Objective: Patients with systemic lupus erythematosus (SLE) have an increased risk of cardiovascular and cerebrovascular events (CCEs). Furthermore, CCE was a significant factor contributing to mortality in patients with SLE. However, no clinical model exists that can predict which patients are at high risk. The purpose of this study was to develop a practical model for predicting the risk of CCE in people with SLE.
Methods: This study was based on the Chinese SLE Treatment and Research Group cohort. A total of 2399 patients, who had a follow-up period of over 3 years and were diagnosed with SLE for less than 1 year at the start of the study, were included. Cox proportional hazards regression and least absolute shrinkage and selection operator regression were used to establish the model. Internal validation was performed, and the predictive power of the model was evaluated.
Results: During the follow-up period, 93 patients had CCEs. The prediction model included nine variables: male gender, smoking, hypertension, age of SLE onset >40, cutaneous involvement, arthritis, anti-β2GP1 antibody positivity, high-dose glucocorticoids and hydroxychloroquine usage. The model's C index was 0.801. Patients with a prognostic index over 0.544 were classified into the high-risk group.
Conclusion: We have developed a predictive model that uses clinical indicators to assess the probability of CCE in patients diagnosed with SLE. This model has the ability to precisely predict the risk of CCE in patients with SLE. We recommended using this model in the routine assessment of patients with SLE.
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http://dx.doi.org/10.1136/rmdopen-2024-004425 | DOI Listing |
JAMA Netw Open
December 2024
Department of Cell Biology, The Province and Ministry Cosponsored Collaborative Innovation Center for Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Key Laboratory of Medical Epigenetics, Tianjin Institute of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Importance: Patients with juvenile idiopathic arthritis (JIA) may develop adult rheumatic diseases later in life, and prolonged or recurrent disease activity is often associated with substantial disability; therefore, it is important to identify patients with JIA at high risk of developing adult rheumatic diseases and provide specialized attention and preventive care to them.
Objective: To elucidate the full extent of the genetic association of JIA with adult rheumatic diseases, to improve treatment strategies and patient outcomes for patients at high risk of developing long-term rheumatic diseases.
Design, Setting, And Participants: In this genetic association study of 4 disease genome-wide association study (GWAS) cohorts from 2013 to 2024 (JIA, rheumatoid arthritis [RA], systemic lupus erythematosus [SLE], and systemic sclerosis [SSc]), patients in the JIA cohort were recruited from the US, Australia, and Norway (with a UK cohort included in the meta-analyzed cohort), while patients in the other 3 cohorts were recruited from US and Western European countries.
Med Sci (Basel)
December 2024
Department of Nephrology, Hospital Cayetano Heredia, Lima 15002, Peru.
Background: Lupus podocytopathy (LP) is a non-immune complex-mediated glomerular lesion in systemic lupus erythematosus (SLE), characterized by the diffuse effacement of podocyte processes without immune complex deposition or with only mesangial immune complex deposition. LP is a rare cause of nephrotic syndrome in SLE patients with implications for prognosis and treatment.
Case Report: We present the case of a 28-year-old woman with a medical history of type 1 diabetes mellitus (T1DM) who presented with lower limb edema, dyspnea, hypercholesterolemia, with nephrotic range proteinuria, without acute kidney injury, and laboratory findings compatible with auto-immune hemolytic anemia.
Curr Issues Mol Biol
December 2024
Department of Medical and Molecular Biology, Faculty of Medical Sciences in Zabrze, Medical University of Silesia, 19 Jordana, 41-800 Zabrze, Poland.
Misshapen/NIKs-related kinase (MINK) 1 belongs to the mammalian germinal center kinase (GCK) family. It contains the N-terminal, conserved kinase domain, a coiled-coil region, a proline-rich region, and a GCK, C-terminal domain with the Citron-NIK-Homology (CNH) domain. The kinase is an essential component of cellular signaling pathways, which include Wnt signaling, JNK signaling, pathways engaging Ras proteins, the Hippo pathway, and STRIPAK complexes.
View Article and Find Full Text PDFDiseases
December 2024
Department of Internal Medicine, Hospital Civil de Guadalajara Fray Antonio Alcalde, Guadalajara 44280, JAL, Mexico.
Background And Objectives: The correlation between diminished 25-hydroxyvitamin D (25-(OH)D) concentrations and heightened disease activity in systemic lupus erythematosus (SLE) patients remains contentious, as clinical studies have yielded conflicting outcomes-some propose a potential link, while others assert no relationship exists. Nonetheless, all studies report a significant prevalence of low 25-(OH)D levels among SLE patients. This study aimed to assess the frequency of low serum levels of 25-(OH)D in Mexican patients with SLE and to evaluate the correlation between 25-(OH)D deficiency or insufficiency and disease activity levels.
View Article and Find Full Text PDFImmunol Med
December 2024
Department of Internal Medicine and Rheumatology, Juntendo University Urayasu Hospital, Urayasu, Japan.
Systemic lupus erythematosus (SLE) is a typical autoimmune disease; although severe disease and refractoriness to existing therapies are still experienced, the number of cases resistant to remission induction has decreased with the establishment of various therapies. However, improving long-term prognosis remains a challenge due to the unavoidable prolonged use of non-selective glucocorticoids. To investigate the additional effect of belimumab in the chronic phase, we included 28 of 46 patients with SLE who were initiated on belimumab between January 2018 and October 2022 for glucocorticoid reduction.
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