Lupus

Systematic lupus erythematosus (SLE) is characterized with various complications which can cause serious organ damage in the human body. Despite the significant improvements in disease management of SLE patients, the non-invasive diagnosis is entirely missing. In this study, we used urinary peptidomic biomarkers for early diagnosis of disease onset to improve patient risk stratification, vital for effective drug treatment.

Urine samples from patients with SLE, lupus nephritis (LN) and healthy controls (HCs) were analyzed using capillary electrophoresis coupled to mass spectrometry (CE-MS) for state-of-the-art biomarker discovery.

A biomarker panel made up of 65 urinary peptides was developed that accurately discriminated SLE without renal involvement from HC patients. The performance of the SLE-specific panel was validated in a multicentric independent cohort consisting of patients without SLE but with different renal disease and LN. This resulted in an area under the receiver operating characteristic (ROC) curve (AUC) of 0.80 (p < 0.0001, 95% confidence interval (CI) 0.65–0.90) corresponding to a sensitivity and a specificity of 83% and 73%, respectively. Based on the end terminal amino acid sequences of the biomarker peptides, an in silico methodology was used to identify the proteases that were up or down-regulated. This identified matrix metalloproteinases (MMPs) as being mainly responsible for the peptides fragmentation.

A laboratory-based urine test was successfully established for early diagnosis of SLE patients. Our approach determined the activity of several proteases and provided novel molecular information that could potentially influence treatment efficacy.

The incidence of end stage renal disease (ESRD) in patients with systemic lupus erythematosus (SLE) is rising. However, the relationship between osteoporotic fractures and SLE in the setting of ESRD remains uninvestigated. The purpose of this study was to compare the frequency of incident osteoporotic fractures in patients with ESRD with and without SLE, to identify risk factors for fractures in patients with SLE and ESRD, and to examine the contribution of these fractures to mortality.

Retrospective cohort study of patients with SLE (n = 716) and a 5% random sample of controls without SLE (n = 4176) in the United States Renal Data System (USRDS) from years 2006–2008 enrolled in Medicare Part D.

Fractures occurred in 10.6% (n = 76) of patients with SLE and ESRD and 12.1% (n = 507) of patients with ESRD without SLE (p = 0.24). Older age (adjusted relative risk 1.02, 95% confidence interval 1.01–1.04) was associated with an increased risk for fracture in patients with SLE and ESRD. In multivariable analyses, vertebral and hip fractures more than doubled the risk for mortality.

The frequency of osteoporotic fractures in patients with SLE and ESRD is similar to the general population of patients with ESRD. Vertebral and hip fractures are significant contributors to mortality in patients with SLE and ESRD. Fracture prevention, in particular, for elderly patients with SLE and ESRD, should be considered.

SLE is not an independent risk factor for fractures in patients with ESRD. However, among patients with SLE and ESRD, vertebral and hip fractures are significant contributors to mortality.

White matter hyperintense (WMHI) lesions are the most common finding in magnetic resonance imaging (MRI) of the brain in patients with systemic lupus erythematosus (SLE).

The objective of this article is to determine the clinical factors associated with an increase in WMHI lesion load among SLE patients.

A total of 83 SLE patients with MRI of the brain from National University of Malaysia Medical Centre were included. The WMHI lesion load was determined using the Scheltens score and Fazekas scale, and their distribution was divided into the deep white matter (DWMHI) and periventricular (PVH) regions. The clinical correlates of WMHI lesions were initially determined using univariate analyses and subsequently multivariable regression analyses were performed to determine the independent factors of increased WMHI lesion load.

