Mortality In Systemic Lupus Erythematosus Research Articles

Proportionate Cardiovascular Mortality in Chronic Inflammatory Disease in Adults in the United States From 1999 to 2019.

Despite a rising prevalence of chronic inflammatory disease (CID), the recent trends in cardiovascular disease (CVD) mortality of patients with CID is scarce. In this study, we investigated patterns of CVD mortality in systemic lupus erythematosus (SLE), inflammatory bowel disease (IBD), and rheumatoid arthritis (RA) compared with the general population. We used the 1999 to 2019 multiple causes of death files from the national center for health statistics to analyze patterns and trends of proportionate CVD mortality in CID compared with the general population. We analyzed a total of 11,154 CVD deaths in IBD, 58,337 CVD deaths in RA, 6227 CVD deaths in SLE, and 17,826,871 CVD deaths in the general population. Between 1999 and 2019, we found that proportionate CVD mortality decreased significantly in the IBD group (25% to 16%), RA group (34% to 25%), and the general population (41% to 31%), but did not change for the SLE group (15% to 15%). Patients with SLE who died of CVD were approximately 10 years younger compared with CVD decedents with RA, IBD, or general population. The White population had higher proportionate CVD mortality than African American (IBD [19% vs 16%-18%] and SLE [14%-16% vs 12-14%], respectively). This study identifies current trends in CVD mortality in the CID population and elucidates current demographics in CVD mortality in CID. Although proportionate CVD mortality decreased in the general population, and in patients with RA and IBD, there was no change among patients with SLE. Further studies are needed to elucidate these differences.

Antimalarials exert a cardioprotective effect in lupus patients: Insights from the Spanish Society of Rheumatology Lupus Register (RELESSER) analysis of factors associated with heart failure

Background/objectivesFactors associated with chronic heart failure (CHF) in patients with systemic lupus erythematosus (SLE) have received little attention. Recent data on the use of hydroxychloroquine in the treatment of SARS-CoV-2 infection have cast doubt on its cardiac safety. The factors associated with CHF, including therapy with antimalarials, were analyzed in a large multicenter SLE cohort. MethodsCross-sectional study including all patients with SLE (ACR-1997 criteria) included in the Spanish Society of Rheumatology Lupus Register (RELESSER), based on historically gathered data. Patients with CHF prior to diagnosis of SLE were excluded. A multivariable analysis exploring factors associated with CHF was conducted. ResultsThe study population comprised 117 patients with SLE (ACR-97 criteria) and CHF and 3,506 SLE controls. Ninety percent were women. Patients with CHF were older and presented greater SLE severity, organ damage, and mortality than those without CHF. The multivariable model revealed the factors associated with CHF to be ischemic heart disease (7.96 [4.01–15.48], p < 0.0001), cardiac arrhythmia (7.38 [4.00–13.42], p < 0.0001), pulmonary hypertension (3.71 [1.84–7.25], p < 0.0002), valvulopathy (6.33 [3.41–11.62], p < 0.0001), non-cardiovascular damage (1.29 [1.16–1.44], p < 0.000) and calcium/vitamin D treatment (5.29 [2.07–16.86], p = 0.0015). Female sex (0.46 [0.25–0.88], p = 0.0147) and antimalarials (0.28 [0.17–0.45], p < 0.000) proved to be protective factors. ConclusionsPatients with SLE and CHF experience more severe SLE. Treatment with antimalarials appears to confer a cardioprotective effect.

Hydroxychloroquine in systemic lupus erythematosus: overview of current knowledge.

The antimalarial hydroxychloroquine (HCQ) has demonstrated several crucial properties for the treatment of systemic lupus erythematosus (SLE). Herein, we reviewed the main HCQ pharmacologic features, detailed its mechanism of action, and summarized the existing guidelines and recommendations for HCQ use in rheumatology with a systematic literature search for the randomized controlled trials focused on lupus. HCQ has been shown to decrease SLE activity, especially in mild and moderate disease, to prevent disease flare and to lower the long-term glucocorticoid need. The numerous benefits of HCQ are extended to pregnancy and breastfeeding period. Based on cohort studies, antithrombotic and metabolic HCQ’s effects were shown, including lipid-lowering properties, which might contribute to an improved cardiovascular risk. Moreover, early HCQ use in antinuclear antibodies positive individuals might delay the progression to SLE. Finally, HCQ has a significant favorable impact on long-term outcomes such as damage accrual and mortality in SLE. Based on these multiple benefits, HCQ is now the mainstay long-term treatment in SLE, recommended by current guidelines in all patients unless contraindications or side effects. The daily dose associated with the best compromise between efficacy and safety is matter of debate. The concern regarding retinal toxicity rather than proper efficacy data is the one that dictated the daily dosage of ⩽5 mg/kg/day actual body weight currently agreed upon.

