Autoimmunity reviews最新文献

{"title":"Characteristics and risk factors for infection in patients with ANCA-associated vasculitis: A systematic review and meta-analysis","authors":"Wenxuan Luo ,&nbsp;Can Liu ,&nbsp;Lei Zhang ,&nbsp;Jie Tang ,&nbsp;Jie Chen ,&nbsp;Yanzao Zhao ,&nbsp;Xuemei Huang ,&nbsp;Xiaoli Zheng ,&nbsp;Long Chen ,&nbsp;Chuanmei Xie ,&nbsp;Xin Wei ,&nbsp;Xiongyan Luo ,&nbsp;Anji Xiong","doi":"10.1016/j.autrev.2024.103713","DOIUrl":"10.1016/j.autrev.2024.103713","url":null,"abstract":"<div><h3>Objective</h3><div>To summarize the characteristics and risk factors for infection in patients with anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV).</div></div><div><h3>Methods</h3><div>PubMed, Embase, and Cochrane Library databases were searched for relevant articles from database inception to November 2023. The prevalence, odds ratio (OR), and mean difference (MD) with 95 % confidence intervals (CIs) were pooled using a random-effects model. Sensitivity and subgroup analysis were also performed.</div></div><div><h3>Results</h3><div>Forty-one studies with 5343 patients with AAV were included, of whom 2890 patients experienced an infection. The pooled prevalence was 54.6 % (95 % CI, 48.4 % to 61.1 %) for all infections and 35.8 % (95 % CI, 31.0 % to 40.8 %) for severe infections; and prevalence of <em>Pneumocystis jirovecii</em> pneumonia, aspergillosis, candidiasis, cryptococcosis, herpes zoster, cytomegalovirus, and specific bacterial infections were pooled. The respiratory system was the most common infection site, followed by blood, urinary tract, skin and soft tissue, and digestive infections. Risk factors for infection included older age, end-stage renal disease, dialysis, diabetes, smoking, kidney and lung involvement, leukopenia; higher Birmingham Vasculitis Activity Score, and serum creatinine and C-reactive protein levels; and lower hemoglobin levels, and platelet and CD4 counts. In addition, use of cyclophosphamide, steroid pulse therapy, plasma exchange, and higher initial glucocorticoid dose were associated with significantly increased risk of infection.</div></div><div><h3>Conclusion</h3><div>In patients with AAV, therapy should take risk factors for infection into account. Risk factors should be modified wherever possible. Physicians should be familiar with the common infection sites and pathogens, and consider empiric therapy covering common pathogens for life-threatening infections.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 2","pages":"Article 103713"},"PeriodicalIF":9.2,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142765914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differences in clinical phenotype, laboratory, and imaging manifestations between AQP4 IgG positive and AQP4 MOG IgG double negative NMOSD: How to correctly diagnose the two","authors":"Fengna Chu ,&nbsp;Mingchao Shi ,&nbsp;Jie Zhu","doi":"10.1016/j.autrev.2025.103761","DOIUrl":"10.1016/j.autrev.2025.103761","url":null,"abstract":"<div><div>Neuromyelitis optica spectrum disorders (NMOSD) is an uncommon autoimmune inflammatory demyelinating disorder of the central nervous system (CNS) and causes severe disability and even death. Aquaporin-4 immunoglobulin G (AQP4-IgG) antibody has been confirmed as the key pathogenic factor for development of NMOSD and leading to repeatting acute attacks. However, 20–40 % of NMOSD patients lack both AQP4-IgG and anti-myelin oligodendrocytes glycoproteins (MOG) IgG, in which the pathogenic factor is still unclear. There are differences in clinical, laboretory and imaiging minifestations between AQP4-IgG positive (AQP4-IgG⁺) and AQP4-IgG/MOG-IgG double negative (AQP4-IgG⁻) NMOSD. Although the treatments applied in NMOSD have made great progress, all treatments are failed in AQP4-IgG⁻ patients. Additionally, it is hard to identify NMOSD with AQP4-IgG⁻ from multiple sclerosis (MS). Therefore, it is suspected and challenged that AQP4-IgG could not be the only pathogenic factor in NMOSD or NMOSD with AQP4-IgG⁻ may be a separate disorder independent of NMOSD AQP4-IgG⁺? It is necessary to find more pathogenic factors and to explore the new pathogenesis and treatments of NMOSD with AQP4-IgG⁻ in the future, which has been a serious problem to be addressed by the neurology community.