SEARCH · PubMed Health

Results for “SLE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 307 records · Page 17Linked to original sources

PubMed2001

UVA-1 cold light treatment of SLE: a double blind, placebo controlled crossover trial.

OBJECTIVE: Treatment of patients with systemic lupus erythematosus (SLE) often implies strong drugs with possibly serious side effects. Thus there is a need for new immunosuppressive treatments. Long wave ultraviolet A (UVA-1) cold light therapy is an anti-inflammatory, immunomodulatory treatment with a possible systemic effect and few side effects. In the current study low dose UVA-1 cold light treatment was tested to determine whether it reduces disease activity in SLE. METHODS: Eleven patients with SLE were treated with UVA-1 cold light treatment and a placebo light treatment in a double blind, placebo controlled, crossover study. In two consecutive 12 week periods the patients were treated in the first three weeks with UVA-1 and placebo treatment or vice versa. The primary variables were the SLE Disease Activity Index (SLEDAI) and SLE Activity Measure (SLAM). RESULTS: The mean SLAM and SLEDAI showed a significant decrease of 30.4% (p=0.0005) and 37.9% (p=0.016) respectively after three weeks of UVA-1 and a non-significant decline of 9.3% (p=0.43) and 12.2% (p=0.54) respectively after three weeks of placebo treatment. In this small trial the difference in reduction of the disease activity indices during UVA-1 compared with during placebo treatment failed to reach the conventional border of significance (p=0.07). The total score of quality of life measure RAND-36 did not improve significantly, but the subscore for vitality did improve. CONCLUSION: Low dose UVA-1 cold light treatment was strongly suggestive of lowering disease activity in this double blind placebo controlled study, and no side effects occurred.

Adolescent↗

PubMed2003

Factors associated with coronary artery calcification in young female patients with SLE.

BACKGROUND: With improved survival rates of patients with systemic lupus erythematosus (SLE), damage such as accelerated atherosclerosis gains increasing importance. OBJECTIVE: To identify the prevalence of coronary artery calcifications (CAC) in asymptomatic patients. METHODS: Electron beam tomography (EBT) was performed in 75 female patients with SLE aged <50. The results were correlated with traditional and SLE related factors associated with CAC. 49 women with symptomatic coronary heart disease (CHD) and 279 women without CHD were also analysed. RESULTS: Overall, 21/75 (28%) patients had CAC. Low HDL cholesterol levels <1.40 mmol/l (p=0.03, OR=1.8, 67% v 39%) and cigarette smoking (p=0.01, OR=5.7, 76% v 44%) were identified as factors associated with CAC. Hypertension and high cholesterol were more common in women with CHD (p<0.01) than in those without CHD. SLE related factors were proteinuria (1331 v 465 mg/day, p=0.02), impaired renal function (p=0.02, OR=2.6, 26% v 6%), and high C3 levels (p=0.04, OR=1.8, 65% v 38%). High C3 levels were also more common in symptomatic CHD (p=0.02). The prevalence of Sm antibodies was lower in patients with CAC (15% v 42%, p=0.03). In a multivariate analysis, cigarette smoking, reduced renal function, high C3, and a cumulative steroid dose above 30 g were the most important CAC associated factors in the lupus cohort. CONCLUSION: A subgroup of patients with SLE with CAC without any clinical symptoms of CHD was identified by EBT. Therefore, EBT is useful for assessing asymptomatic atherosclerosis in this group.

Adult↗

PubMed2006

Clearance of apoptotic cells in human SLE.

Systemic lupus erythematosus (SLE) is characterized by a diverse array of autoantibodies, particularly against nuclear antigens, thought to derive from apoptotic and necrotic cells. Impaired clearance functions for dying cells may explain accumulation of apoptotic cells in SLE tissues, and secondary necrosis of these cells may contribute to the chronic inflammation in this disease. The exposure of phosphatidylserine (PS) and altered carbohydrates on dying cells are important recognition signals for macrophages. Furthermore, serum factors such as complement, DNase I, pentraxins (e.g. C-reactive protein) and IgM contribute to efficient opsonization and uptake of apoptotic and necrotic cells. Defects in these factors may impact the development of SLE in humans and mice in a variety of ways. We observed impaired clearance of apoptotic cells in lymph nodes and skin biopsies of humans with lupus, as well as intrinsic defects of macrophages differentiated in vitro from SLE patients' CD34+ stem cells, demonstrating that apoptotic cells are not properly cleared in a subgroup of patients with SLE. This altered mechanism for the clearance of dying cells may represent a central pathogenic process in the development and acceleration of this autoimmune disease.

