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PubMed1998

Systemic lupus erythematosus (SLE): changing concepts and challenges for the new millennium.

SLE is still the prototype experimental animal and human autoimmune disease. The clinical manifestations are so diverse that some have come to regard it as the incumbent 'luetic heir apparent' of the late 20th century. The aberrations of the immune disturbance have up until now defied clear explanation but have certainly generated a level of academic and research interest far greater than the frequency of the disease would initially suggest. The clear understanding of the immune derangements in SLE will probably lead to the understanding of the core mechanisms of the immune system and thus to better ways of its specific manipulation in the management of many other conditions including cancer. Research currently being undertaken on the mechanisms of control of immunologically mediated inflammation and the possible use of immunogenetic therapy in the treatment of various forms of SLE will hopefully further improve SLE related morbidity and mortality.

Adult↗

PubMedDate not supplied

In vitro spontaneous and UVB-induced lymphocyte apoptosis are not specific to SLE.

We studied in vitro spontaneous and ultraviolet light (UV)-induced lymphocyte apoptosis in patients with systemic lupus erythematosus (SLE, n = 11), cutaneous lupus erythematosus (CLE, n = 8), and other collagen diseases (n = 6), as well as normal individuals (n = 6). Apoptosis was confirmed by the presence of a 180 bp DNA ladder on gel electrophoresis. UVB-induced apoptosis was observed in 4 of 11 patients with SLE (36.3%), 3 of 8 patients with CLE (37.5%) and 2 of 6 patients (33.3%) with other collagen diseases. There was no clinical correlation between clinical photosensitivity and UV-induced apoptosis. Similarly, spontaneous apoptosis was also found in lymphocytes from patients with diseases other than SLE. No apoptosis was found in normal subjects with or without UVB irradiation (25 mJ/cm2). These data suggest that UV-induced lymphocyte apoptosis may not be specific to SLE but may be common in collagen diseases.

Adolescent↗

PubMed1996

[A SLE case with toxic shock syndrome after delivery].

We experienced a SLE patient with TSS after delivery. A 32-year-old SLE patient was transferred to our division due to fever, diarrhea, erosive rash, pericardial effusion, myalgia, low blood pressure, thrombocytopenia and hypoproteinemia which appeared two days after transvaginal delivery. At the time of admission, we considered these symptoms as the exacerbation of SLE, and treatment with high doses of steroid was started. It was when TSST-1-producing-MRSA was cultured from the vagina and uterus that TSS was suspected. 2 g/day of vancomycin was administered and her symptoms improved. As observed in this case, it is important to consider TSS as one of the complications seen with SLE patients after delivery.

Adult↗

PubMed2005

Type I interferon correlates with serological and clinical manifestations of SLE.

BACKGROUND: Systemic lupus erythematosus (SLE) is an autoimmune disease affecting multiple organ systems triggered by the production of autoantibodies. Previous clinical studies in humans and murine models suggest that type I interferons (IFNs) are important for the initiation and potentiation of SLE activity. METHODS: 65 consecutive patients with SLE were identified from the University of California, San Francisco Lupus Clinic with moderate-severe disease activity. 94 serological samples were collected. Type I IFN levels and the ability of plasma to induce expression of several surface markers of dendritic cell maturation were measured. RESULTS: Type I IFN levels correlated with the presence of cutaneous manifestations, and there was a trend towards correlation with renal disease. No correlation was found between type I IFN levels and neurological disease. Type I IFN levels correlated positively with the SLEDAI score and anti-dsDNA levels and inversely with C3 levels. Interestingly, type I IFN levels were highest in African American patients. SLE plasma also induced the expression of MHC class I, CD38, and CD123 on monocytes, and was blocked by the addition of a monoclonal antibody to IFNAR1. CONCLUSIONS: The pathogenic role of type I IFN is suggested by the induction of cell surface markers for dendritic cell maturation. The potential therapeutic utility of antibodies directed to either type I IFN or IFNAR1/IFNAR2 may be of interest in further studies.

Adult↗

PubMed1977

Involvement of the eye in SLE and scleroderma. A study using fluorescein angiography in addition to clinical ophthalmic assessment.

