumatology, global health inequity relates to the uneven distribution of healthcare resources, accessibility, and health outcomes among children with rheumatic conditions across various countries, regions, and socioeconomic groups. This inequity can manifest in various ways. This review article provides an overview of common rheumatic diseases, such as juvenile idiopathic arthritis and systemic lupus erythematosus, which significantly contribute to and are affected by disparities in global healthcare.</div><div>Subsequently, we delve into the inequalities in accessing patient care, encompassing issues related to diagnosis and treatment. Additionally, we address challenges in educational advancement and identify research gaps within the field of pediatric rheumatology. We also reveal successful global collaborations, such as a Global Task Force for Pediatric Musculoskeletal Health and special working groups among international organizations, aimed at bridging the disparities gap. Through these efforts, we try to enhance understanding, cooperation, and resource allocation to ensure equal access to quality care worldwide for children with rheumatic conditions. Futhermore, we present a case study from Thailand, highlighting their successful initiatives in developing pediatric rheumatology within their healthcare system.</div></div>","PeriodicalId":50983,"journal":{"name":"Best Practice & Research in Clinical Rheumatology","volume":"38 3","pages":"Article 101983"},"PeriodicalIF":4.5,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141789825","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}
引用次数: 0
How to treat monogenic SLE? 如何治疗单基因系统性红斑狼疮？
IF 4.5 2区 医学
Best Practice & Research in Clinical Rheumatology Pub Date : 2024-09-01 DOI: 10.1016/j.berh.2024.101962
{"title":"How to treat monogenic SLE?","authors":"","doi":"10.1016/j.berh.2024.101962","DOIUrl":"10.1016/j.berh.2024.101962","url":null,"abstract":"<div><div>Systemic lupus erythematosus is a rare and life-threatening autoimmune disease characterized by autoantibodies against double-stranded DNA, with an immunopathology that remains partially unclear. New insights into the disease have been provided by the discovery of key mutations leading to the development of monogenic SLE, occurring in the context of early-onset disease, syndromic lupus, or familial clustering. The increased frequency of discovering these mutations in recent years, thanks to the advent of genetic screening, has greatly enhanced our understanding of the immunopathogenesis of SLE. These monogenic defects include defective clearance of apoptotic bodies, abnormalities in nucleic acid sensing, activation of the type-I interferon pathway, and the breakdown of tolerance through B or T cell activation or lymphocyte proliferation due to anomalies in TLR signalling and/or NFκB pathway overactivation. The translation of genetic discoveries into therapeutic strategies is presented here, within the framework of personalized therapy.</div></div>","PeriodicalId":50983,"journal":{"name":"Best Practice & Research in Clinical Rheumatology","volume":"38 3","pages":"Article 101962"},"PeriodicalIF":4.5,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141321892","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}
引用次数: 0
38.3 Primary Immunodeficiencies: When is it not just “JIA” 38.3 原发性免疫缺陷：何时不仅仅是 "JIA"。
IF 4.5 2区 医学
Best Practice & Research in Clinical Rheumatology Pub Date : 2024-09-01 DOI: 10.1016/j.berh.2024.101960
