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Objectives: Data on the economic consequences of systemic lupus erythematosus (SLE) and lupus nephritis (LN) are scarce in Europe. We aimed to estimate the total direct costs attributable to SLE and LN in France, at the nationwide level.
Methods: Patients with SLE and LN were identified in the French nationwide health insurance database (SNDS). Prevalent SLE patients for the year 2019 were age- and sex-matched (1:1) with non-SLE controls. Direct costs (in 2019 euros) were assigned from a societal and a third-party payer perspective, using official sources.
Results: A total of 29,135 SLE patients, including 4357 (14.5%) with lupus nephritis, were matched to non-SLE controls. The median overall direct cost for SLE was €4795 versus €1910 for controls from a third-party payer perspective (P<0.0001). From a societal perspective the overall direct cost of SLE patients was higher (€5894) compared to non-SLE matched controls (€2601, P<0.0001), for hospitalizations (+€1305 versus non-SLE controls), medications (+€872), consultations (+€343) and transportation (+€193). The overall median cost for LN was €9800 versus €3918 for SLE patients without LN, from third-party payer perspective, and €11,279 versus €4950 from a societal perspective (P<0.0001, for both). At a national level, the extra cost of SLE compared to non-SLE controls was M€104.9 with hospitalizations contributing to 39.6% of this extra cost.
Conclusions: The direct extra costs of SLE and LN are substantial in France, particularly for hospitalizations, outpatient medications, consultations, and transportations. By identifying and addressing major drivers of SLE costs, healthcare providers and policymakers can work towards more cost-effective strategies for managing SLE.
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http://dx.doi.org/10.1016/j.jbspin.2024.105827 | DOI Listing |
Curr Opin Immunol
September 2025
Univ. Grenoble Alpes, CNRS, CEA, UMR5075, IBS, Laboratoire d'Immunologie, CHU Grenoble Alpes, Grenoble, France.
The complement system plays a paradoxical role in systemic lupus erythematosus physiopathology, acting both as a protective mechanism and as a driver of tissue injury, depending on disease stage. Neutrophil extracellular traps (NETs) further exacerbate disease activity by promoting complement activation and autoantigen exposure, forming an amplifying inflammatory loop. Lupus nephritis remains challenging to monitor using conventional complement biomarkers such as CH50, C3, and C4; the utility of anti-C1q, anti-ficolin, and anti-C1s antibodies, along with tissue-based markers such as renal C4d and C5b-9 deposits, as markers of disease activity and prognosis, is discussed.
View Article and Find Full Text PDFSemin Arthritis Rheum
August 2025
Grupo IRIDIS (Investigation in Rheumatology and Immune-Diseases), Instituto de Investigación Sanitaria Galicia Sur, (IISGS), Hospital Universitario Vigo, Vigo, Spain.
Introduction: Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disorder characterized by multi-organ involvement and variable clinical manifestations. Recurrent clinical patterns suggest distinct phenotypes, where cluster analysis of autoantibodies could identify prognostic subtypes.
Objectives: To define and describe serological clusters and their clinical-epidemiological characteristics, as well as their association with comorbidities, disease activity measures, severity, and damage.
Lupus
September 2025
Department of Pharmacy, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
ObjectiveTo systematically compare the clinical effectiveness and safety of Belimumab, Rituximab and Voclosporin in the treatment of lupus nephritis based on network meta-analysis method.MethodsSystematic search of registered clinical trials in four major databases (Pubmed, Embase, Web of Science, The Cochrane Register of Clinical Trials) and ClinicalTrials.gov.
View Article and Find Full Text PDFSci Adv
September 2025
Department of Medicine, Altman Clinical and Translational Research Institute, University of California, San Diego, La Jolla, CA 92093, USA.
Protein tyrosine phosphatase nonreceptor type 22 (PTPN22) is encoded by a gene strongly associated with lupus and other autoimmune diseases. PTPN22 regulates T cell receptor (TCR) signaling through dephosphorylation of the kinases lymphocyte-specific protein tyrosine kinase (LCK) and zeta-chain-associated protein kinase 70 (ZAP70). The regulation of PTPN22 remains poorly understood.
View Article and Find Full Text PDFInt Immunol
September 2025
Division of Innate Immunity, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Toll-like receptor 7 (TLR7) is an endosomal sensor that responds to both pathogen-derived and self-derived single-stranded RNA (ssRNA). Responses of TLR7 to self-derived ssRNA have been implicated in the development of autoimmune diseases, such as systemic lupus erythematosus (SLE). TLR7 antagonists and inhibitory anti-TLR7 monoclonal antibodies (mAbs) can protect lupus-prone NZBWF1 mice from lethal nephritis.
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