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 4","pages":"Article 103761"},"PeriodicalIF":9.2,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143073564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Current landscape of monogenic autoinflammatory actinopathies: A literature review","authors":"P. Mertz ,&nbsp;V. Hentgen ,&nbsp;G. Boursier ,&nbsp;J. Delon ,&nbsp;S. Georgin-Lavialle","doi":"10.1016/j.autrev.2024.103715","DOIUrl":"10.1016/j.autrev.2024.103715","url":null,"abstract":"<div><div>Autoinflammatory diseases (AID) are conditions leading to a hyperactivation of innate immunity without any underlying infection, and may be poly- (e.g. Still's disease) or monogenic. The number of monogenic AID is continuously expanding, with the discovery of novel pathologies and pathophysiological mechanisms, facilitated in part by easier access to pangenomic sequencing. Actinopathies with autoinflammatory manifestations represent a newly emerging subgroup of AID, associated with defects in the regulation of actin cytoskeleton dynamics. These diseases typically manifest in the neonatal period and variably combine a primary immunodeficiency of varying severity, cytopenia (particularly thrombocytopenia), autoinflammatory manifestations primarily affecting the skin and digestive system, as well as atopic and autoimmune features.</div><div>Diagnosis should be considered primarily when encountering an early-onset autoinflammatory skin and digestive disorder, along with a primary immunodeficiency and either thrombocytopenia or a bleeding tendency. Some of these diseases exhibit specific features, such as a risk of macrophage activation syndrome (MAS) or a predisposition to atopy or lymphoproliferation. The complete pathophysiology of these diseases is not yet fully understood, and further studies are required to elucidate the underlying mechanisms, which could guide therapeutic choices. In most cases, the severity of the conditions necessitates allogeneic marrow transplantation as a treatment option.</div><div>In this review, we discuss these novel diseases, providing a practical approach based on the main associated biological abnormalities and specific clinical characteristics, with a special focus on the newly described actinopathies <em>DOCK11</em> and <em>ARPC5</em> deficiency. Nonetheless, genetic testing remains essential for definitive diagnosis, and various differential diagnoses must be considered.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 2","pages":"Article 103715"},"PeriodicalIF":9.2,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting interleukin-6 pathways in giant cell arteritis management: A narrative review of evidence","authors":"Maxime Samson ,&nbsp;Bhaskar Dasgupta ,&nbsp;Anthony M. Sammel ,&nbsp;Carlo Salvarani ,&nbsp;Christian Pagnoux ,&nbsp;Rula Hajj-Ali ,&nbsp;Wolfgang A. Schmidt ,&nbsp;Maria C. Cid","doi":"10.1016/j.autrev.2024.103716","DOIUrl":"10.1016/j.autrev.2024.103716","url":null,"abstract":"<div><div>Giant cell arteritis (GCA) is a chronic inflammatory vasculitis with a significant impact on vascular and patient health. It may present with non-specific symptoms and can lead to severe complications if not managed effectively. This narrative review explores the treatment of GCA with interleukin-6 (IL-6) pathway inhibitors, focusing on key studies from selected databases published between 2018 and 2024. The findings reveal that the current treatment primarily involves glucocorticoids (GCs), but their long-term use is associated with adverse effects. Targeting the IL-6 pathway offers therapeutic benefits by reducing inflammation and sparing GC use. Tocilizumab, a humanized immunoglobulin G1κ monoclonal antibody that blocks the IL-6 receptor, has demonstrated efficacy in achieving sustained remission and improving quality of life in people with GCA. However, challenges remain in understanding the optimal duration of therapy, managing relapse upon discontinuation, and addressing long-term structural vascular outcomes. Additional research is needed to further elucidate the complex pathogenesis of GCA and to optimize treatment strategies to achieve sustained remission both clinically and histologically while minimizing adverse effects. This review provides a comprehensive overview of the evidence of IL-6 inhibition in GCA management, highlighting both its therapeutic benefits and the challenges associated with its use.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 2","pages":"Article 103716"},"PeriodicalIF":9.2,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-vitamin D antibodies","authors":"Jozélio Freire de Carvalho ,&nbsp;Thelma L. Skare ,&nbsp;Ana Tereza Amoedo Martinez ,&nbsp;Yehuda Shoenfeld","doi":"10.1016/j.autrev.2024.103718","DOIUrl":"10.1016/j.autrev.2024.103718","url":null,"abstract":"<div><h3>Background</h3><div>Low vitamin D levels are commonly observed in autoimmune diseases, suggesting a potential role in disease pathogenesis. The presence of anti-vitamin D antibodies may contribute to these deficiencies and influence autoimmune processes.