Rapamycin relieves lupus nephritis by regulating TIM-3 and CD4+CD25+Foxp3+ Treg cells in an MRL/lpr mouse model

Lupus nephritis (LN) is a severe consequence of systemic lupus erythematosus (SLE) and is an important driver of morbidity and mortality in SLE. Treg cells and TIM-3 play an important role in the pathogenesis of LN. The beneficial effect of rapamycin on LN has been confirmed in both mouse models and patients, but the effect of rapamycin on Treg cells and TIM-3 is not yet completely understood. In this study, rapamycin treatment attenuated proteinuria, histological damage, and renal deposition of C3, and improved renal function. Spleen and renal draining lymph node weight and serum levels of anti-dsDNA antibodies were also improved by rapamycin. Furthermore, the frequency of Treg cells and Treg functional molecules, such as cytotoxic T cell antigen 4 (CTLA-4), interleukin 10 (IL-10), and transforming growth factor β1 (TGF-β1), increased significantly after treatment with rapamycin in MRL/lpr mice. We also found that expression of TIM-3 was significantly decreased in CD4+ T cells and Treg cells in mice treated with rapamycin. In summary, the study demonstrated that rapamycin treatment induced preferential expansion of CD4+CD25+Foxp3+ Tregs with increased expression of CTLA-4, IL-10, and TGF-β1, and decreased TIM-3 expression, thereby ameliorating lupus nephritis in the MRL/lpr mouse model.

Urinary Sediments as Predictors of the Histopathology of Lupus Nephritis.

Lupus nephritis (LN) is a major risk factor for morbidity and mortality in systemic lupus erythematosus (SLE). Urinalysis has an invaluable role in the diagnosis of various renal and urological diseases. Examinations of the urinary sediment using phase contrast microscopy (PCM) may add more information to help earlier diagnoses of LN. This cross-sectional study aimed to assess the possible role of the components of urinary sediment examined using PCM in discriminating the proliferative classes of LN (III and IV ± V) from the non-proliferative classes (I, II, and V), and to detect the correlation between the components of urinary sediment and indices of both activity and chronicity found by the renal biopsy. The study was conducted on 40 SLE patients for whom a renal biopsy was indicated. Clinical, demographic, and laboratory data and the results of the histopathological renal biopsy were collected. The morning before the renal biopsy; urine samples were collected from every patient and examined by PCM. Receiver operating characteristic curves were used to detect the area under the curve to predict proliferative LN. The correlations of counts of leukocytes, erythrocytes, all dysmorphic erythrocytes, acanthocytes, and stomatocytes with the indices of activity and chronicity were significant (activity: P = 0.027, P = 0.015, P = 0.033, P = 0.040, and P <0.001*; chronicity: P = 0.035, P = 0.009, P = 0.027, P = 0.010, and P <0.001, respectively). For patients with SLE, urinary sediment examinations can suggest a renal biopsy for the histopathology of LN.

Extraglomerular immune complex deposition in lupus nephritis.

Lupus nephritis (LN) is a common manifestation and a major cause of morbidity and mortality in systemic lupus erythematosus (SLE) patients. It is characterized by glomerular and often extraglomerular immune complex deposition. Given the emerging importance of the tubulointerstitial compartment, we conducted a retrospective study of 78 LN biopsies to enumerate the spectrum of extraglomerular immune complex deposition that can be observed in lupus nephritis by electron microscopy and to identify possible clinical or pathologic correlates. The presence of tubulointerstitial immune complex deposition often accompanied interstitial inflammation, but some discrepancies were also seen. As target antigens are identified, correlation with glomerular, tubulointerstitial, and vascular immune complex deposition will be of increasing interest.

Promising Roles of Exosomal microRNAs in Systemic Lupus Erythematosus.

Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by the loss of immune tolerance. Lupus nephritis (LN) is still a major cause of the morbidity and mortality of SLE. In clinical practice, diagnosis, and therapy of SLE is complicated and challenging due to lack of ideal biomarkers. Exosomes could be detected from numerous kinds of biological fluids and their specific contents are considered as hallmarks of autoimmune diseases. The exosomal miRNA profiles of SLE/LN patients significantly differ from those of the healthy controls making them as attractive biomarkers for renal injury. Exosomes are considered as optimal delivery vehicles owing to their higher stable, minimal toxicity, lower immunogenicity features and specific target effects. Endogenous miRNAs can be functionally transferred by exosomes from donor cells to recipient cells, displaying their immunomodulatory effects. In addition, it has been confirmed that exosomal miRNAs could directly interact with Toll-like receptors (TLRs) signaling pathways to regulate NF-κB activation and the secretion of inflammatory cytokines. The present Review mainly focuses on the immunomodulatory effects of exosomal-miRNAs, the complex interplay between exosomes, miRNAs and TLR signaling pathways, and how the exosomal-miRNAs can become non-invasive diagnostic molecules and potential therapeutic strategies for the management of SLE.

All-cause mortality in systemic rheumatic diseases under treatment compared with the general population, 2015–2019

ObjectivesTo compare current all-cause mortality rates in rheumatoid arthritis (RA), ankylosing spondylitis (AS), psoriatic arthritis (PsA), systemic lupus erythematosus (SLE) and systemic sclerosis (SSc) versus general population.MethodsIn this population-based, retrospective...

Norcantharidin ameliorates the development of murine lupus via inhibiting the generation of IL-17 producing cells

Systemic lupus erythematosus (SLE) is a devastating autoimmune disorder associated with severe organ damage. The abnormality of T cell apoptosis is considered as an important pathogenetic mechanism of SLE. Norcantharidin (NCTD), a derivative of Cantharidin, is an efficacious anti-cancer drug by inhibiting cell proliferation and inducing cell apoptosis. Besides, NCTD has also been proved to protect the function of kidneys, while damaged renal function is the most important predictor of morbidity and mortality in SLE. All these suggest the potential effects of NCTD in SLE treatment. In this study we investigated whether NCTD exerted therapeutic effects in a mouse SLE model. Lupus prone female MRL/lpr mice were treated with NCTD (1, 2 mg·kg−1·d−1, ip) for 8 weeks. We showed that NCTD administration significantly decreased mortality rate, diminished the expression of anti-dsDNA IgG antibody, a diagnostic marker for SLE, as well as restored renal structure and function in MRL/lpr mice. Moreover, NCTD administration dose-dependently inhibited lymphoproliferation and T cell accumulation in the spleens of MRL/lpr mice. We further revealed that NCTD specifically inhibited DN T cell proliferation and Th17 cell differentiation both via blocking activation of signal transducer and activator of transcription 3 (STAT3) signaling pathway. On the other hand, NCTD did not affect T cell apoptosis in MRL/lpr mice. Taken together, our data suggest that NCTD may be as a promising therapeutic drug through targeting T cells for the treatment of SLE.

Cardiovascular disease in systemic lupus erythematosus.

There is a well-known increased risk for cardiovascular disease that contributes to morbidity and mortality in systemic lupus erythematosus (SLE). Major adverse cardiovascular events and subclinical atherosclerosis are both increased in this patient population. While traditional cardiac risk factors do contribute to the increased risk that is seen, lupus disease-related factors, medications, and genetic factors also impact the overall risk. SLE-specific inflammation, including oxidized lipids, cytokines, and altered immune cell subtypes all are likely to play a role in the pathogenesis of atherosclerotic plaques. Research is ongoing to identify biomarkers that can help clinicians to predict which SLE patients are at the greatest risk for cardiovascular disease (CVD). While SLE-specific treatment regimens for the prevention of cardiovascular events have not been identified, current strategies include minimization of traditional cardiac risk factors and lowering of overall lupus disease activity.

Evaluation of a Patient-reported Frailty Tool in Women With Systemic Lupus Erythematosus.

