Lupus最新文献

Aim: To investigate the radial peripapillary capillary plexus vessel density (RPCP-VD) and peripapillary retinal nerve fiber layer thickness (pRNFLT) of systemic lupus erythematosus (SLE) and neuropsychiatric SLE patients (NPSLE) using disc optical coherence tomography angiography (OCTA) and investigate the association between these parameters and SLE disease activity index (SLEDAI-2K).

Methods: A total of 64 'right eyes (36 SLE patients, 28 healthy controls (HCs)) were included in this cross-sectional case-control study. Ten (27.7%) patients had neuropsychiatric involvement. RPCP-VD and pRNFLT of patients were evaluated in all peripapillary sectors. RPCP-VD and pRNFLT of NPSLE, non-NPSLE, and HCs were compared. The correlation between SLEDAI-2K and OCTA findings was evaluated.

Results: SLE patients' RPCP-VDs were significantly lower compared with the HCs except for two sectors (p < .005). There was not a significant difference in pRNFLT of SLE patients and HCs. There was not a correlation between SLEDAI-2K and RPCP-VD in any subsectors but there was a significantly negative correlation between pRNFLT in tempo-inferior and inferior-temporal sectors. When compared with non-NPSLE-patients, NPSLE patients had significantly lower inferior-hemi (p = .001), inferior-nasal VDs (p = .003), and peripapillary (p = .012), superior-hemi (p = .038), inferior-hemi (p = .026), inferior-nasal (p = .002) and inferior-temporal (p = .012) pRNFLTs. A negative correlation was found between NPSLE and pRNFLT.

Conclusion: SLE patients may have early subclinical vascular involvement leading to decreased RPCP-VD. A negative correlation between the SLEDAI-2K and pRNFLT in the temporal subsectors of all SLE patients may show an association between the disease activity and temporal pRNFL thinning. The presence of neuropsychiatric involvement may also be associated with decreased RPCP-VD and pRNFLT.

Systemic lupus erythematosus (SLE) is a complex multi-organ autoimmune disease marked by the production of autoantibodies against nuclear structures, formation of immune complexes, and chronic inflammation triggered by their tissular deposition. SLE is characterized by alternating periods of relapse and remission and each flare has the potential to cause new organ damage related to either the disease process or the medication toxicity. Despite remarkable progress across its multiple domains, SLE is still an area with many unmet needs, calling for innovative and practical solutions. The efforts of the drug development programme in lupus have led to considerable growth in the last decade, owing to the approval of belimumab, anifrolumab, and voclosporin. The increasing understanding of the pathogenesis of the disease has enabled the exploration of novel therapeutic strategies. New discoveries in the intricate cytokine kaleidoscope of lupus have made the concept of targeted therapy an attractive and promising research focus. JAK inhibitors are oral targeted therapies approved for a wide variety of diseases across the Rheumatology, Gastroenterology, Dermatology, and Haematology fields. Multiple JAKis are currently being investigated in SLE. This paper aims to summarize existing data coming from both clinical trials and case reports regarding the use of JAK inhibitors in SLE.

Background: Lupus nephritis (LN) is the most serious complication of systemic lupus erythematosus (SLE), and plasma exosomes may serve as a bridge. MicroRNAs (miRNAs) are abundant in exosomes, so this study aimed to explore the role of exosome-derived miRNA in the development of LN.

Methods: The publicly available data containing plasma exosomal miRNAs in SLE patients and healthy controls were researched, and differential expression and functional enrichment analysis of exosomal miRNA was conducted. Then, plasma exosomes from SLE patients were extracted, and the accuracy of differential expression and functional enrichment analysis was preliminarily verified. PKH26 dye was used to label exosomes to detect whether exosomes can enter HK2 cells. Evaluation of plasma exosomes impact on cell viability was done by utilizing CCK-8 assay. Flow cytometry was used to measure cell apoptosis.