Animals↗

PubMed1980

The clinical significance of the antinuclear antibody test as a screening procedure for DNA antibodies in SLE.

During the two-year period (1st October 1974-30th September 1976), 2979 sera were tested for DNA antibodies by the Farr test. One thousand six hundred and ninety-five of these were tested because they had high ANA titres (1/256 or greater). In this group 285 sera were found to have raised DNA binding capacities (DNA-bc), 86 of which were found in patients having diagnoses other than SLE. When the diagnoses were reviewed following the finding of a raised DNA-bc, 55 of these patients were found to be suffering from SLE. Of the 1284 sera tested for DNA antibodies without the prior ANA screening procedures, 288 were positive, 36 of which came from patients not considered to have SLE; 30 of these patients were subsequently shown to have SLE. Thus the DNA-bc test is an important tool in the diagnosis of SLE, and the ANA test appears to be a valuable screening procedure. The level of DNA-bc was not of any diagnostic value.

Antibodies, Antinuclear↗

PubMed2000

Increased cervical dysplasia in intravenous cyclophosphamide-treated patients with SLE: a preliminary study.

To determine if intravenous cyclophosphamide (IV-C) causes an excess of cervical dysplasia and/or cancer in systemic lupus erythematosus (SLE) patients, a retrospective review was conducted. Patients with SLE who received IV-C between 1988-98 (study group) were compared with a group of SLE patients who had not received IV-C (control group). Of the 79 IV-C-treated SLE patients identified, we excluded 18 because of absence of pertinent data. We found 10 cases of cervical dysplasia in the remaining 61 patients, compared to 2 in 49 non-exposed patients (P<0.04). Comparison of the two groups revealed no difference in: mean years of disease duration, months of follow-up and age. The non-exposed patients were more likely to be on estrogen and hydroxychloroquine but less often on steroids and azathioprine. The study group with and without dysplasia were assessed; we found no difference in the mean, or total IV-C dose, smoking and estrogen use. There was a significant decrease in time to dysplasia in those, given IV-C, with previous dysplasia compared to those without. These preliminary data suggests that IV-C causes an increased number of abnormal Papanicolaou (Pap) smears in SLE patients, particularly those with previous dysplasia.

Adult↗

PubMed1993

HLA antigens and complement C4 allotypes in patients with chronic biologically false positive (CBFP) seroreactions for syphilis: a follow-up study of SLE patients and CBFP reactors.

We report a follow-up of our previous study of HLA markers in 118 unrelated patients: 49 with definite systemic lupus erythematosus (SLE) (group 1), 32 with definite or probable SLE and chronic biologically false positive (CBFP) seroreactions for syphilis (group 2), and 37 CBFP reactors (group 3). Definite SLE was confirmed in 28 (90.3%) of the patients in group 2, equally in HLA B8- and HLA B7-positive patients. Three of the CBFP reactors developed SLE, two (40%) out of five HLA B8-positive as compared to one (6.6%) out of 15 HLA B7-positive CBFP reactors (P = 0.07). Fourteen patients died (groups 1 and 2). Eight of the 24 HLA B8-positive patients died in contrast to one of the 20 HLA B7-positive patients (P < 0.02). Of the CBFP reactors, 70.9% had complement C4 null alleles as compared to 47.9% in controls (P = 0.05) and 50% had C4A null alleles as compared to 17.8% in controls (P < 0.05). C4B null alleles were found in 28.6% (28.6% in controls, P is not significant). The null alleles for C4A were not solely in a linkage disequilibrium with the HLA B8 DR3 haplotype. CBFP reactors with C4A null alleles had a higher risk of developing SLE, lupus-like disease or symptoms such as photosensitivity, cutaneous vasculitis and/or autoantibodies than did those with no C4A null alleles (P < 0.02).

