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PubMed1994

Epidemiology, genetics, etiology, and environment relationships of systemic lupus erythematosus.

Systemic lupus erythematosus continues to provide a major etiologic challenge. Current investigation is focusing on the possibilities of environmental factors, including infection. How these factors are related to genetic factors, including the major histocompatibility complex and more recently observed defects in apoptosis genes, remains unclear. Ethnic and geographic studies of systemic lupus erythematosus are providing important clues, as are continued clinical observations on the various subsets of disease and the patterns of therapeutic response. Different pathogenic mechanisms are constantly being uncovered and in turn need to be related to the various etiologies.

Contraceptives, Oral↗
PubMed1990

Identification of human immunodeficiency virus hybridizing sequences in the peripheral blood of a patient with systemic lupus erythematosus.

Systemic lupus erythematosus, a multisystemic disorder, is considered a prototype of the autoimmune diseases. Although its cause remains unknown, a viral etiology has been proposed. We report that a rapid and sensitive messenger RNA in situ hybridization technique detected hybridizing sequences to the human immunodeficiency virus type in the peripheral blood cells of a woman with systemic lupus erythematosus in whom the presence of acquired immuno-deficiency syndrome was reasonably excluded.

Adult↗
PubMed2001

The role of Epstein-Barr virus in systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a devastating autoimmune disease with no known cure. Lupus patients suffer from a myriad of clinical symptoms which variably include arthritis, pleuritis, pericarditis, vasculitis, and nephritis. The underlying mechanisms behind these clinical findings and the etiologic events preceding and causing disease onset, however, remain largely unknown. For many years, investigators have suspected that Epstein-Barr virus might somehow be involved in the etiology and/or pathogenesis of systemic lupus. Numerous studies have examined this possibility from various angles and have arrived at different conclusions. This work reviews these historical papers in the context of new results and presents a hypothetical role for this virus as an etiological environmental trigger for SLE.

Antibodies, Viral↗
PubMed2002

A role for the Cr2 gene in modifying autoantibody production in systemic lupus erythematosus.

Systemic lupus erythematosus is an autoimmune disease characterized by autoantibody production against nuclear Ags. Recent studies suggest that the Cr2 gene, which encodes for complement receptor (CR)1 and CR2, is important in disease susceptibility. Because the precise disease phenotype related to this gene, in isolation or in relation to other genetic loci, is not known, we analyzed C57BL/6 mice with a targeted mutation in Cr2 (C57BL/6.Cr2(-/-)) with or without a concomitant mutation in Fas (C57BL/6.lpr Cr2(-/-)). The Cr2(null) mutation in a C57BL/6.lpr background markedly increases the serum concentrations of IgG1 and IgG2b and the levels of antinuclear and anti-dsDNA Abs as compared with C57BL/6.lpr controls. There is also a trend for higher concentrations of IgG2a and IgG3. In contrast, isolated deficiencies in either these CRs or Fas have a limited effect in the production of anti-dsDNA Abs. Moreover, the Cr2(null) mutation does not affect other disease manifestations. These findings demonstrate that abnormalities in CR1 and CR2 may be linked to the production of autoantibodies by modifying the effect of other systemic lupus erythematosus susceptibility genes. Phenotypic expression of other disease manifestations need additional Cr2-independent genetic factors.

Animals↗
PubMed2003

Apoptosis in systemic lupus erythematosus.

Systemic lupus erythematosus is a complex, multisystem autoimmune disease characterized by production of high-titer autoantibodies directed against ubiquitously expressed self-antigens. Autoantigens in systemic lupus erythematosus are highly diverse in terms of structure and location in control cells, but become clustered in and on the surface blebs of apoptotic cells. The past several years have provided significant evidence that the apoptotic cell plays a central role in tolerizing B cells and T cells to both tissue-specific and ubiquitously expressed self-antigens, and may drive the autoimmune response in systemic autoimmune disease. The authors review the significant recent advances in this area. Recent studies suggest that predisposing factors to subsequent development of systemic autoimmunity may be the incomplete induction of tolerance to apoptotic antigens, potentially through abnormal apoptotic signaling and effector pathways, decreased apoptotic cell clearance, or abnormal signaling thresholds on responding lymphocytes. In such genetically susceptible hosts, proinflammatory events at the host-environment-immune system interface that lead to the binary change in the response to apoptotic material from tolerance to immunity may be responsible for initiation of autoimmunity and subsequent disease amplification. Such pathways may be amenable to therapeutic and preventive interventions.