General examination of the eye was carried out in 22 patients with systemic lupus erythematosus (SLE) and in 10 with scleroderma. 3 of the SLE and 2 of the scleroderma patients had keratoconjunctivitis sicca. Fluorescein angiography showed abnormalities of the retinal vasculature in one of a subgroup of 12 SLE patients and one of 10 scleroderma patients. None of the 12 SLE patients had abnormalities of the choroidal vasculature, while 5 of the 10 scleroderma patients had patchy areas of nonperfusion of the choroidal capillary bed.

Eye Diseases↗

PubMed1984

Beta 2-microglobulin and its binding activity in serum from patients with SLE.

Repeated determinations of beta 2-microglobulin (beta 2m) and beta 2-microglobulin binding activity (beta 2m ba) in serum were performed during a follow-up of 23 patients with SLE. beta 2m was determined by a radioimmunoassay. Individual mean values were raised in 65% of the patients. The mean value for all patients, 2.9 mg/l, was significantly higher than that of the controls. The beta 2m concentrations parallelled the clinical disease activity in several cases with different disease manifestations. The beta 2m ba was determined by precipitation of 125I-labelled beta 2m with polyethylene glycol. Increased beta 2m ba was found in 26% of the SLE patients with the 90th percentile in 40 healthy subjects being taken as the upper normal limit. There were, however, no significant differences between the mean values for beta 2m ba in the patients and the controls. Patients with systemic lupus erythematosus (SLE), suffering exacerbation of their disease, had a higher mean beta 2m ba than those with less active disease. Variations of the serum beta 2m ba occurred especially in patients with active disease but did not seem to reflect the clinical course. The beta 2m ba was recovered in the IgG peak when SLE serum was subjected to gel chromatography on Sephadex G-200.

Adolescent↗

PubMed2000

Anti-ribosomal P protein antibodies detected by immunoblotting in patients with connective tissue diseases: their specificity for SLE and association with IgG anticardiolipin antibodies.

OBJECTIVE: To assess the prevalence and clinical and serological associations of anti-ribosomal P protein antibodies (anti-P antibodies) in patients with connective tissue diseases (CTDs) and investigate the immunobiological nature of autoantibody clustering in which anti-P antibodies play a part. METHODS: IgG anti-P antibodies in the sera of 267 patients with CTDs and 31 healthy subjects were analysed by immunoblotting performed on cytoplasmic extract of Raji cells. 60 patients with systemic lupus erythematosus (SLE), 32 systemic sclerosis, 46 primary Sjögren's syndrome, 16 poly/dermatomyositis, 11 rheumatoid arthritis, 8 undifferentiated CTD, 72 overlap CTD, and 22 primary antiphospholipid syndrome were studied. Anti-P antibodies were affinity purified by elution from nitrocellulose bound antigen and tested by ELISA for their binding activity to cardiolipin. RESULTS: Anti-P antibodies were detected in 16 (6%) patients and in none of the controls: 12/60 SLE (20%) and 4/80 undifferentiated/overlap patients with CTD (5%). A close association of IgG antibodies with P proteins and with cardiolipin was seen in lupus sera (p=0.0009, odds ratio 18.33). Anti-P antibodies from 9 of 12 anti-P lupus serum samples could be affinity purified and none of the affinity purified fractions cross reacted with ELISA plate coated cardiolipin. CONCLUSIONS: Anti-P immunoreactivity is a specific marker of SLE and lupus-like disease and its detection is recommended as a powerful diagnostic tool. Anti-P antibodies are strongly clustered with IgG anticardiolipin antibodies in lupus sera, even if they are independently elicited. This suggests that their cognate autoantigens play a part in a common pathogenetic pathway in SLE.

Antibodies, Anticardiolipin↗

PubMed2003

Correlations of Y chromosome microchimerism with disease activity in patients with SLE: analysis of preliminary data.