Adolescent↗

PubMed1999

Prevalence of soft tissue calcifications in patients with SLE and effects of alfacarcidol.

OBJECTIVE: To clarify the prevalence and etiology of ectopic calcification in patients with systemic lupus erythematosus (SLE), especially under the active vitamin D3 administrations and to reveal the risk factors of ectopic calcification. METHODS: Sixty patients with SLE, excluding the patients on dialysis were studied. We examined radiographs of hands, forearms, upper and lower extremities, and pelvises of all patients to evaluate ectopic calcification. RESULTS: The prevalence of ectopic calcification in SLE was 40% (24 out of 60 patients), found in 6.7% (4 patients) in peripheral arteries, 33.3% (20 patients) in periarticular area and 16.7% (10 patients) in other soft tissues. The incidence of lupus nephritis and nephrotic syndrome were significantly higher (respectively: P=0. 0144 and P=0.0348) in the calcification-positive than negative group. Total protein levels (7.04+/-0.6 g/dl) of patients in the calcification-positive group were decreased significantly (P=0.0056) compared with 7.48+/-0.55 g/dl in the negative group. However, other biochemical parameters were not significantly different between the two groups. Sixty-three percent of the SLE patients with ectopic calcification received alfacarcidol, which is significantly (P=0. 0007) higher than the 19% in patients without calcification. CONCLUSION: It is suggested that the alfacarcidol therapy and lupus nephritis could increase the risk of ectopic calcification in SLE patients.

Adult↗

PubMed2000

Toxic effects of SLE serum on normal monocytes in vitro: cell death induced by apoptosis related to complement dysfunction.

The aim of this study was to assess toxic effects of systemic lupus erythematosus (SLE) serum on blood peripheral mononuclear cells from healthy donors and to evaluate if complement activation was involved. Monocytes from a healthy donor were incubated with 20 sera from ten SLE patients in both high and low disease activity states. After incubation non-adherent cells were analysed by flow cytometry. Serum from six SLE patients induced an increased cell death, four in active disease only, one in the inactive state and one in the active and the inactive state. Five of these sera, three with high and two with low disease activity, induced an increased apoptosis in the monocytes. Proportion of apoptotic cells correlated inversely with C1q and C3 concentration in the active disease sera, but not with disease activity as evaluated by SLEDAI. Apoptosis could be induced by addition of active C1s or antigen/antibody complexes to normal serum before incubation. Serum with complexes added induced increased tumour necrosis factor-alpha secretion from mononuclear cells, but SLE patient sera did not. The results demonstrate that the toxic effect of serum from SLE patients on healthy monocytes is explained by induction of apoptosis. The induction process is suggested to be connected with complement activation in the serum.

Adolescent↗

PubMed2001

CD4 positive peripheral T cells from patients with systemic lupus erythematosus (SLE) are clonally expanded.

T cell activation was analysed in peripheral CD4+ T cells from both systemic lupus erythematosus (SLE) patients with active and inactive disease as well as in normal healthy donors (NHD) to investigate the involvement of CD4+ T cells in the etiopathogenesis of SLE. CD4+ T cell receptor (TCR) beta-chain transcripts, containing the complementarity determining region 3 (CDR3), were amplified by reverse transcriptase-polymerase chain reaction (RT-PCR) and analysed by high-resolution polyacrylamide gel electrophoresis. In addition the CDR3 of both clonally activated as well as heterogeneous Vbeta families from SLE patients were analysed at the molecular level. We observed a restricted CDR3 length polymorphism in peripheral CD4+ T cells from SLE patients compared with NHD, more pronounced in patients with high disease activity. Furthermore, in some Vbeta families single peaks in the histogram indicated nearly monoclonal T cell expansion. Sequencing of selected TCR beta-chains revealed a increased content of acidic amino acids in the CDR3 encoded by either proximal Jbeta elements or N nucleotides. We conclude that CD4+ T cells from peripheral blood of SLE patients display features of a secondary antigen driven immune response. The bias of the CDR3 towards acidic amino acids suggests the involvement of positively charged antigens.