MRI of the brain of 46 patients who had WMHI lesions were compared with 37 patients with normal MRI. We found significant association between the presence of WMHI lesions and age, presence of cerebral infarcts, positive antiphospholipid antibody (aPL), active disease, neuropsychiatric lupus (NPSLE) and disease damage. Age, SLEDAI scores, cerebral infarcts and disease damage were significantly associated with higher DWMHI and PVH Scheltens scores. Meanwhile, patients with active lupus nephritis (LN), lower serum albumin and more severe proteinuria were associated with larger Fazekas WMHI lesions. Multivariable regression analysis revealed that the independent factors associated with presence of WMHI lesions were positive aPL and SLEDAI scores (p < 0.05). Higher WMHI Scheltens scores in both DWMHI and PVH were associated with presence of cerebral infarct but higher PVH lesion load was significantly associated with active SLE disease.

Presence of WMHI lesions in SLE was significantly associated with cerebral infarcts, aPL and high general SLE activity, suggesting both inflammation and ischaemia as the underlying pathology of these lesions.

The aim of this study was to measure presenteeism (productivity impairment while the patient is at work) and the related risk factors in patients with systemic lupus erythematosus (SLE) from Argentina.

A total of 130 consecutive (1997 American College of Rheumatology (ACR) criteria) working patients with SLE were assessed using a standardized data collection form. Sociodemographic, disease and work-related variables were collected. The Work Productivity and Activity Impairment (WPAI) questionnaire was performed.

Overall, 130 patients were included in the analysis; 91% were women, and the mean age was 39 years (range 19–77). A total of 43% were White, 43% Mestizo and 13% Amerindian. Overall, 38% were single and 38% were married. A total of 75% had more than 12 years of formal education. The median disease duration was 7 years (interquartile range 25–75 (IQR) 4–13). Median Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) score was 0 (IQR 0–2), and median Systemic Lupus International Collaborating Clinics/ACR Damage Index (SLICC-SDI) score was 0 (IQR 0–1). Lupus quality of life (LupusQoL) domains scores were: physical health 87 (IQR 70–96), emotional health 78 (IQR 54–91), burden to others 75 (IQR 50–92), intimate relationships 87 (IQR 50–100), and body image 85 (IQR 70–100). Absenteeism was 8%, presenteeism was 19%, and overall work impairment (absenteeism + presenteeism) was 26%. In the multiple regression analysis, considering presenteeism as dependent variable, (adjusting by age, disease duration, >12 years of education, Non-white race, Visual Analogue Scale (VAS) pain, VAS fatigue, SLICC-SDI, LupusQoL, physical and emotional domains), we found that SLICC-SDI (odds ratio (OR) 1.68, confidence interval (CI) 1–2.7) and Non-white race (OR 3.27, CI 1.04–10) were related to presenteeism and >12 years of education (OR 0.30, CI 0.09–0.98) and higher scores of LupusQoL emotional health domain (OR 0.95, CI 0.92–0.98) were protective.

organ damage and Non-white race were significantly associated with presenteeism while >12 years of education and higher scores of LupusQoL emotional health domain were protective.

Anti-double stranded DNA antibodies are a very heterogeneous group of antibodies, quite specific for systemic lupus erythematosus. Newer technologies, such as addressable laser bead immunoassays (ALBIA), show great potential as a diagnostic application. The production of anti-double stranded DNA antibodies is often encountered in inflammatory arthritis; however, literature reports that the actual onset of drug induced lupus in patients treated with biological drugs is a rare event. False positive results for anti-double stranded DNA and anti-nucleosome antibodies detected in patients with inflammatory arthritis treated with different biologics prompted the investigation of full autoantibody profiles to evaluate each biomarker’s diagnostic performance in systemic lupus erythematosus. The aim of the study was to compare the diagnostic performance of anti-double stranded DNA antibody and anti-nucleosome antibody methods and to evaluate the value of simultaneously measuring anti-double stranded DNA and anti-nucleosome antibodies, along with other anti-nuclear antibody analytes, as biomarkers for systemic lupus erythematosus, using a more appropriate control cohort including inflammatory arthritis patients with a non-clinical drug induced lupus.

Anti-double stranded DNA and anti-nucleosome antibody levels were evaluated in 247 patient samples: 70 systemic lupus erythematosus, 177 disease controls (including 97 inflammatory arthritis during treatment with different biologics) using the Bio-Rad BioPlex® 2200.