BACKGROUND: Recently it has been suggested that microchimerism may have a significant role in the aetiopathogenesis of some autoimmune diseases. OBJECTIVES: To evaluate the incidence of microchimerism in systemic lupus erythematosus (SLE), to quantify the phenomenon, to evaluate changes of microchimerism during follow up, and to correlate these data with clinical and laboratory variables. METHODS: Patients were selected for the study on the basis of the following criteria: (a) pregnancy with at least one male offspring; (b) no history of abortion and blood transfusion. Microchimerism was detected using a competitive nested polymerase chain reaction for a specific Y chromosome sequence and an internal competitor designed ad hoc. Disease activity and organ involvement were also evaluated. RESULTS: Sixty samples from 22 patients with SLE and 24 healthy controls were examined. Microchimerism was seen in 11 (50%) patients and 12 (50%) controls. The mean number of male equivalent cells was 2.4 cells/100 000 (range 0.1-17) in patients with SLE and 2.5 (range 0.2-1.8) in healthy controls. No differences in the incidence of microchimerism or in the number of microchimeric cells were found between patients and healthy controls. Patients with a history of lupus nephritis had a higher mean number of fetal cells than patients with no such history. Disease activity did not appear to correlate with microchimerism. CONCLUSIONS: The preliminary data suggest that microchimerism does not interfere with the disease course of SLE, although further analysis on larger groups will be necessary to confirm these observations.

Adolescent↗

PubMed2005

Treatment of SLE with anti-CD20 monoclonal antibody.

Systemic lupus erythemaotsus (SLE) is an autoimmune disease involving multiple organ systems and characterized by anti-nuclear antibodies. While T cells and dendritic cells may play major roles in SLE, several lines of evidence strongly suggest a central role for B cells. This article will review the role of B cells in human SLE as well as the currently available data on the treatment of SLE by depleting B cells with anti-CD20 (rituximab).

Antibodies, Monoclonal↗

PubMed2026

Stigma, discrimination-related events, and determinants among adult people living with systemic lupus erythematosus (SLE): Systematic review and indicator-level meta-analysis.

BackgroundSystemic lupus erythematosus (SLE) is a complex autoimmune disease with 0.4 million new cases diagnosed annually. With its wide variety of visible and invisible manifestations, people living with SLE report being exposed to stigmatization, which impacts their personal and professional lives. However, the current literature is unclear on whether healthcare management teams assess this concern during follow-up. This study aims to synthesize existing evidence on the prevalence and determinants of stigma among people living with SLE.MethodsThis systematic review and meta-analysis gathered evidence from observational studies identified from three databases on 16 July 2025. Dual independent screening, data extraction, and risk-of-bias assessment (using the Newcastle-Ottawa Scale) were performed. Results were synthesized using descriptive statistics, narrative synthesis, and indicator-level meta-analyses.ResultsWithin the past two decades, 11 studies comprising 2254 people living with SLE reported and measured stigma- and discrimination-related events using various scales. Stigma was found to be prevalent across its three constructs: interpersonal, perceived, and intrapersonal stigma. This review demonstrated that people living with SLE reported a moderate overall burden of stigma (34.71 [95% CI 26.15, 43.27]), with average stigma scores indicating psychological impact. Additionally, nearly one in two persons (46% [95% CI 28-66%]) experienced at least one form of stigma or discrimination, most commonly social isolation and unfair treatment. Mental health associations were correlated with higher stigma burden.ConclusionThis review demonstrates that stigma and discrimination are not just social challenges but also critical determinants of health. With cautious interpretation, pooled evidence reveals a consistent high prevalence of stigma and discrimination, which act as "toxic" stressors, creating a vicious cycle with psychological stress and psychiatric manifestations and disease activity. There is an urgent clinical need to move beyond a mere biological approach to disease assessment and management and to begin screening for the "invisible" burden of invalidation and discrimination.

Humans↗

PubMed1994

Decreased mRNA levels coding for poly(ADP-ribose) polymerase in lymphocytes of patients with SLE.