Amino Acid Sequence↗

PubMed2001

AVEMAR (a new benzoquinone-containing natural product) administration interferes with the Th2 response in experimental SLE and promotes amelioration of the disease.

The potential of oral treatment with AVEMAR (AVEMAR), a new benzoquinone-containing fermentation product of wheat germ, on features of experimental systemic lupus erythematosus (SLE) in naive mice, induced by idiotypic manipulation, was studied. We assessed the effect of AVEMAR on the profile of autoantibody production and the response of Th1/Th2 related cytokines as well as the clinical picture of experimental SLE in the SLE-induced mice. When the product was given in the pre-immunization period, down-regulation of autoantibody production (anti-dsDNA, mouse 16/6 Id, and anti-histones) following treatment with AVEMAR was noted (eg anti-dsDNA decreased from 0.898+/-0.097 OD at 405 nm to 0.519+/-0.103 OD following treatment). This effect was sustained for at least 4 weeks after discontinuation of the therapy. Serological manifestations associated with a delay in Th2 response (IL-4 and IL-10) were recorded (eg IL-4 decreased from 91.7+/-8.11 to 59.55+/-7.78 ng/ml in splenocyte condition media). The mice showed normal ESR, WBC and less than 100 mg/dl of protein in the urine in comparison to > 300 mg/dl protein in the SLE non-treated mice. In conclusion, oral intake of AVEMAR can ameliorate the clinical manifestations of experimental SLE, via affecting the Th1/Th2 network inhibiting Th2 response.

Animals↗

PubMed2002

Scleroderma-like nailfold capillaroscopic abnormalities are associated with anti-U1-RNP antibodies and Raynaud's phenomenon in SLE patients.

This study aimed to evaluate the association between nailfold capillary abnormalities and the presence of Raynaud's phenomenon (RP), anti-U1-RNP, and anti-cardiolipin (aCL) antibodies in SLE patients. One-hundred SLE patients were studied. Widefield nailfold capillaroscopy was considered abnormal according to five criteria. Intercapillary distance, capillary width and capillary length were registered by videomorphometry in two fingers in 100 patients and in four fingers in 40 of these patients. Both the presence of alterated capillaroscopy and the presence of scleroderma-pattern (SD-pattern), characterized by the presence of avascular areas and enlarged or giant loops, were associated with the isolated presence of RP (P < 0.001) or anti-U1-RNP antibodies (P < 0.01), as well as with the simultaneous presence of RP and anti-U1RNP antibodies (P < 0.001). There was a negative association between the presence of aCL antibodies and SD-pattern (P < 0.05). Higher figures for the videomorphometric parameters capillary width, intercapillary distance and capillary length (measured on four fingers) were observed in patients with RP. Patients presenting both RP and anti-U1-RNP antibodies showed higher figures for intercapillary distance and capillary width. This study demonstrated significant association between nailfold capillaroscopic abnormalities and either RP or anti-U1-RNP antibodies in SLE patients. The association of RP, anti-U1-RNP antibodies, and 'scleroderma-like' findings on nailfold capillaroscopy (SD-pattern) in patients with SLE may suggest a new SLE subset with subclinical features of systemic sclerosis.

Adult↗

PubMed2002

Antiribosomal P protein antibodies in Chilean SLE patients: no association with renal disease.