Anti-nucleosome antibodies demonstrated greater clinical sensitivity and specificity than anti-double stranded DNA antibodies. At the manufacturers’ cut-off range, considering the two markers as a single or combined test, the “anti-double stranded DNA test or anti-nucleosome antibodies” was the most sensitive combination (0.400) with the best negative likelihood ratio (0.62) and negative predictive value (0.803).

Anti-nucleosome antibodies are a more sensitive and specific biomarker of systemic lupus erythematosus than anti-double stranded DNA antibodies. Anti-nucleosome antibodies and anti-double stranded DNA antibodies are independent and complementary markers of systemic lupus erythematosus diagnosis and, therefore, are strongly suggested as combined tests (positive predictive value = 0.938). Moreover, the combined use of the two tests may help to overcome the decreased specificity percentage of the anti-double stranded DNA test, when considering an inflammatory arthritis cohort under biological therapies. The ALBIA method for anti-nuclear specificity detection allows a full autoantibody assessment, resulting in a much higher clinical specificity for systemic lupus erythematosus in the presence of ≥3 positive markers and significantly more positive likelihood ratio when ≥2 positive markers are present.

The objective of this paper is to analyze the role of bone marrow-derived mesenchymal stem cells (BM-MSCs) on the differentiation of T follicular helper (Tfh) cells in lupus-prone mice.

Bone marrow cells were isolated from C57BL/6 (B6) mice and cultured in vitro, and surface markers were identified by flow cytometry. Naïve CD4⁺ T cells, splenocytes and Tfh cells were isolated from B6 mice spleens and co-cultured with BM-MSCs. The proliferation and the differentiation of CD4⁺ T cells and Tfh cells were analyzed by flow cytometry. Lupus-prone MRL/Mp-lpr/lpr (MRL/lpr) mice were treated via intravenous injection with expanded BM-MSCs, the differentiation of Tfh cells was detected, and the relief of lupus nephritis was analyzed.

MSCs could be successfully induced from bone marrow cells, and cultured BM-MSCs could inhibit T cell proliferation dose-dependently. BM-MSCs could prevent Tfh cell development from naïve CD4⁺ T cells and splenocytes. BM-MSCs could inhibit IL-21 gene expression and cytokine production and inhibit isolated Tfh cells and STAT3 phosphorylation. In vivo study proved that BM-MSCs intravenous injection could effectively inhibit Tfh cell expansion and IL-21 production, alleviate lupus nephritis, and prolong the survival rate of lupus-prone mice.

BM-MSCs could effectively inhibit the differentiation of Tfh cells both in vitro and in vivo. BM-MSC treatment could relieve lupus nephritis, which indicates that BM-MSCs might be a promising therapeutic method for the treatment of SLE.

We evaluated the efficacy and safety of tacrolimus in systemic lupus erythematosus patients with refractory thrombocytopenia.

We retrospectively reviewed the data for 20 systemic lupus erythematosus patients with refractory thrombocytopenia and treated with tacrolimus during the period January 2013 to January 2015. In addition to glucocorticoids, all patients were treated with tacrolimus, 1 mg taken twice daily. The clinical effect of tacrolimus treatment in patients was evaluated by analysis of platelet counts at baseline and after one, three and six months of tacrolimus treatment. Levels of anti-double-stranded DNA antibodies and complement C3, C4 were determined individually.

After one month of tacrolimus treatment, three patients (15%) did not respond, three patients (15%) achieved a complete response and the other 14 patients (75%) achieved a partial response. After three months of tacrolimus treatment, the platelet counts of all patients were significantly improved. A partial response was seen in 14 patients (75%) and the complete response rate increased to 25% (five patients). After six months, all patients attained partial response or complete response without relapse, and the rate of complete response increased to 75%. Compared to pretreatment, anti-double-stranded DNA antibody levels and the disease activity index score were markedly decreased after tacrolimus treatment. The levels of serum C3 and C4 were increased significantly (P < 0.05).