Results: Plasma exosomes were successfully extracted and identified. Through differential expression analysis of the pulbilic data and subsequent qPCR validation, we observed that miR-20b-5p is overexpressed in plasma exosomes of SLE patients, whereas miR-181a-2-3p is downregulated. Then functional enrichment analysis revealed that these differential miRNAs primarily regulate processes such as apoptosis, autophagy, and inflammation. Then, flow cytometry analysis conducted after co-incubation of plasma exosomes and peripheral blood mononuclear cells confirmed that exosomes can indeed regulate apoptosis. And plasma exosomes can successfully enter HK2 cells without affecting cell activity. In addition, plasma exosomes promote HK2 cell apoptosis and autophagy. Overexpression of miR-181a-2-3p could inhibit HK2 cells apoptosis and upregulate the expression of bcl2, and beclin1. At the same time, a trend towards increased apoptosis rates was observed in HK2 overexpressed miR-20b-5p, although the difference did not reach statistical significance. And miR-20b-5p can enhance the expression of caspase3 and becin1 while suppressing the expression of bcl2 and LC3β.

Conclusion: Our research indicates that the abundant presence of miR-20b-5p and the depletion of miR-181a-2-3p in plasma exosomes of SLE patients may mediate the promotion of apoptosis and autophagy in HK2 cells, thereby causing kidney damage and the development of LN.

Background: Laboratory-based biomarkers accurately presenting systemic lupus erythematosus (SLE) disease activity may have a practical value in clinical routine. As shown in many other conditions, complete blood count (CBC)-derived biomarkers may also play a role in SLE.

Objectives: We aimed to study for the first time the pan-immune-inflammation value (PIV, monocytes x platelets x neutrophils/lymphocytes) and the more established systemic immune-inflammation index (SII, neutrophils x platelets /lymphocytes) in SLE patients and correlate it with serological and clinical findings including disease outcomes.

Methods: In this retrospective multicentric investigation, we reviewed the clinical records of 148 SLE who had an available CBC at baseline. The latter served for the determination of the neutrophil-to-lymphocyte ratio (NLR), SII, and the PIV. Control groups were studied as well. Univariable as well as multivariable statistics were employed.

Results: The values for baseline systemic immune-inflammation biomarkers (SIIB) studied were significantly (p < 0.0001) higher than those observed in healthy controls but comparable to those obtained from patients with other inflammatory conditions. Multivariable analysis revealed that ANA titer > 1:640 remained the only significant (p < 0.0001) baseline predictor of SLE flare (odds ratio: 7.6, 95% CI 3.1 to 18.8). Improvement of SLE following treatment was associated with the absence of lymphopenia as well as ANA > 1:640 (p = 0.041). The SLEDAI-2K significantly correlated with NLR, SII, CRP, lymphocytes, and monocytes only on univariable testing.

Conclusions: Compared to healthy controls the CBC-based SIIB investigated are significantly increased in SLE patients. However, SIIB do not appear to be useful in managing SLE clinically. Nevertheless, we confirm that higher ANA titers can predict flares of SLE.

Introduction: Systemic Lupus Erythematosus (SLE) can be diagnosed using the 2012 criteria of the Systemic Lupus International Collaborating Clinics (SLICC) and, more recently, the 2019 criteria of the European League Against Rheumatism/American College of Rheumatology (EULAR/ACR). Hematological involvement is scored differently by these classifications. Our objective was to compare both criteria in a cohort of children with autoimmune cytopenia (AIC)-associated SLE.

Method: We included 79 patients with childhood-onset AIC as the first manifestations of SLE.