{"title":"38.3 Primary Immunodeficiencies: When is it not just “JIA”","authors":"","doi":"10.1016/j.berh.2024.101960","DOIUrl":"10.1016/j.berh.2024.101960","url":null,"abstract":"<div><div><span>Juvenile Idiopathic Arthritis<span> (JIA) is sometimes considered a diagnosis of exclusion as the name signifies that no cause is evident for this form of arthritis. Despite this JIA has some classical clinical features and many categories are defined based on the phenotype</span></span><strong>.</strong><span> Since there is no diagnostic test for JIA, diseases that can mimic JIA, including Primary Immunodeficiencies (PID) can sometimes be misdiagnosed as JIA. The clues to suspecting PIDs are early age of onset, presence of family history, increased susceptibility to infections, unusual features like urticaria<span>, interstitial lung disease, sensorineural hearing loss and poor response to conventional therapy, amongst others. This review will highlight the basics of PIDs and will discuss PIDs that can present with arthritis and hence can be confused with JIA.</span></span></div></div>","PeriodicalId":50983,"journal":{"name":"Best Practice & Research in Clinical Rheumatology","volume":"38 3","pages":"Article 101960"},"PeriodicalIF":4.5,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141293916","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}
引用次数: 0
Challenges and complications in juvenile localized scleroderma: A practical approach 幼年局部硬皮病的挑战与并发症：实用方法。
IF 4.5 2区 医学
Best Practice & Research in Clinical Rheumatology Pub Date : 2024-09-01 DOI: 10.1016/j.berh.2024.101987
Clare E. Pain , Kathryn S. Torok
{"title":"Challenges and complications in juvenile localized scleroderma: A practical approach","authors":"Clare E. Pain ,&nbsp;Kathryn S. Torok","doi":"10.1016/j.berh.2024.101987","DOIUrl":"10.1016/j.berh.2024.101987","url":null,"abstract":"<div><div>Juvenile localized scleroderma is characterised by inflammation which drives fibrosis in skin and soft tissues. The more severe subtypes of localized scleroderma such as linear and craniofacial are more common in children. Additionally, extracutaneous involvement is seen in half of all children and is associated with poorer treatment outcomes and health-related quality of life. Evidence for the management of craniofacial and extracutaneous involvement is lacking and therefore poses a challenge to clinicians. This review aims to provide a practical approach to management of these most challenging features of juvenile localized scleroderma through case studies where we present the available evidence, current recommendations and considerations for management.</div></div>","PeriodicalId":50983,"journal":{"name":"Best Practice & Research in Clinical Rheumatology","volume":"38 3","pages":"Article 101987"},"PeriodicalIF":4.5,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142300235","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}
引用次数: 0
Preface: Pediatric rheumatology 前言：小儿风湿病学。
IF 4.5 2区 医学
Best Practice & Research in Clinical Rheumatology Pub Date : 2024-09-01 DOI: 10.1016/j.berh.2024.102004
Christiaan Scott, Petra Hissink Muller
{"title":"Preface: Pediatric rheumatology","authors":"Christiaan Scott,&nbsp;Petra Hissink Muller","doi":"10.1016/j.berh.2024.102004","DOIUrl":"10.1016/j.berh.2024.102004","url":null,"abstract":"","PeriodicalId":50983,"journal":{"name":"Best Practice & Research in Clinical Rheumatology","volume":"38 3","pages":"Article 102004"},"PeriodicalIF":4.5,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142300237","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}
引用次数: 0
Non-coding DNA variants for risk in lupus 红斑狼疮风险的非编码 DNA 变异。
IF 4.5 2区 医学
Best Practice & Research in Clinical Rheumatology Pub Date : 2024-05-01 DOI: 10.1016/j.berh.2024.101937
{"title":"Non-coding DNA variants for risk in lupus","authors":"","doi":"10.1016/j.berh.2024.101937","DOIUrl":"10.1016/j.berh.2024.101937","url":null,"abstract":"<div><p>Systemic Lupus Erythematosus (SLE) is a multifactorial autoimmune disease that arises from a dynamic interplay between genetics and environmental triggers. The advent of sophisticated genomics technology has catalyzed a shift in our understanding of disease etiology, spotlighting the pivotal role of non-coding DNA variants in SLE pathogenesis. In this review, we present a comprehensive examination of the non-coding variants associated with SLE, shedding light on their role in influencing disease risk and progression. We discuss the latest methodological advancements that have been instrumental in the identification and functional characterization of these genomic elements, with a special focus on the transformative power of CRISPR-based gene-editing technologies. Additionally, the review probes into the therapeutic opportunities that arise from modulating non-coding regions associated with SLE. Through an exploration of the complex network of non-coding DNA, this review aspires to decode the genetic puzzle of SLE and set the stage for groundbreaking gene-based therapeutic interventions and the advancement of precision medicine strategies tailored to SLE management.