Frailty is associated with mortality in systemic lupus erythematosus (SLE), but how best to measure frailty is unclear. We aimed to compare 2 frailty metrics, the self-reported Fatigue, Resistance, Ambulation, Illnesses, and Loss of weight (FRAIL) scale (FS) and the Fried phenotype (FP), in SLE to evaluate differences between frail and nonfrail women and whether frailty is associated with self-reported disability. Adult women aged < 70 years with validated SLE and mild/moderate disease enrolled in this cross-sectional study between August 2018 and October 2019. Correlation and agreement between the FS and the FP were determined. Differences in sociodemographic and disease characteristics, patient-reported outcome measures (PROMs), and biomarkers between frail and nonfrail participants were evaluated, as well as the association of frailty with Valued Life Activities disability. Of 67 participants, 27% and 18% were frail according to the FS and the FP, respectively. Correlation (r = 0.51; P < 0.0001) and agreement (κ = 0.46; P = 0.0004) between the FS and the FP were significant. Frail women had greater disease damage, high-sensitivity C-reactive protein, and interleukin 6, and worse PROMs according to both frailty definitions. Both frailty measures were associated with self-reported disability after adjustment for age, comorbidity, and disease activity and damage; this relationship was attenuated for the FP. Frailty prevalence was high in this cohort of women with SLE using both frailty definitions, suggesting that frailty may be accelerated in women with SLE, particularly when based exclusively on self-report. Frailty remained associated with self-reported disability in adjusted analyses. The FS may be an informative point-of-care tool to identify frail women with SLE.

Combining C reactive protein and serum albumin to predict 90-day mortality in systemic lupus erythematosus with serious community-acquired infections

ObjectiveSerious infections in SLE are common and have emerged as the major cause of death. However, effective methods to identify poor prognosis are still lacking. Therefore, we aimed to determine...

PSY15 Rate and Characteristics of All-Cause Mortality Among Elderly Systemic Lupus Erythematosus Patients

Systemic lupus erythematosus (SLE) is associated with increased morbidity and mortality. In this study, we sought (1) to examine the mortality rate difference between elderly SLE patients versus controls, and (2) to identify characteristics associated with mortality in SLE using machine learning (ML).

Diagnostic significance of circulating miR-485-5p in patients with lupus nephritis and its predictive value evaluation for the clinical outcomes.

Lupus nephritis (LN) is one of the main risk factors contributing to morbidity and mortality of systemic lupus erythematosus (SLE). This study aimed to investigate the potential role of miR-485-5p in human LN. Quantitative real-time polymerase chain reaction was used for the measurement of miR-485-5p levels. The levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) in serum were determined by enzyme-linked immunosorbent assay. The diagnostic role of miR-485-5p in LN was evaluated by the receiver operating characteristic (ROC) curve. The impact of miR-485-5p on end-stage renal disease (ESRD) was compared by Kaplan-Meier analysis and Cox regression analysis. The target gene was determined by a dual-luciferase reporter assay system. MiR-485-5p was highly expressed in SLE and LN patients compared with the healthy controls, and LN patients had the highest level of miR-485-5p. The expression level of miR-485-5p in active LN patients was significantly increased compared with that in nonactive cases. MiR-485-5p expression showed a positive correlation with the levels of estimated glomerular filtration rate, serum creatinine, proteinuria, SLE disease activity index score, and inflammatory cytokines. The ROC analysis results indicated that serum miR-485-5p was a promising biomarker for the early diagnosis of LN, and it can distinguish active LN patients from nonactive ones. Phosphatase and tensin homolog was a direct target of miR-485-5p, and negatively associated with serum miR-485-5p levels. More ESRD events were observed in cases with high miR-485-5p expression, miR-485-5p was an independent factor for the risk of ESRD in LN patients. Serum miR-485-5p might be a novel promising diagnostic marker for LN and has potential predictive value for ESRD risk in LN patients.