Poly(ADP-ribose) metabolism is altered in patients with SLE. In order to localize the defect, the levels of poly(ADP-ribose) polymerase-specific mRNA were measured from dot blots of total RNA from peripheral blood lymphocytes. In this preliminary study, eleven patients with SLE and two with antiphospholipid syndrome were compared to three controls. It was found that the mean levels of specific mRNA were ten fold lower in the PBL from SLE patients compared to controls and no overlap of values was seen between the two groups. No such decrease was seen in the PBL from the patients with antiphospholipid syndrome. It is concluded that the defect in poly(ADP-ribose) polymerase metabolism that is seen in SLE patients occurs at the level of transcription or mRNA turnover.

Adult↗

PubMed1996

Biochemical characterization of ADP-ribose polymer metabolism in SLE.

The metabolism of poly(ADP-ribose) in peripheral blood mononuclear (PBM) cells was studied in 13 patients with systemic lupus erythematosus (SLE) and in 12 age and sex matched controls. Poly(ADP-ribose) polymerase activity was measured as the net accumulation of ADP-ribose polymers during the conversion of 32P-NAD to poly(ADP-ribose) in PBM cells in vitro. The control population showed a mean activity of 418 +/- 91(s.d.)pmol ADP-ribose/10 min/10(6) cells. The SLE population was more heterogeneous and showed a lower mean of 225 +/- 147(s.d.)pmol ADP-ribose/10 min/10(6) cells. The mechanism of decreased ADP-ribose polymer accumulation was investigated. Measurements of turnover of the ADP-ribose polymers and its substrate, NAD+, showed that diminished ADP-ribose polymer accumulation in SLE subjects resulted from decreased poly(ADP-ribose) synthesis and not from altered rates of polymer turnover or NAD utilization. Western blot analyses of enzyme protein levels, kinetic studies of poly(ADP-ribose) polymerase activity and analyses of polymer size distribution suggested that the mechanisms of poly(ADP-ribose) synthesis in SLE cells is not altered but that the number of active poly(ADP-ribose) polymerase molecules is reduced.

Adult↗

PubMed1997

SLE mortality in an oriental population.

We analysed the causes of 67 deaths, over a 4 y period, in our oriental population with systemic lupus erythematosus (SLE). The median disease duration was 48 +/- 60.5 months (range 1-250 months). The mean age at diagnosis and death were 30 and 35.1 y respectively. SLE alone accounted for death in 30 patients (44.8%), infection in 27 (40.3%), pulmonary embolism in 5 (7.5%), malignancy in 4 (5.9%) and rheumatic heart disease in 1 (1.5%). The major organ involvement in those with active disease at death were SLE related thrombocytopenia (n = 23/44, 52.3%), nephritis (n = 21/44), 47.7%), cerebral lupus (n = 16/44, 36.4%), and pulmonary haemorrhage (n = 12/44, 27.3%). As in other series, SLE and infection were the principal causes of death in our population. During this 4 y period, there was no late death due to atherosclerosis.

Adolescent↗

PubMed2003

SLE--systemic lupus erythematosus: a BLySful, yet BAFFling, disorder.

BLyS/BAFF (B-lymphocyte stimulator/B-cell activating factor) is a vital B-cell survival factor. Overexpression of BLyS in mice may lead to systemic-lupus-erythematosus-like (SLE-like) disease, and BLyS overexpression is common in human SLE. Treatment of SLE-prone mice with a BLyS antagonist ameliorates disease progression and enhances survival, making BLyS an attractive therapeutic target in human disease. However, several unresolved issues remain, including what is the contributory role of APRIL (a tumor-necrosis-factor superfamily member related to BLyS) in the 'autoimmunogenic' effects of BLyS, identification of the 'optimal' BLyS antagonist, and identification of those SLE patients most likely to benefit from BLyS antagonist therapy.

Animals↗

PubMed2000

Validation of a Chinese version of the Medical Outcomes Study Family and Marital Functioning Measures in patients with SLE.