Results: The median age at SLE diagnosis was 14.5 years (1.1-21.4 years). The SLICC criteria were fulfilled by 76/79 (96%) patients and the EULAR/ACR criteria by 72/79 (91%) patients during follow-up. The SLICC and EULAR/ACR criteria were discordant (not concomitantly fulfilled) in 25/79 (32%) patients. Non-hematological clinical manifestations were more frequently observed in SLE diagnosis when the criteria were concordant (30/54, 56%) than when they were not (5/25, 20%) (p = 0.004). In 16/25 (64%) discordant patients, the SLICC criteria allowed earlier diagnosis of SLE. Finally, the attribution of a maximum weight of 6 to the hematological involvement of the EULAR/ACR criteria increased the sensitivity thereof from 63/79 (80%) to 76/79 (96%) in our population.

Conclusion: The SLICC 2012 and EULAR/ACR 2019 criteria do not effectively diagnose SLE in children when AIC is the predominant feature. The SLICC criteria appear to be more effective in this population of SLE patients. An increase in the maximum weight of hematological involvement to 6 increases the sensitivity of the EULAR/ACR criteria for SLE diagnosis in children.

Background: Systemic lupus erythematosus (SLE) is a complex autoimmune disorder characterized by a malfunction of the body's immune defense system.

Objective: The objective of the present investigation was to examine the expression and diagnostic significance of NRIR in SLE and to prove whether it is involved in the progression of SLE.

Methods: The study involved 110 participants, including 55 healthy individuals and 55 SLE patients. The expression levels of NRIR, miR-31-5p, and ICAM-1 were measured using qRT-PCR. The ROC curve was performed to assess the diagnostic significance of NRIR in SLE patients. Pearson correlation analysis was utilized to explore the relationship between NRIR and other indicators. Cytokines including IL-4, IL-6, and IL-21, along with IgG levels, were assessed using ELISA. The interaction between NRIR and miR-31-5p was validated using a dual-luciferase reporter assay.

Result: Upregulated expression of NRIR was observed in individuals with SLE, serving a diagnostic function for SLE. Additionally, abnormal expression of NRIR impacted the viability of CD4⁺ T cells within SLE patients. NRIR could negatively modulate the expression of miR-31-5p.

Conclusion: LncRNA NRIR may be a potential biomarker for SLE and is likely involved in the progression of SLE.

Objective: Systemic Lupus Erythematosus (SLE) is a complex autoimmune disease predominantly affecting women. Despite advances in treatment, recent developments in single-cell RNA sequencing (scRNA-seq) and Mendelian randomization (MR) continue to facilitate the need for precision medicine.

Methods: Data obtained from the GSE135779 dataset underwent quality control, normalization, and dimensionality reduction using Seurat and MonacoImmuneData. Marker genes identified subgroups for analysis with CellChat and ClusterProfilerR. MR analysis of these genes' eQTLs was performed to establish causal relationships with SLE using IEU Open GWAS project data.

Results: Single-cell analysis revealed distinct cellular subtypes and highlighted increased monocyte levels in patients with SLE. MR analysis revealed 12 genes, particularly interferon induced protein with tetratricopeptide repeats 3 (IFIT3), causally related to SLE. Gene ontology and the Kyoto encyclopedia of genes and genomes analyses identified pathways significant to SLE pathogenesis. Visualization of these genes at the single-cell level revealed their role in disease progression. Cell communication differences between IFIT3-positive and -negative groups were also observed.

Conclusion: This study demonstrates the potential of scRNA-seq and MR in identifying critical factors in SLE pathogenesis, thereby supporting the need for targeted therapies. Identifying IFIT3, among other genes, as central to SLE progression opens new avenues for precision medicine approaches in SLE management.

Introduction: Systemic Lupus Erythematosus (SLE) is a chronic multi-systemic autoimmune disease that mainly affects young females. SLE's chronicity and high level of complications yield frequent clinic visitations & hospital admissions, increasing the necessity to investigate the healthcare system and improve patient satisfaction and quality of life.

Objective: This study aimed to understand SLE patients' points of view on the healthcare system in Jordan, especially given the chronic nature of the disease. With a clearer understanding, improvements can be made to benefit both the patients and the healthcare system.

Methods: A cross-sectional study of 79 patients following up at the University of Jordan Hospital, rheumatology clinics were interviewed over the phone.