P087 Mortality trends from systemic lupus erythematosus in Cuba: 2001-2014

Abstract Background/Aims There is little research on the mortality of Cuban patients with systemic lupus erythematosus (SLE), with not enough impact to recognize SLE as a health problem in the country. Our aim was to identify time trends and geographic variability in the mortality of Cuban patients with SLE. Methods Mortality data of decedents over 15 years old were retrieved from the Cuban Ministry of Public Health mortality database, based on International Classification of Disease (ICD), Tenth Revision (ICD-10, code M32). We computed age-standardized mortality rate (ASMR) for each year and province as the estimated number of deaths per million inhabitants and its 95% confidence interval (95% CI) using World Health Organization reference population. The 2001-2014 time trends were analyzed using Jointpoint software. Results Between 2001 and 2014, 1,054 deaths from SLE were found, mostly women (89.0%), white (54.4%) with a median age of 43 years (interquartile range: 34-53). In 2014 the ASMR caused by SLE per million inhabitants was 14.4 (95% CI: 10.9 to 18.4) in women and 1.3 (95% CI: 0.5 to 3.2) in men. A growing time trend was identified in the ASMR by SLE throughout the period (average annual percentage change [AAPC]: 1.6; 95% CI: 0.6 to 2.6), highest in males (AAPC: 5.6; 95% CI: 1.7 to 9.7) than in females (AAPC: 1.2; 95% CI: 0.3 to 2.0). The highest mortality in women was concentrated in the provinces of Camagüey, Las Tunas and Granma, and in the case of men, in Havana and Ciego de Ávila. Conclusion The variation in the magnitude of the risk of dying from SLE over time and geographic areas indicates the possible influence of biological, environmental, socioeconomic and health systems factors. The growing trend in SLE mortality in Cuba demands its recognition as an important health problem and immediate actions that help mitigate it. Disclosure H. Hernández Negrín: None.

All-cause and cause-specific mortality in systemic lupus erythematosus: a population-based study.

To investigate all-cause and cause-specific mortality in SLE patients between two time periods, 1997-2005 and 2006-14. We used an administrative health database from the province of British Columbia, Canada to match all incident SLE patients to 10 non-SLE individuals on sex, age and index date. Cohorts were divided into two subgroups, according to diagnosis year: early cohort 1997-2005 and late cohort 2006-14. The outcome was death [all-cause, renal disease, cancer, infection, cardiovascular disease (CVD) and other]. Hazard ratios (HR) and 95% CIs were estimated using univariate and multivariable Cox models. Among 6092 SLE patients and 60 920 non-SLE individuals, there were 451 and 1910 deaths, respectively. The fully adjusted all-cause mortality HR (95% CI) in the overall SLE cohort was 1.85 (1.66, 2.06), with no statistically significant improvement between early and late cohorts [1.95 (1.69, 2.26) vs 1.74 (1.49, 2.04)]. There was excess mortality from renal disease [3.04 (2.29, 4.05)], infections [2.74 (2.19, 3.43)] and CVD [2.05 (1.77, 2.38)], but not cancer [1.18 (0.96, 1.46)], in the overall SLE cohort. There was no statistically significant improvement in cause-specific mortality between early and late cohorts for renal disease [3.57 (2.37, 5.36) vs 2.65 (1.78, 3.93)], infection [2.94 (2.17, 3.98) vs 2.54 (1.84, 3.51)] and CVD [1.95 (1.60, 2.38) vs 2.18 (1.76, 2.71)]. There was no increase in cancer-related mortality in either cohort [1.27 (0.96, 1.69) vs 1.10 (0.82, 1.48)]. This population-based study demonstrates a persisting mortality gap in all-cause and cause-specific deaths in SLE patients, compared with the general population.

Mortality in a cohort of Egyptian systemic lupus erythematosus patients: retrospective two-center study

BackgroundSystemic lupus erythematosus is a debilitating autoimmune disease with major contribution to the worldwide morbidity and mortality. This study aimed to investigate the causes of mortality in systemic lupus erythematosus (SLE) patients and the relation between clinical activity, disease-associated end-organ damage, laboratory markers and mortality.ResultsAmong the 771 patients who were successfully followed up, 34 patients (4.4%) died. The leading causes of death were infectious causes (35.29%), cardiopulmonary causes (26.48%), renal causes (14.7%), unknown causes (14.7%), neuropsychiatric causes (5.88%), and lastly gastrointestinal causes (2.94%). Subjects who died had lower complement 3 level, more anemia, lymphopenia, neutropenia, leukocytosis, thrombocytopenia, decreased glomerular filtration rate, higher incidence of infection, end-stage renal disease, and cardiopulmonary complications. Higher glucocorticoid dosage with more immunosuppressant (mofetil and cyclophosphamide) treatment was observed in patients who died. SLE disease Activity Index and Systemic Lupus International Collaborating Clinics damage index were both significantly higher in deceased persons. Multivariable hazards regression analysis revealed that lymphopenia (p = 0.017), decreased glomerular filtration rate < 50% (p = 0.002) with end-stage renal disease (p = 0.001), and high steroid daily use of > 40 mg (p = 0.016) were independent risk factors for the mortality of SLE patients.ConclusionInfections and cardiopulmonary complications are the leading causes of death in two centers caring for Egyptian SLE patients. Lymphopenia, end-stage renal failure, and high steroid daily use were associated with poor outcomes.