Our survey revealed that a six-month course of tacrolimus is a safe and effective treatment for systemic lupus erythematosus patients with refractory thrombocytopenia.

We aimed to investigate risk of hepatitis B virus reactivation in systemic lupus erythematosus patients with different hepatitis B virus infection statuses receiving immunosuppressive therapy.

We retrospectively analyzed systemic lupus erythematosus patients with positive hepatitis B surface antigen or anti-hepatitis B core IgG antibody who underwent immunosuppressive therapies from January 2001 to December 2012 at a medical center in Taiwan for evidence of hepatitis B virus reactivation.

During this period, 906 out of 3125 patients who were diagnosed with systemic lupus erythematosus received screening tests for hepatitis B virus. Thirty-eight patients were identified as hepatitis B surface antigen-positive. Fifteen of 38 (39.5%) hepatitis B surface antigen-positive patients developed hepatitis B virus reactivation, and 53.3% of these patients experienced severe hepatitis flare. Three of 157 hepatitis B surface antigen-negative/anti-hepatitis B core IgG antibody-positive patients (1.9%) experienced hepatitis B surface antigen seroreversion after immunosuppressive therapy. Five patients received prophylactic or preemptive antiviral therapy and none of them developed hepatitis B virus flares. A daily dose of prednisolone greater than 5 mg was a risk factor for hepatitis B reactivation by multivariate logistic analysis.

The risk of hepatitis B virus reactivation is high in lupus patients receiving immunosuppressive therapy. Antiviral prophylaxis or preemption can effectively reduce the incidence of hepatitis B virus reactivation in lupus patients.

Osteonecrosis is a serious comorbidity in patients with systemic lupus erythematosus. The aims of this study were to describe the prevalence of symptomatic osteonecrosis, determine the pattern of joint involvement, identify the outcomes and investigate predictive factors in a large cohort of patients with systemic lupus erythematosus followed prospectively.

At the Toronto Lupus Clinic patients have been followed prospectively according to a standard protocol since 1970. Osteonecrosis is recorded if patients are symptomatic and is confirmed by imaging. The site of osteonecrosis is recorded and whether or not surgery was performed. For determination of prevalence, pattern and outcome of osteonecrosis a longitudinal cohort design was performed. For the predictive factors, only patients with incident osteonecrosis were included and were matched for gender, year of entry to clinic (within 5 years), year of birth (within 5 years) and disease duration (within 3 years) with systemic lupus erythematosus patients without osteonecrosis.

Of 1729 patients with systemic lupus erythematosus registered in the database, 234 (13.5%) developed symptomatic osteonecrosis in 581 sites. Hips and knees were most commonly affected and 47% of the patients had multiple sites involved. More than half of the joints involved at first occurrence of osteonecrosis had surgery. Univariate analysis identified black race, damage, elevated cholesterol and glucocorticosteroids as predictive factors, but glucocorticosteroids remained as the primary predictor for the development of osteonecrosis on multivariable analysis.

Despite advancements in the assessment and treatment of systemic lupus erythematosus, symptomatic osteonecrosis continues to be a significant comorbidity. Strategies to minimize glucocorticosteroid use are necessary to prevent this serious complication.

Dilute Russell’s viper venom time (dRVVT) is indispensible in lupus anticoagulant (LA) detection yet commercial reagents from different suppliers perform variably, no gold standard assays exist and therapeutic anticoagulation interference is problematic.

The objective of this study was to compare a new formulation dRVVT with two currently available dRVVTs.

Life Diagnostics (LD) dRVVT and Stago PTT-LA were routinely used for lupus anticoagulant detection, plus Taipan snake venom time/ecarin time (TSVT/ET) for patients on warfarin or rivaroxaban. Siemens dRVVT and the new HYPHEN BioMed (HBM) dRVVT were tested with 193 patient samples. Group 1, 59 non-anticoagulated patients (NAPs) LA-positive in LD dRVVT; Group 2, 15 PTT-LA-positive/dRVVT-negative NAPs; Group 3, 24 LA-positive warfarinized patients; Group 4, 13 patients on rivaroxaban; Group 5, 62 LA-negative thrombotic NAPs; Group 6, 20 warfarinized, non-antiphospholipid syndrome patients.