Result: The majority of patients were satisfied overall with the treatment services and medications as rated on a Likert scale of 1-5 (4.28 ± 1.01 and 4.19 ± 0.96, respectively) despite a quarter of patients complaining of adverse effects from the medications. The use of oral corticosteroids was significantly associated with a lower General Satisfaction Rate (p = 0.050), while high income (1000 Jordanian Dinars and above) and fatigue contributed to a lower Medication Satisfaction Rate (p = 0.016 and 0.000, respectively). A good physician-patient relationship was the most commonly cited reason for general satisfaction (73.4%) and was positively associated with the general (p = 0.000) and medication satisfaction (p = 0.004) rates.

Conclusion: SLE patients perceived high satisfaction rates despite adverse effects and symptoms. These higher satisfaction rates were seen predominantly due to good physician-patient relationships.

Objectives: This multicenter longitudinal study investigated the prevalence of gastrointestinal (GI) manifestations in lupus patients and determined the risk factors associated with mortality.

Methods: This study is part of the Oman Lupus Study, which included 1160 patients who met the classification criteria for systemic lupus erythematosus (SLE) from January 2006 to February 2020. All patients were screened for GI symptoms and involvement.

Results: We identified 91 patients with GI manifestations, with a prevalence rate of 8.53% in the pediatric group and 7.75% in the adult group, and this difference was not statistically significant (p = .755). Ischemic colitis was significantly associated with longer disease duration (p < .001) and positivity for B2-glycoprotein I (B2GPI) autoantibodies (p < .0001). Moreover, a significant correlation was found between ischemic colitis and hematologic manifestations (p = .001), lupus nephritis (p = .007), pulmonary complications (p = .000-.039), and some cardiac complications (p = .012-.269). Mortality rates were greater in patients with GI involvement (24.37%), including those with ischemic colitis (p = .005), chronic peritonitis (p < .001), and spleen/liver infarction (p = .001). Sepsis, thrombocytopenia, and different internal organ involvement rates were significantly associated with increased mortality.

Conclusion: This research provides significant insights into GI manifestations in lupus patients. A higher mortality rate was found to be associated with organ involvement, disease duration, autoantibody profile, and specific complications. Considering this fact, it is vital to prioritize management strategies to improve clinical outcomes in this group of patients.

Background: Systemic lupus erythematosus (SLE) increases the risk of interstitial lung disease (ILD). SLE is also linked to an elevated risk of type 2 diabetes mellitus (T2DM). However, the impact of T2DM on ILD risk in patients with SLE is still unclear. This study aimed to compare the prevalence of ILD in patients with SLE based on the presence of T2DM (SLE + T2DM+) or its absence (SLE + T2DM-).

Methods: This was a retrospective cohort study using the 2019-2020 National Inpatient Sample database. Adult SLE patients were identified and stratified by T2DM status. Comparable cohorts were created using propensity score matching, resulting in 10,532 patients in each cohort. Multivariate logistic regression assessed the association between T2DM and ILD.

Results: T2DM was associated with a lower prevalence of ILD in patients with SLE (OR 0.798, 95% CI: 0.695-0.918, p = .002), occurring in 371 (3.5%) patients with T2DM compared to 463 (4.4%) patients without T2DM. Specifically, this difference was mainly driven by pulmonary fibrosis, which was significantly less frequent in the T2DM group (1.3% vs 1.8%, OR 0.7, 95% CI: 0.560-0.875, p = .002). No differences were found in secondary outcomes, including death rates, length of hospital stay, ARDS, pneumothorax, pleural effusion, or pulmonary arterial hypertension.

Conclusion: Our study suggests that T2DM significantly reduced ILD risk in patients with SLE, specifically diminishing pulmonary fibrosis prevalence. Further research should explore mechanisms for this protective association between T2DM and ILD development in SLE. These findings may guide management strategies for this vulnerable population.