</div></div><div><h3>Objective</h3><div>To review and analyze studies investigating the occurrence of anti-vitamin D antibodies in autoimmune diseases.</div></div><div><h3>Results</h3><div>Three studies, comprising a total of 345 patients, were reviewed. The autoimmune conditions included systemic lupus erythematosus (SLE), scleroderma (SSc), primary antiphospholipid antibody syndrome (pAPS), and pemphigus vulgaris (PV). Patient mean ages ranged from 26.8 to 31 years, with the proportion of female participants ranging from 87 % to 96 %. The duration of disease varied between 6.3 and 12.3 years. Serum vitamin D levels ranged from 11.71 ± 7.21 to 28.4 ± 9.6 ng/mL, with 57.1 % to 82.1 % of patients presenting vitamin D deficiency. The prevalence of anti-vitamin D antibodies was reported as follows: 87 % in SSc, 11 % in PV, 4 % to 6.1 % in SLE, and 3.5 % in pAPS. Associations with other disease markers were also noted: in SLE, anti-vitamin D antibodies were associated with anti-dsDNA antibodies; while in SSc, their presence was linked to the disease itself.</div></div><div><h3>Conclusion</h3><div>Anti-vitamin D antibodies were identified in 3.5 % to 87 % of patients with SLE, SSc, pAPS, and PV. These antibodies are associated either with the autoimmune condition itself or with other autoantibodies, suggesting their potential role in disease mechanisms and progression.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 2","pages":"Article 103718"},"PeriodicalIF":9.2,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142799346","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic and genomic associations in antiphospholipid syndrome: A systematic review","authors":"Joseph Zouein ,&nbsp;Nabih Naim ,&nbsp;Diane M. Spencer ,&nbsp;Thomas L. Ortel","doi":"10.1016/j.autrev.2024.103712","DOIUrl":"10.1016/j.autrev.2024.103712","url":null,"abstract":"<div><h3>Background</h3><div>Numerous genes have been associated with APS in the literature. In recent years, microRNA (miRNA) and long non-coding RNA (lncRNA) have also been shown to modulate the expression of APS-related genes.</div></div><div><h3>Objective</h3><div>We performed a systematic review to identify all studies reporting on genetic mechanisms that have been shown to be associated with APS.</div></div><div><h3>Methods</h3><div>An extensive literature search was performed in the PubMed, Cochrane and Web of Science databases gathering all available articles through February 2024. We only selected case-control studies that met inclusion criteria and that focused on genetic contributors and modifiers related to primary APS.</div></div><div><h3>Results</h3><div>Sixty studies were selected for data extraction. Selected studies were grouped into 8 broad categories for review and analysis: (1) gene expression studies; (2) thrombophilia genotypes; (3) single nucleotide polymorphisms (SNPs); (4) interferon-inducible genes; (5) microRNA studies; (6) long non-coding RNA (lncRNA) studies; (7) DNA methylation studies; and (8) differential gene expression studies. Several genes have been identified as associated with APS by more than one approach, including <em>TF</em>, complement associated genes, and interferon-inducible genes. It has been demonstrated that miRNA and lncRNA may alter the expression of important genes in patients with APS.</div></div><div><h3>Conclusion</h3><div>This systematic review has helped highlight important genes implicated in APS. Most importantly, pathways such as thrombosis/hemostasis, complement and interferon appear to be involved. Further studies are needed to help uncover important genes that could serve as biomarkers.