Accepting that the Life Diagnostics reagents were acting as a pseudo-gold standard, Siemens dRVVT detected 56/59, (95%) Group 1 LA and HBM dRVVT 46/59, (76%), one each from Group 2, and Siemens dRVVT detected one in Group 5. The lower HBM dRVVT detection rate mainly concerned weaker LA, where between-reagent concordance is problematic. All Group 3 patients appeared LA-positive in undiluted plasma with Siemens dRVVT, as did 16/24 (67%) with HBM dRVVT but the fewer LA-positives in mixing tests better mapped to clear LA-positives with LD dRVVT. LD and Siemens dRVVTs exhibited 87% and 95% false-positivity for Group 6 whilst HBM dRVVT had none. Increasing the cut-off improved accuracy. Applying higher cut-offs improved accuracy in Group 4 patients.

HBM dRVVT exhibited improved specificity, mainly due to less interference by anticoagulation, but reduced sensitivity, compared to the other dRVVTs employed.

Several studies have evaluated the prevalence of rheumatoid factor (RF) and anti-citrullinated proteins antibodies (ACPA) in systemic lupus erythematosus (SLE) patients but no data are available on the anti-carbamylated proteins (anti-CarP), a new biomarker for rheumatoid arthritis (RA). We evaluated the anti-CarP prevalence in SLE patients with joint involvement and the associations with different phenotypes.

Seventy-eight SLE patients with joint involvement were enrolled (F/M 73/5; mean ± SD age 47.6 ± 11.2 years; mean ± SD disease duration 214.3 ± 115.6 months). As control groups, we evaluated SLE patients without joint manifestations (N = 15), RA (N = 78) and healthy individuals (HS, N = 98). Anti-CarP were assessed by home-made ELISA in all patients and controls, RF and ACPA in SLE patients with joint involvement (commercial ELISA kit).

The prevalence of anti-CarP in SLE patients with joint involvement was similar to RA (p = NS) and significantly higher compared with SLE without joint involvement and HS (p < 0.0001, p < 0.0001, respectively). Four patients were positive for all three antibodies: seventy-five percent of these showed Jaccoud arthropathy. Fourty-five percent of ACPA-ve/RF-ve patients were anti-CarP + ve.

The evaluation of anti-CarP in SLE joint involvement demonstrated a prevalence of almost 50%, similar to RA and significantly higher than SLE without joint involvement and HS.

In this study, we aimed to assess the relative efficacy and safety of intravenous (IV) or subcutaneous (SC) belimumab compared with those of placebo in patients with active systemic lupus erythematosus (SLE).

We performed a Bayesian network meta-analysis to combine the direct and indirect evidence from randomized controlled trials (RCTs) examining the efficacy and safety of belimumab 1 mg/kg and 10 mg/kg IV administration, and belimumab 200 mg SC injection, and placebo in patients with active SLE despite having received standard therapy.

Five RCTs (3460 patients) met the inclusion criteria. The SLE Responder Index (SRI) response rate at week 52 was significantly higher in the belimumab 10 mg/kg group than in the placebo group (OR 2.63, 95% CrI 2.14–3.23). Similarly, the SRI response rates were significantly higher in the belimumab 1 mg/kg, and belimumab 200 mg SC groups than in the placebo group (OR 2.42, 95% CrI 1.90–3.09; OR 1.71, 95% CrI 1.27–2.29). Ranking probability based on surface under the cumulative ranking curve (SUCRA) indicated that belimumab 10 mg/kg had the highest probability of being the best treatment for achieving the SRI response (SUCRA = 0.9174), followed by belimumab 1 mg/kg (SUCRA = 0.7338), belimumab 200 mg SC (SUCRA = 0.3487), and placebo (SUCRA = 0.0000). However, a sensitivity test by omitting one outlier study showing low SRI response rate compared with the other three studies (11% vs. 33%, 40%, 48%) showed that belimumab 200 mg SC and belimumab 10 mg/kg had the highest probability of being the best treatment for achieving the SRI response (SUCRA = 0.7903, SUCRA = 0.7456), followed by belimumab 1 mg/kg, and placebo. The number of serious adverse events (SAEs) did not differ significantly among the four treatment options.