Lupus retinopathy: epidemiology and risk factors.

Lupus retinopathy is a clinical manifestation of systemic lupus erythematosus in the visual system. It is generally asymptomatic; however, it can become a threatening condition. It is closely associated with the inflammatory activity and higher mortality of systemic lupus erythematosus. Lupus retinopathy has several different clinical presentations, such as lupus microangiopathy, vascular occlusion, vasculitis, hypertensive retinopathy associated with lupus nephritis, and autoimmune retinopathy. Although the prevalence and associated factors of lupus retinopathy have been well defined in some parts of the world, there are no data from Latin America, including Brazil. As lupus retinopathy is generally asymptomatic, without a routine fundoscopy, it has been probably underestimated. This review is intended to discuss the epidemiology and risk factors of lupus retinopathy.

Systematic Evaluation of Urinary VCAM1 as Novel Biomarker for Prognosis of Lupus Nephritis.

Lupus nephritis was established as the major cause of morbidity and mortality in systemic lupus erythematosus (SLE) patients. This severity could be monitored by laboratory prognosis with accuracy and specificity for the disease. Recently, various SLE laboratory investigations still have had improper prognosis and also possibly causing tissue injury in the patients. The present study thus aimed to systematically explore a novel urinary protein for further development into a prognosis biomarker in patients. Several urinary proteins that previously were reported with abnormal expression in SLE patients between 2014 - 2019 were comprehensively collected. These proteins were also analyzed for functional category and sites of expression using STIRNG, FUNRICH, and Uniport database. Thereafter, the level of altered protein candidate was then validated by western blotting, correlation analysis, and diagnostic performance. Vascular cell adhesion molecule-1 (VCAM1) protein was found in higher levels and also specific in SLE patients with nephritis. Moreover, VCAM1 has a role in immune response, inflammation, is expressed on plasma membrane of renal cells, and has the ability to secret into urine. The level of VCAM1 in urine of SLE patients was significantly higher than in healthy controls. The area under ROC curve (AUC) was also 0.891. Furthermore, the level of VCAM1 was dramatically associated with the severity of renal insufficiency (r = 0.738). VCAM1 may be a novel urinary biomarker for reliable prognosis of nephritis severity in SLE patients.

FIB-4 index associated with mortality risk of patients with systemic lupus erythematosus: a large retrospective cohort study

IntroductionA considerable proportion of patients with systemic lupus ery­thematosus (SLE) have liver enzyme abnormalities. We evaluated whether fibrosis-4 (FIB-4) was associated with increased mortality of SLE patients.Material and methodsA multicenter retrospective cohort study was conducted based on medical records of first-admission SLE patients who were hospitalized during 1999–2009 in Jiangsu province. FIB-4 was estimated by age, platelet (PLT) count, alanine aminotransferase (ALT), aspartate aminotransferase (AST), and FIB-4. A Cox model and a restricted cubic spline (RCS) model were used to estimate hazard ratio (HR) and 95% confidence interval (95% CI).ResultsDuring up to 15 years of follow-up, 226 deaths were observed among 2331 SLE patients. Increased overall mortality was associated with abnormal groups of PLT, ALT, AST, and high FIB-4 (≥ 1.92), with adjusted HRs (95% CI) of 1.58 (1.19–2.11), 1.54 (1.14–2.07), 1.58 (1.17–2.12), and 1.88 (1.42–2.50), respectively. Moreover, significant dose-response relationships were found between mortality of SLE and those indexes, and it was nonlinear for PLT (p &lt; 0.001), ALT (p = 0.046) and FIB-4 (p &lt; 0.001), but not AST (p = 0.109). In cause-specific analyses, high FIB-4 index was directly associated with death from liver failure and indirectly associated with other death from infection and neuropsychiatric impairment. We found no significant differences of areas under curves (AUCs) between FIB-4 index and the disease activity index score of SLE.ConclusionsThis is the first report to describe the nonlinear association between FIB-4 index and increased mortality of SLE patients. The FIB-4 index may be used as an independent prognostic indicator for SLE patients.