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 2","pages":"Article 103712"},"PeriodicalIF":9.2,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142765916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Caspase family in autoimmune diseases","authors":"Wangzheqi Zhang ,&nbsp;Huang Wu ,&nbsp;Yan Liao ,&nbsp;Chenglong Zhu ,&nbsp;Zui Zou","doi":"10.1016/j.autrev.2024.103714","DOIUrl":"10.1016/j.autrev.2024.103714","url":null,"abstract":"<div><div>Programmed cell death (PCD) plays a crucial role in maintaining tissue homeostasis, with its primary forms including apoptosis, pyroptosis, and necroptosis. The caspase family is central to these processes, and its complex functions across different cell death pathways and other non-cell death roles have been closely linked to the pathogenesis of autoimmune diseases. This article provides a comprehensive review of the role of the caspase family in autoimmune diseases such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), type 1 diabetes (T1D), and multiple sclerosis (MS). It particularly emphasizes the intricate functions of caspases within various cell death pathways and their potential as therapeutic targets, thereby offering innovative insights and a thorough discussion in this field. In terms of therapy, strategies targeting caspases hold significant promise. We emphasize the importance of a holistic understanding of caspases in the overall concept of cell death, exploring their unique functions and interrelationships across multiple cell death pathways, including apoptosis, pyroptosis, necroptosis, and PANoptosis. This approach transcends the limitations of previous studies that focused on singular cell death pathways. Additionally, caspases play a key role in non-cell death functions, such as immune cell activation, cytokine processing, inflammation regulation, and tissue repair, thereby opening new avenues for the treatment of autoimmune diseases. Regulating caspase activity holds the potential to restore immune balance in autoimmune diseases. Potential therapeutic approaches include small molecule inhibitors (both reversible and irreversible), biological agents (such as monoclonal antibodies), and gene therapies. However, achieving specific modulation of caspases to avoid interference with normal physiological functions remains a major challenge. Future research must delve deeper into the regulatory mechanisms of caspases and their associated complexes linked to PANoptosis to facilitate precision medicine. In summary, this article offers a comprehensive and in-depth analysis, providing a novel perspective on the complex roles of caspases in autoimmune diseases, with the potential to catalyze breakthroughs in understanding disease mechanisms and developing therapeutic strategies.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 2","pages":"Article 103714"},"PeriodicalIF":9.2,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142784088","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A20 haploinsufficiency diagnosis beyond systemic lupus erythematosus: A systematic review of the literature","authors":"Rémi Philip ,&nbsp;Inès Elhani ,&nbsp;Sophie Gallou ,&nbsp;Hubert De Boysson ,&nbsp;Nicolas Martin Silva ,&nbsp;Sophie Georgin-Lavialle ,&nbsp;Samuel Deshayes ,&nbsp;Achille Aouba","doi":"10.1016/j.autrev.2024.103722","DOIUrl":"10.1016/j.autrev.2024.103722","url":null,"abstract":"<div><div>Systemic lupus erythematosus (SLE) is an autoimmune disease whose pathophysiology remains incompletely understood, involving genetic and epigenetic factors. However, an increasing small subset of patients present with monogenic lupus, providing insight into the pathogenesis of the disease. This systematic review focuses on SLE associated with A20 haploinsufficiency (HA20), a monogenic disorder associated with tumor necrosis factor alpha-induced protein 3 gene (<em>TNFAIP3)</em> variants. Besides the mainly auto-inflammatory phenotypic expression of HA20 mimicking Behçet's disease spectrum, some of its clinical and biological manifestations are part of the spectrum of autoimmune diseases, including glomerulonephritis as well as the frequent presence of antinuclear antibodies, sometimes with anti-DNA specificity. Among all the 191 HA20 patients reported in the literature, we identified 16 patients (8.4 %) with a compatible diagnosis of SLE. When estimable, the SLICC 2012 and EULAR/ACR 2019 classification criteria were positive for 92.9 % of them. A majority had multi-system involvement, mainly cutaneous (81.3 %), musculoskeletal (56.3 %), and/or renal (56.3 %) manifestations. They also seemed to exhibit differences compared to other SLE patients: higher prevalence of fever, chronic cutaneous lupus erythematosus, oral and genital ulcers, neuropsychiatric manifestations, autoimmune cytopenia, and elevated biologic inflammatory markers. This review highlights the necessity of considering <em>TNFAIP3</em> variants in SLE patients with early-onset disease, familial history, and/or specific clinical manifestations suggestive of autoinflammatory diseases. Recognizing HA20-SLE patients may improve our understanding of SLE pathogenesis and lead to better therapeutic strategies for these patients.