</p></div>","PeriodicalId":50983,"journal":{"name":"Best Practice & Research in Clinical Rheumatology","volume":"38 2","pages":"Article 101937"},"PeriodicalIF":4.5,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140013651","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}
引用次数: 0
Immune checkpoints in autoimmune vasculitis 自身免疫性血管炎中的免疫检查点
IF 4.5 2区 医学
Best Practice & Research in Clinical Rheumatology Pub Date : 2024-05-01 DOI: 10.1016/j.berh.2024.101943
{"title":"Immune checkpoints in autoimmune vasculitis","authors":"","doi":"10.1016/j.berh.2024.101943","DOIUrl":"10.1016/j.berh.2024.101943","url":null,"abstract":"<div><p><span>Giant cell arteritis<span><span><span> (GCA) is a prototypic autoimmune disease with a highly selective tissue tropism for medium and large arteries. Extravascular GCA manifests with intense systemic inflammation and </span>polymyalgia rheumatica; vascular GCA results in vessel wall damage and stenosis, causing </span>tissue ischemia<span>. Typical granulomatous infiltrates in affected arteries are composed of CD4</span></span></span><sup>+</sup><span> T cells and hyperactivated macrophages, signifying the involvement of the innate and adaptive immune system. Lesional CD4</span><sup>+</sup> T cells undergo antigen-dependent clonal expansion, but antigen-nonspecific pathways ultimately control the intensity and duration of pathogenic immunity. Patient-derived CD4<sup>+</sup><span> T cells receive strong co-stimulatory signals through the NOTCH1 receptor and the CD28/CD80-CD86 pathway. In parallel, co-inhibitory signals, designed to dampen overshooting T cell immunity, are defective, leaving CD4</span><sup>+</sup><span> T cells unopposed and capable of supporting long-lasting and inappropriate immune responses. Based on recent data, two inhibitory checkpoints are defective in GCA: the Programmed death-1 (PD-1)/Programmed cell death ligand 1 (PD-L1) checkpoint and the CD96/CD155 checkpoint, giving rise to the “lost inhibition concept”. Subcellular and molecular analysis has demonstrated trapping of the checkpoint ligands in the endoplasmic reticulum, creating PD-L1</span><sup>low</sup><span> CD155</span><sup>low</sup> antigen-presenting cells. Uninhibited CD4<sup>+</sup><span> T cells expand, release copious amounts of the cytokine Interleukin (IL)-9, and differentiate into long-lived effector memory cells. These data place GCA and cancer on opposite ends of the co-inhibition spectrum, with cancer patients developing immune paralysis due to excessive inhibitory checkpoints and GCA patients developing autoimmunity due to nonfunctional inhibitory checkpoints.</span></p></div>","PeriodicalId":50983,"journal":{"name":"Best Practice & Research in Clinical Rheumatology","volume":"38 2","pages":"Article 101943"},"PeriodicalIF":4.5,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140871112","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}
引用次数: 0
Dendritic cells and antigen-specific immunotherapy in autoimmune rheumatic diseases 树突状细胞和自身免疫性风湿病中的抗原特异性免疫疗法。
IF 4.5 2区 医学
Best Practice & Research in Clinical Rheumatology Pub Date : 2024-05-01 DOI: 10.1016/j.berh.2024.101940