Belimumab at 1 and 10 mg/kg IV and belimumab 200 mg SC in combination with standard therapy was an efficacious intervention for active SLE, and was not associated with a significant risk of SAEs.

There is a decreased risk of breast cancer in systemic lupus erythematosus (SLE) versus the general population; little is known regarding the receptor status of breast cancers in SLE, or treatment.

Breast cancer cases occurring after SLE diagnosis were ascertained through linkage with tumor registries. We determined breast cancer positivity for estrogen receptors (ER), progesterone receptors (PR), and/or Human Epidermal Growth Factor Receptor 2 (HER2), as well as cancer treatment.

We obtained information on ER, PR, and/or HER2 status for 63 SLE patients with breast cancer. Fifty-three had information on ER and/or PR status; 36 of these (69%) were ER positive. Thirty-six of the 63 had information on HER2 status; of these, 26 had complete information on all three receptors. Twenty-one of these 26 (81%) were HER2 negative; seven of 26(27%) were triple negative. All but one patient underwent surgery; 11.5% received both non-tamoxifen chemotherapy and radiotherapy, 16.4% radiotherapy without non-tamoxifen chemotherapy, and 14.7% received non-tamoxifen chemotherapy without radiotherapy.

ER positivity was similar to historical general population figures, with a trend toward a higher proportion of triple-negative breast cancers in SLE (possibly reflecting the relatively young age of our SLE patients).

The objective of this report is to evaluate the prevalence and clinico-serological correlations of anti-α-enolase antibody (Ab) in patients with systemic lupus erythematosus (SLE).

Thirty-two untreated patients with SLE and 20 age- and sex-matched healthy controls were evaluated by rheumatologic examinations. The serum levels of anti-α-enolase Ab were measured by an enzyme-linked immunosorbent assay (ELISA). Clinical, biochemical and serological markers of disease activity were measured by standard laboratory procedure.

The serum levels of anti-α-enolase Ab in SLE patients were higher significantly than those in healthy controls. Moreover, patients with lupus nephritis displayed significantly higher levels of serum anti-α-enolase Ab than those without renal involvement. The serum anti-α-enolase Ab levels were positively correlated with serum whole IgG and 24-hour urine protein and negatively correlated with serum D-dimer level.

These data suggest that anti-α-enolase Ab associates with active renal disease in SLE and might reflect a state of active autoimmunity and fibrinolysis inhibition.

T-cell activation may be one of the pathogenic mechanisms of systemic lupus erythematosus (SLE). After repeated antigenic stimulation, T-cells undergo different modifications, leading to the differentiation into effector memory T-cells (CCR7−CD45RA−) and terminally differentiated effector memory (TDEM) T-cells (CCR7−CD45RA+). Similarly, down-modulation of CD28 may lead to the expansion of the CD28− T-cells, a subpopulation with peculiar effector activities. The aim of this study was the characterization of T-cell phenotype in a cohort of patients with SLE according to disease activity and damage index.

Phenotypic analysis of peripheral blood T lymphocytes of 51 SLE patients and 21 healthy controls was done by flow-cytometry. SLE disease activity was evaluated by SLE Disease Activity Index-2000 (SLEDAI-2K) and damage by the Systemic Lupus International Collaborating Clinics/American College of Rheumatology damage index (SDI). The variations between different groups were evaluated by Mann–Whitney test. Bonferroni correction was applied to adjust for multiple comparisons (p^adj). Spearman rank test was used to evaluate the correlations between quantitative variables.