Apoptosis↗
PubMed1986

Autoimmunity, fetal losses, lupus anticoagulant: beginning of systemic lupus erythematosus or new autoimmune entity with gynaeco-obstetrical expression?

Among the various autoantibodies commonly found in women with systemic lupus erythematosus, the so-called lupus anticoagulant has been described in association with fetal losses. Recently, women with repeated spontaneous abortions and lupus anticoagulant, but no apparent systemic lupus erythematosus have been described. We have studied prospectively the possible connections between fetal losses and autoimmunity in a large control study of 130 idiopathic habitual aborters. These non-pregnant patients without any antecedent autoimmune disease were explored for the presence for autoantibodies especially lupus anticoagulant. Ten percent of the patients exhibit an antithromboplastin antibody (lupus anticoagulant) and half of this group possesses a striking association of biological manifestations of autoimmunity. In conclusion, two points appear: firstly, statistical correlation is demonstrated between antithromboplastin antibody and habitual abortion; secondly, doubt remains about the significance of the association between autoimmunity, fetal losses and antithromboplastin: beginning of systemic lupus erythematosus or new autoimmune entity with gynaeco-obstetrical expression.

Abortion, Habitual↗
PubMed2000

The Systemic Lupus International Collaborating Clinics/American College of Rheumatology (SLICC/ACR) Damage Index for Systemic Lupus Erythematosus International Comparison.

OBJECTIVE: To compare patients with systemic lupus erythematosus (SLE) from different centers with respect to demographics and Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index (SLICC/ACR DI) scores, and to assess whether the SLICC/ACR DI changed over time, and whether initial DI scores were related to outcome. METHODS: Members of SLICC completed DI scores and patient demographics on patients followed in their centers. Information was provided at 2, 5-10, and > 10 years of followup. Data were entered on computer and analyzed on SPSS/PC+ and SAS using descriptive statistics and analysis of variance. RESULTS: Information for 1297 patients within 2 years of first clinic visit was submitted from 8 centers. There were 1187 women and 110 men with a mean age at diagnosis of SLE of 32 years. Seven hundred sixty-two were Caucasian, 423 were black, and the remainder were of other races. There were more blacks in the American centers than in Canadian or European centers. Five centers provided information for the 3 time periods. The DI increased over time. Ninety-nine patients had died. Higher SLICC/ACR DI scores were documented in patients who went on to die. CONCLUSION: The SLICC/ACR DI is a valid measure for damage in SLE.

American Medical Association↗
PubMed2002

High predictive value of the Systemic Lupus International Collaborating Clinics/American College of Rheumatology damage index for survival in systemic lupus erythematosus.

OBJECTIVE: We previously reported high Systemic Lupus International Collaborating Clinics (SLICC) scores in fatal cases of systemic lupus erythematosus (SLE) from our inception cohort. This study was done to clarify if the SLICC damage scores 5 years after diagnosis predicted the outcome. METHODS: We studied 80 patients with SLE (70 women, 10 men), all enrolled and diagnosed during the years 1981 through 1991 in our inception cohort, and all alive 5 years after inclusion into the cohort. In all patients the SLICC/American College of Rheumatology (ACR) damage index (DI) was scored at 5 years after SLE diagnosis, and these scores were tested for predictive value. The outcomes were survival or late mortality within the following median observation period of 7 years. All surviving patients were followed through 1999, and no patient was lost to followup. RESULTS: At study entry, 5 years after the diagnosis of SLE, 37 patients had no damage to score with SLICC. Of the remaining 43 patients, 25 had a score of 1 and 18 had a score of 2 or more. In total, 14 fatalities occurred within 7 years after study entry, 7 among the 18 with initial SLICC/ACR DI of 2 or more compared with 7 fatalities among the 62 with less or no damage (p < 0.01). Cardiovascular or cerebrovascular SLICC/ACR DI items were more common in fatal cases than in survivors (p < 0.001). A SLICC score at 5 years of 2 or more increased the relative risk for fatality by 3.4 (95% CI 1.5-14.4), and had a predictive value of 38%. A SLICC score of 0 at 5 years gave an odds ratio in favor of survival of 0.06 (95% CI 0.0-0.5) and had a predictive value for survival of 97%. During an extended followup for one more year the predictive value of damage for fatalities was even more pronounced (p = 0.003, log-rank). CONCLUSION: SLICC damage scores registered 5 years after SLE diagnosis have a high predictive value for survival during the following median observation time of 7 years. These data provide strong evidence that the items included in the SLICC score are clinically relevant.

Adult↗
PubMed2000

Lipids, cardiovascular disease and atherosclerosis in systemic lupus erythematosus.

