Systemic lupus erythematosus (SLE) patients are susceptible to marantic endocarditis (ME) due to a hypercoagulable state. The literature regarding the epidemiology and outcomes of ME in SLE patients is limited. All patients ≥18 years who had SLE with and without ME between 2007 and 2019 were identified from the National Inpatient Sample in the United States (US). Predictors of inpatient mortality for SLE patients with ME were analyzed. Between 2007 and 2019, there were 508,818 hospitalizations for SLE, of which 785 (0.2%) had ME. Of SLE patients with ME, 33 (4.2%) died while hospitalized over the study period. On multivariate analysis, female sex (adjusted odds ratio (aOR), 95% confidence intervals: 24.72 (3.21, 190.27)), age <34 years (aOR: 6.81 (1.80, 25.79)), anemia (aOR: 3.41 (1.12, 10.40)), antiphospholipid syndrome (aOR: 13.50 (3.83, 47.64)), stroke complicating ME (aOR: 9.64 (3.24, 28.71)), and acute kidney injury (aOR: 3.74 (1.06, 13.20)) were all associated with increased inpatient mortality among SLE patients with ME ( < .05 for all). Between 2007 to 2019, ME occurred in 0.2% of SLE hospitalizations, with a 4.2% average inpatient mortality over the study period. Female sex, antiphospholipid syndrome, and stroke were most strongly associated with increased inpatient mortality.
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http://dx.doi.org/10.1177/00033197241288666 | DOI Listing |
Nat Genet
January 2025
Department of Statistical Genetics, Osaka University Graduate School of Medicine, Suita, Japan.
Aberrant immune responses to viral pathogens contribute to pathogenesis, but our understanding of pathological immune responses caused by viruses within the human virome, especially at a population scale, remains limited. We analyzed whole-genome sequencing datasets of 6,321 Japanese individuals, including patients with autoimmune diseases (psoriasis vulgaris, rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), pulmonary alveolar proteinosis (PAP) or multiple sclerosis) and coronavirus disease 2019 (COVID-19), or healthy controls. We systematically quantified two constituents of the blood DNA virome, endogenous HHV-6 (eHHV-6) and anellovirus.
View Article and Find Full Text PDFArch Immunol Ther Exp (Warsz)
January 2025
Department of Human Physiology, Medical University of Lublin, Lublin, Poland.
Systemic lupus erythematosus (SLE) is an autoimmune disease whose pathogenesis is not fully understood to date. One of the suggested mechanisms for its development is NETosis, which involves the release of a specific network consisting of chromatin, proteins, and enzymes from neutrophils, stimulating the immune system. One of its markers is citrullinated histone H3 (H3Cit).
View Article and Find Full Text PDFClin Rheumatol
January 2025
Rheumatology Department, Faculty of Medicine, Cairo University, Cairo, Egypt.
Objective: The objective of this study is to present the clinical characteristics of immunoglobulin G4-related diseases (IgG4-RD) patients and describe associated overlap with autoimmune rheumatic diseases (ARDs).
Patients And Methods: This cross-sectional study included 81 patients with IgG4-RD who were recruited from 13 specialized rheumatology departments and centers across the country in collaboration with the Egyptian College of Rheumatology (ECR). Patients underwent a thorough history-taking and clinical examination.
Lupus
January 2025
Mansoura Nephrology and Dialysis Unit, Mansoura University, Mansoura, Egypt.
Background: Endoplasmic reticulum stress with protein misfolding has been introduced as a key pathogenetic mechanism in lupus nephritis (LN). Pregnancy is thought to exaggerate proteostasis, which leads to the accumulation of potentially pathogenic misfolded proteins in the urine, serum, and placenta particularly in women with preeclampsia. The detection of misfolded proteins is made using Congo red stain, which is referred to as congophilia.
View Article and Find Full Text PDFFront Immunol
January 2025
Innovation & Research Department, OriCell Therapeutics Co. Ltd., Shanghai, China.
Systemic lupus erythematosus (SLE) and lupus nephritis (LN) are debilitating autoimmune disorders characterized by pathological autoantibodies production and immune dysfunction, causing chronic inflammation and multi-organ damage. Despite current treatments with antimalarial drugs, glucocorticoids, immunosuppressants, and monoclonal antibodies, a definitive cure remains elusive, highlighting an urgent need for novel therapeutic strategies. Recent studies indicate that chimeric antigen receptor T-cell (CAR-T) therapy has shown promising results in treating B-cell malignancies and may offer a significant breakthrough for non-malignant conditions like SLE.
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