The objective was to validate a Chinese translation of the Medical Outcomes Study Family and Marital Functioning Measures (FFM and MFM) in patients with systemic lupus erythematosus (SLE). Chinese-speaking SLE patients (n = 69) completed a self-administered questionnaire containing the FFM and MFM and assessing demographic and socio-economic status twice within a 2 week period. SLE activity, disease-related damage and quality of life were assessed using the BILAG, SLICC/ACR Damage Index and SF-36 Health Survey, respectively. Scale psychometric properties were assessed through factor analysis, Cronbach's alpha, quantifying test-retest differences and known-groups construct validity. Factor analysis identified 1 factor corresponding to the FFM and 2 factors corresponding to the MFM. Internal consistency for the FFM was excellent (alpha = 0.92) while that for the MFM was acceptable (alpha = 0.62). Mean (s.d.) test-retest differences were 0.06 (1.54) points for the FFM and 0.03 (2.08) points for the MFM. 11 and 10 of 13 a priori hypotheses relating the FFM and MFM, respectively, to demographic, disease and quality of life variables were confirmed, supporting the construct validity of these scales. The Chinese FFM and MFM are valid and reliable measures of family and marital functioning in Chinese-speaking SLE patients, with psychometric properties very similar to the source English version.

Adolescent↗

PubMed2000

Complement component 9 deficiency is not a susceptibility factor for SLE.

Almost all complement component 9 (C9) deficiency in Japan shows Arg95 Stop mutation of C9 gene. Therefore, we studied the prevalence of Arg95Stop mutation of C9 gene among 78 patients with SLE to elucidate the association of SLE and C9 deficiency. The Arg95Stop carrier frequency showed no significant difference between SLE patients and controls. Thus, C9 deficiency is not implicated in SLE susceptibility.

Complement C9↗

PubMed2001

Disassociation of sex hormone levels and cytokine production in SLE patients.

This study examines whether changes in the cytokine milieu of patients with systemic lupus erythematosus (SLE) are associated with abnormal levels of sex hormone levels in serum. The concentration of 17beta-estradiol (E2), progesterone (Pg) and dehydroepiandrosterone-sulphate (DHEAS) was monitored in sera from 128 lupus patients and 96 controls, and correlated with the activity of their cytokine secreting cells. Results indicate that SLE patients have (i) significantly fewer cells secreting IFNgamma, (ii) increased serum E2 and Pg levels, and (iii) reduced serum DHEAS levels compared to normal controls. However, the observed abnormalities in the cytokine milieu of SLE patients did not correlate with abnormalities in serum sex hormone levels. Instead, the association between IFNgamma production and DHEAS levels evident in healthy controls is absent in SLE patients, suggesting that cells from lupus patients are defective in their ability to produce IFNgamma in response to physiologic stimuli. Similarly, the normal correlation between IL-4 production and E2 levels was lost in patients with severe disease. Thus, while it remains possible that increased E2 and reduced DHEAS levels in lupus patients may help induce cytokine abnormalities early in disease, the subsequent cytokine imbalance does not correlate with sex hormone levels.

Adolescent↗

PubMed2001

Suppression of experimental systemic lupus erythematosus (SLE) in mice via TNF inhibition by an anti-TNFalpha monoclonal antibody and by pentoxiphylline.

We have previously shown that the clinical manifestations of experimental systemic lupus erythematosus (SLE) correlate with an early increased secretion of TNFalpha and IL-1. In the present study, we examined the efficacy of two therapeutic modalities which lower TNFalpha production or activity, on the clinical manifestations of the disease. Experimental SLE was induced in naive C3H.SW mice by injection of the human anti-DNA monoclonal antibody (mAb) bearing the common idiotype, 16/6 Id. Two weeks after booster injections, treatment with either an anti-TNFalpha mAb, or pentoxiphylline (PTX) was started, for a period of 6 weeks. Production of TNFalpha (by splenocytes) and IL-1 (by peritoneal macrophages) was determined 3 and 7 months after disease induction. The experimental mice were also followed for disease manifestations. Both treatment protocols, with anti-TNFalpha mAb and with PTX, reduced the production of the two pro-inflammatory cytokines. TNFalpha and IL-1, in mice with experimental SLE. Anti-DNA antibodies were significantly lower in the mice treated with either protocol. In addition, a significantly lower rate of leukopenia, proteinuria and immune complex deposition was observed in treated mice. Abrogation of TNFalpha and IL-1 production in the early stages of experimental SLE by an anti-TNFalpha mAb or by PTX improves the clinical status of mice afflicted with this autoimmune disease.

Animals↗