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 2","pages":"Article 103722"},"PeriodicalIF":9.2,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142821856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IgG4 in the gut: Gastrointestinal IgG4-related disease or a new subtype of inflammatory bowel disease","authors":"Sarah Bencardino ,&nbsp;Cosimo Simone Matichecchia ,&nbsp;Jacopo Fanizza ,&nbsp;Laurent Peyrin-Biroulet ,&nbsp;Emanuel Della-Torre ,&nbsp;Silvio Danese ,&nbsp;Ferdinando D’Amico","doi":"10.1016/j.autrev.2024.103720","DOIUrl":"10.1016/j.autrev.2024.103720","url":null,"abstract":"<div><div>IgG4-related disease (IgG4-RD) is a chronic inflammatory condition characterized by tissue infiltration with IgG4-positive plasma cells, leading to fibrosis and organ dysfunction. While primarily affecting the pancreas, bile ducts, and salivary glands, IgG4-RD can also involve the gastrointestinal tract, raising questions about its relationship with inflammatory bowel disease (IBD).</div><div>Recent studies suggest that patients with IBD may exhibit histological and serological features consistent with IgG4-RD, such as a dense lymphoplasmacytic infiltration, a storiform-type of fibrosis and a prominent IgG4 immune response. This overlap represents a diagnostic challenge, as differentiating between primary IBD and IgG4-RD involving the gut is crucial for appropriate treatment.</div><div>Further research is essential to delineate the prevalence of tissue and serum IgG4 expression in patients with IBD. This approach could classify subtypes of IBD, enabling advancements in non-invasive diagnosis and monitoring as well as personalized therapies. The purpose of this review is to summarize the available evidence regarding intestinal involvement in IgG4-RD and the role of both serum and tissue IgG4 in inflammatory bowel diseases IBD.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 2","pages":"Article 103720"},"PeriodicalIF":9.2,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142799349","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Risk factors associated with thrombocytopenia in systemic lupus erythematosus: A systematic review and meta-analysis","authors":"Ze Yang ,&nbsp;Yanzuo Wu ,&nbsp;Shuo Huang ,&nbsp;Jie Bao ,&nbsp;Li Xu ,&nbsp;Yongsheng Fan","doi":"10.1016/j.autrev.2024.103721","DOIUrl":"10.1016/j.autrev.2024.103721","url":null,"abstract":"<div><h3>Background</h3><div>Systemic lupus erythematosus (SLE) frequently manifests with thrombocytopenia (TP), a hematologic complication that heightens the risk of severe outcomes and increases mortality. This meta-analysis aims to evaluate the potential risk factors associated with TP in SLE patients, providing insights into the demographic features, clinical features, and laboratory findings that contribute to this condition.</div></div><div><h3>Methods</h3><div>A comprehensive literature search was conducted across eight databases from inception to September 1, 2024. Study quality was assessed using the Newcastle-Ottawa Scale. Meta-analysis was conducted using univariate and multivariate analyses with Revman 5.3, while heterogeneity was addressed through subgroup and sensitivity analyses. Publication bias was assessed using funnel plots and Egger tests via Stata 15.0.</div></div><div><h3>Results</h3><div>Seventeen high-quality studies meeting the inclusion criteria were incorporated into this meta-analysis. Independent risk factors for TP in SLE included age (Demographic Features), serositis, splenomegaly, blood system involvement, and renal involvement (Clinical Features), as well as cardiac involvement, anemia, leukocytopenia, low C3/C4, ACA, and CRP (Laboratory Findings). Arthritis and rash were protective factors. Subgroup analysis addressed heterogeneity caused by unit and sample size differences. Sensitivity analysis comparing the consistency between fixed-effects model (FEM) and random-effects model (REM) confirmed the reliability of the findings, and both funnel plots and Egger tests suggested no publication bias.</div></div><div><h3>Conclusion</h3><div>This meta-analysis identified several potential independent risk factors for TP in SLE. Early screening and timely intervention for patients with these risk factors are essential to reduce the likelihood of TP, prevent severe organ damage, and improve overall prognosis.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 2","pages":"Article 103721"},"PeriodicalIF":9.2,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142816832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}