The objective of this work was to determine the frequency and clinical associations of anti-ribosomal P protein antibodies (Anti-P) in a cohort of Chilean patients with systemic lupus erythematosus (SLE). Between 1996 and 1998, 141 consecutive patients with SLE were examined prospectively according with a standard protocol. Disease activity was measured by MEX-SLEDAI in 138 patients. Anti-P positivity was determined by double immune diffusion or Western blot and ELISA. Anti-P was found in 21 (15%) patients. In the Anti-P positive patients recent onset SLE (disease duration of 1 year or less) was more frequent (P = 0.018). Anti-P was found in 23% of 83 patients with active SLE vs 4% of the 55 patients with inactive SLE (Yates corrected P = 0.00479). An association with anti-dsDNA antibodies by Farr assay was observed. Anti-P positive patients had a median Farr of 65 IU/ml (1.4-1240) and Anti-P negative of 12 IU/ml (1.4-992; P-value = 0.0084). During the study only two patients had lupus psychosis and they were Anti-P positive. No association was found with liver disease (six patients, two with Anti-P antibodies) or active glomerulonephritis (22 patients four with Anti-P). Our data shows that the presence of Anti-P antibodies supports the clinical diagnosis of lupus psychosis.

Adolescent↗

PubMed1999

Systemic lupus erythematosus (SLE) and hair treatment: a large community based case-control study.

OBJECTIVE: To investigate the association of hair treatment, including permanent and non-permanent dyes, bleach, highlights and lowlights on the development of systemic lupus erythematosus (SLE). METHODS: 150 SLE patients and 300 controls from Nottingham, UK were interviewed in a case-control study. Controls were matched to cases for gender and year of birth. All patients met at least four of the American Rheumatology Association criteria for SLE. Controls were randomly selected from the Nottingham Family Health Services Authority register. Information was collected via an interview-administered questionnaire concerning demographic variables and hair treatment. RESULTS: For hair treatment no significant associations were observed between ever using permanent colouring, non-permanent colouring, bleach or lowlights, and disease. Nevertheless a significant association (OR 0.55, 95% CI 0.31-0.95) was observed between 'ever having' used highlights and disease with cases having used highlights less frequently than their healthy counterparts. No significant differences were observed in duration of usage of hair bleach, permanent colouring, non-permanent colouring, highlights and lowlights between cases and controls. CONCLUSIONS: Hair treatment or duration of hair treatment usage is not significant in the aetiology of SLE. Although patients with SLE were less likely in this study to have highlights than controls, for all other hair treatments no differences were observed.

Case-Control Studies↗

PubMed1999

Cytokine-mediated down-regulation of B cell activity in SLE: effects of interleukin-2 and transforming growth factor-beta.

We have recently reported that transforming growth factor-beta (TGF-beta) co-stimulates interleukin-2 (IL-2) activated CD8+ T cells to down-regulate antibody production. In SLE, lymphocyte production of both IL-2 and TGF-beta is decreased. Here we report that a brief treatment of PBMC from SLE patients with IL-2 and TGF-beta can result in marked inhibition of spontaneous polyclonal IgG and autoantibody production. Peripheral blood mononuclear cells (PBMC) from 12 patients with active SLE were exposed to IL-2 with or without TGF-beta for three days, washed and cultured for seven more days. The mean decrease in IgG secretion was 79%. The strongest inhibitory effect was observed in cases with the most marked B cell hyperactivity. Spontaneous production of anti-nucleoprotein (NP) antibodies was observed in four cases and cytokine treatment of PBMC decreased autoantibody production by 50-96%. IL-2 inhibited Ig production by either TGF-beta-dependent or independent mechanisms in individual patients. In a study of anti-CD2 stimulated IgG production in a patient with active SLE, we documented that IL-2 and TGF-beta reversed the enhancing effects of CD8+ T cells on IgG production and induced suppressive activity instead. These results raise the possibility that cytokine-mediated down-regulation of B cell hyperactivity in SLE may have therapeutic potential.

Adolescent↗

PubMed2003

SLE and infections.