{"title":"Dendritic cells and antigen-specific immunotherapy in autoimmune rheumatic diseases","authors":"","doi":"10.1016/j.berh.2024.101940","DOIUrl":"10.1016/j.berh.2024.101940","url":null,"abstract":"<div><p>Dendritic cells (DCs) are professional antigen-presenting cells and trigger downstream immune responses to antigen while integrating cellular pathogen and damage-associated molecular pattern (PAMP and DAMP) or immunomodulatory signals. In healthy individuals, resting and tolerogenic DCs draining skin and intestine facilitate expansion of regulatory T cells (Treg) to maintain peripheral antigen-specific immune tolerance. In patients with rheumatic diseases, however, DCs activated by PAMPs and DAMPs expand self-reactive effector T cells, including follicular helper T cells that promote the expansion of activated autoreactive B cells, chronic inflammation and end-organ damage. With the development of cellular and nanoparticle (NP)-based self-antigen-specific immunotherapies we here consider the new opportunities and the challenges for restoring immunoregulation in the treatment and prevention of autoimmune inflammatory rheumatic conditions through DCs.</p></div>","PeriodicalId":50983,"journal":{"name":"Best Practice & Research in Clinical Rheumatology","volume":"38 2","pages":"Article 101940"},"PeriodicalIF":4.5,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1521694224000111/pdfft?md5=bf169639c49fdd2ca495145dff4e0c7d&pid=1-s2.0-S1521694224000111-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140133185","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}
引用次数: 0
Potential therapeutic targets of fibrosis in inflammatory rheumatic diseases 炎症性风湿病纤维化的潜在治疗目标。
IF 4.5 2区 医学
Best Practice & Research in Clinical Rheumatology Pub Date : 2024-05-01 DOI: 10.1016/j.berh.2024.101945
{"title":"Potential therapeutic targets of fibrosis in inflammatory rheumatic diseases","authors":"","doi":"10.1016/j.berh.2024.101945","DOIUrl":"10.1016/j.berh.2024.101945","url":null,"abstract":"<div><p><span>Fibrosis<span> is commonly associated with chronic rheumatic diseases, and causes substantial morbidity and mortality. Treatment of fibrosis is extremely challenging but is badly needed, as approved antifibrotic therapies fibrosis do not halt its progression, which will be discussed with a focus on </span></span>pulmonary fibrosis<span>. Findings from recent studies indicate several therapeutic targets for treating fibrosis. Interleukin-11 is emerging as a fibrogenic<span> cytokine whose activity can be blocked with neutralizing monoclonal antibodies. Fibroblast activation protein (FAP) is highly expressed by activated fibroblasts in inflammatory and fibrotic tissues. Targeting FAP with different modalities has been extensively explored as adjunct treatment for cancer, which can also apply to treating fibrosis in rheumatic diseases.</span></span></p></div>","PeriodicalId":50983,"journal":{"name":"Best Practice & Research in Clinical Rheumatology","volume":"38 2","pages":"Article 101945"},"PeriodicalIF":4.5,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140867478","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}
引用次数: 0
Granzyme K+ CD8 T cells in autoimmunity 自身免疫中的颗粒酶 K+ CD8 T 细胞
IF 4.5 2区 医学
Best Practice & Research in Clinical Rheumatology Pub Date : 2024-05-01 DOI: 10.1016/j.berh.2024.101930
{"title":"Granzyme K+ CD8 T cells in autoimmunity","authors":"","doi":"10.1016/j.berh.2024.101930","DOIUrl":"10.1016/j.berh.2024.101930","url":null,"abstract":"<div><p>CD8 T cells expressing granzyme K are enriched in synovial tissue from patients with rheumatoid arthritis and in tissues affected by several other autoimmune diseases. The roles these cells play in autoimmune disease is under active investigation, and several recent studies have begun to shed light on this question. Putting this cell type into functional perspective is especially important given their enrichment at the sites of disease. This review summarizes available evidence for the presence of CD8 T cells and other granzyme K-expressing cells in tissues in autoimmune diseases and discusses the effects these cells may have on the pathogenesis of autoimmune conditions.</p></div>","PeriodicalId":50983,"journal":{"name":"Best Practice & Research in Clinical Rheumatology","volume":"38 2","pages":"Article 101930"},"PeriodicalIF":4.5,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139658949","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}
引用次数: 0
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