CD4+ lymphopenia was found among SLE patients. Patients showed a trend for a higher percentage of TDEM among the CD4+ T-cell subpopulation in comparison with healthy controls (p = .04). SLE patients were divided into two groups according to disease activity: patients with SLEDAI-2K ≥ 6 (n = 13) had a higher percentage of circulating CD4+ T-cells with CD28− phenotype (p^adj= .005) as well as those with an effector memory (p^adj= .004) and TDEM (p^adj= .002) phenotype and a trend of decrease of regulatory T-cells (TREGs) (p = .02), in comparison with patients with low disease activity (n = 38). Patients with damage (SDI ≥ 1) tended to show an expansion of TDEM among CD4+ T-cells as compared with patients with no damage (p = .01). In SLE patients an inverse correlation was found between the percentages of TREGs and those of TDEM (p < .01) or CD4 + CD28− (p < .01) T-cells.

CD4+ T-cell subpopulations displaying phenotype characteristics of effector lymphocytes are proportionally expanded in patients with active SLE and a higher damage index. These findings may suggest a role of effector T-cells in the pathogenesis of the disease and in the mechanisms of damage in SLE.

The objective of this paper is to compare adverse pregnancy outcomes between normal pregnancies and pregnancies with systemic lupus erythematosus (SLE), particularly focusing on uncomplicated SLE with remission.

A retrospective cohort study was conducted by accessing the Maternal-Fetal Medicine (MFM) Unit database and the full medical records of the women. The records of singleton pregnancies with SLE and no underlying disease were assigned as the study group and their medical records were reviewed. The low-risk pregnancies were randomly selected as the controls. The adverse pregnancy outcomes were compared between the control group vs women with SLE, control group vs uncomplicated SLE, and between the subgroups within the study group.

Of 28,003 births during the study period, 1400 controls and 140 pregnancies with SLE were compared. The rates of fetal loss, preterm birth, small-for-date, low birth weight and preeclampsia were significantly higher in the study groups with a relative risk of 5.6 (95% CI: 2.9–10.9), 3.2 (95% CI: 2.5–4.1), 3.5 (95% CI: 2.4–4.9), 4.2 (95% CI: 3.4–5.3) and 2.9 (95% CI: 1.9–4.4), respectively. The increased rates of most adverse outcomes were still noted even in the cases of uncomplicated SLE. Among women with SLE, lupus nephritis, chronic hypertension, antiphospholipid syndrome, active disease at the onset of pregnancies, and proteinuria were significantly associated with such outcomes.

Pregnancies with SLE, even in uncomplicated cases with remission, increase the risk of poor pregnancy outcomes. The presence of lupus nephritis, chronic hypertension, antiphospholipid syndrome, active disease at the onset of pregnancies, and proteinuria were significantly associated with such outcomes.

To determine the incidence, duration and cause of hospitalization in a cohort of Danish patients with systemic lupus erythematosus (SLE). In addition, we investigated risk factors for admission and prolonged hospital stay.

A total of 155 SLE patients from a population-based cohort were included in the study during a period of 70 months, from January 2007 to October 2012. Data on frequency, cause and duration of hospitalizations were obtained by review of medical charts. Data on disease manifestations, organ damage and treatment were collected prospectively.

A total of 101 of the 155 SLE patients (65%) had one or more hospitalization during the study period. The incidence rate of all hospitalizations was 0.50 per year. Leading causes of admission were complications to SLE or its treatment, but infections were also common. Mean duration of hospital stay was 6.4 ± 10.5 days, and SLE Disease Activity Index 2000 (SLEDAI-2K) on admission emerged as a risk factor for prolonged hospital stay.

Danish SLE patients experience frequent admissions to hospital. Complications to SLE or its treatment, as well as infections, are leading causes of admission. High SLEDAI-2K on admission is a risk factor for prolonged hospital stay.