Infections are common in systemic lupus erythematosus (SLE), and remain a source of mortality. The types of infections (such as pneumonia, urinary tract infection, cellulitis, and sepsis) in SLE patients are similar to the general population and include the same pathogens (Gram-positive and Gram-negative). SLE patients may also develop opportunistic infections, especially when treated with immunosuppressive agents. As a high-risk population, identification and treatment of chronic infections such as tuberculosis, hepatitis B, or human immunodeficiency virus (HIV), are important prior to the institution of immunosuppression to prevent reactivation or exacerbation of the infection. A common caveat is to distinguish between a lupus flare and an acute infection; judicious use of corticosteroids and cytotoxic drugs is critical in limiting infectious complications. The risk factors associated with susceptibility to disease include severe flares, active renal disease, treatment with moderate or high doses of corticosteroids and/or immunosuppressive agents, and others. Genetic factors (complement deficiencies, mannose-binding lectin, Fcgamma III, granulocyte macrophage colony-stimulating factor [GM-CSF], osteopontin) may predispose certain SLE patients to develop infections. Parameters including C-reactive protein (CRP) and adhesion molecules may help to differentiate an infectious disease from an exacerbation of the disease. Finally, the mechanism of molecular mimicry by specific microbial agents may play a role in the induction of SLE.

Bacterial Infections↗

PubMed2001

Of mice and men: the relevance of the mouse to the study of human SLE.

A number of mouse models have been utilized to study the pathophysiology of immune complex (IC) disease, and the hallmark IC disease systemic lupus erythematosus (SLE). Many of these studies have provided exciting new insights into IC-mediated inflammation and autoimmunity. However, numerous differences exist between mice and humans that suggest that mouse studies are not always applicable to human disease. These differences can be found in the biological systems that interact with circulating IC, in the specifics of disease presentation, and in the general physiology of the two species. Furthermore, although the mechanisms of SLE-like autoimmune disease in the mouse are being defined through analyses of the murine models of SLE, it remains to be proven that these mechanisms are relevant to human SLE. Thus, generalizing the results of the mouse studies to human SLE and other human IC diseases must be done with caution.

Animals↗

PubMed2003

Delay in the diagnosis of SLE: the importance of arthritis/arthralgia as the initial symptom.

Despite the current diagnostic and serologic testing for SLE, the interval between the onset of symptoms and the diagnosis is still long. In this study, we aimed to show the interval between the initial symptoms and the diagnosis of SLE and to investigate the presence of any relationship between the interval and the initial symptoms. One hundred and thirty-six patients were diagnosed with SLE using the 1982 ARA criteria. The mean age of the patients at diagnosis was 29.9 +/- 10.5 years. The mean interval between the onset of symptoms and the diagnosis of SLE was 21.82 +/- 30.32 months. The subjects were evaluated twice, at intervals of < or = 3 and < or = 12 months after the onset of symptoms. Although arthritis and/or arthralgia were the most common initial symptoms (60.3%), only 26.8% of the patients with these symptoms were diagnosed earlier than 3 months after the onset. If the first initial symptoms were butterfly rash or pericarditis, pleuritis, spontaneous abortion or cognitive dysfunction, they led to early diagnosis. In conclusion, since arthritis and/or arthralgia are the most common initial symptoms of the disease, every young woman with these symptoms should be carefully evaluated for SLE.

Adult↗

PubMed1978

Anti-DNA antibody determination in systemic lupus erythematosus (SLE). Predictive value as compared with the LE-cell test.

All pathological LE-cell tests and anti-DNA antibody determinations were registered in a prospective study over a period of 9 months at a department of internal medicine with rheumatology as a subspecialty. The results were compared with the clinical diagnosis of the patients, and correlated to SLE disease activity, as evaluated clinically and by blood analysis of five acute-phase reactants. Of 159 positive LE-cell tests, 43 were from patients with SLE, giving a diagnostic value of 27%. Of 37 positive anti-DNA antibody values, 30 were from patients having SLE, giving a diagnostic value of 81%. All of the 7 false-positive anti-DNA antibody determinations were only slightly above the normal range (22--26%: normal range less than or equal to 21%). No correlation was found between the activity of the SLE and the degree of the positive LE-cell test. Pathological levels of anti-DNA antibodies were always found when the patient had active SLE--clinically and by elevation of acute phase reactants. On the other hand, it was impossible to evaluate the disease activity from the level of the anti-DNA antibody test. It is concluded that the anti-DNA antibody determination should be preferred to the LE-cell test in the evaluation of patients with connective tissue diseases.

Antibodies↗