Systemic lupus erythematosus is commonly associated with early onset cardiovascular disease and is often associated with hyperlipidaemia. This review examines the evidence for an increased prevalence of both CHD and hyperlipidaemia in SLE and mechanisms by which autoimmunity in SLE could accelerate the progression of atheroma. It postulates how lipid lowering therapies used in cardiological disease might help reduce the incidence of CHD in SLE.

Arteriosclerosis↗
PubMed2002

A novel susceptibility locus on chromosome 2 in the (New Zealand Black x New Zealand White)F1 hybrid mouse model of systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is inherited as a complex polygenic trait. (New Zealand Black (NZB) x New Zealand White (NZW)) F(1) hybrid mice develop symptoms that remarkably resemble human SLE, but (NZB x PL/J)F(1) hybrids do not develop lupus. Our study was conducted using (NZW x PL/J)F(1) x NZB (BWP) mice to determine the effects of the PL/J and the NZW genome on disease. Forty-five percent of BWP female mice had significant proteinuria and 25% died before 12 mo of age compared with (NZB x NZW)F(1) mice in which >90% developed severe renal disease and died before 12 mo. The analysis of BWP mice revealed a novel locus (chi(2) = 25.0; p < 1 x 10(-6); log of likelihood = 6.6 for mortality) designated Wbw1 on chromosome 2, which apparently plays an important role in the development of the disease. We also observed that both H-2 class II (the u haplotype) and TNF-alpha (TNF(z) allele) appear to contribute to the disease. A suggestive linkage to proteinuria and death was found for an NZW allele (designated Wbw2) telomeric to the H-2 locus. The NZW allele that overlaps with the previously described locus Sle1c at the telomeric part of chromosome 1 was associated with antinuclear autoantibody production in the present study. Furthermore, the previously identified Sle and Lbw susceptibility loci were associated with an increased incidence of disease. Thus, multiple NZW alleles including the Wbw1 allele discovered in this study contribute to disease induction, in conjunction with the NZB genome, and the PL/J genome appears to be protective.

Alleles↗
PubMed2001

[Significance of anti-nucleosome (anti-chromatin) auto-antibodies in systemic lupus erythematosus].

Systemic lupus erythematosus is characterised by the presence of antinuclear autoantibodies (ANA). Native DNA, histone proteins and small nuclear ribonucleoproteins (snRNP) are the main targets of these ANA-s, but some of them may derive against the entire chromatin, which is composed of the listed elements, and also against its fundamental unit, that is nucleosome. Authors investigated at the first time the frequency and the concentration of anti-nucleosome antibodies in a group of 107 consecutively selected Hungarian lupus patients. They calculated correlation between these parameters and the activity as well as organ--mainly kidney--manifestations of the disease. The frequencies of positive anti-nucleosome, anti-dsDNA and anti-histone antibodies were 39.2, 28.0 and 47.6%, respectively. All the three autoantibodies were present more frequently in cases with lupus nephritis, and this correlation was significant by statistical respect. Also a positive correlation was found between the concentration of these autoantibodies and activity of the diseases (SLE-DAI). Results suggest that long disease duration (mean 8.5 year) and consequently low disease activity (mean DAI: 3.28) may stand at the background of the relatively low occurrence of the measured ANA-s. Besides anti-dsDNA, the determination of anti-nucleosome and anti-histone antibodies can be useful in the diagnosis and monitoring of SLE. Authors discuss the possible role of anti-nucleosome autoantibodies in the pathogenesis of lupus nephritis.

Adult↗
PubMed2004

[Lipid profile in patients with systemic lupus erythematosus, with special focus on lipoprotein(a) in lupus nephritis].

Systemic lupus erythematosus (SLE) is a multifactorial polysystemic autoimmune disorder. Although life expectance in SLE has been improved by adequate immune suppressive therapy, the importance of chronic renal failure has not been reduced. Among late complications of the disease accelerated atherosclerosis attempts increasing attention. Dyslipoproteinemia and increased concentration of lipoproteins are important risk factors of atherosclerotic cardiovascular complication in SLE. Serum lipid parameters of 50 patients with lupus were examined in the present work. Thirty patients had histologically proven lupus nephritis (LN+), while the other group did not have renal involvement (LN-). Serum triglyceride, total cholesterol, LDL-C and apolipoprotein B (apoB) concentrations were significantly higher in the lupus nephritis (LN+) group. On the other hand, HDL-C and apoAI levels were also elevated in patients with LN. As a consequence of that, LDL-C/HDL-C and the apoB/apoAI ratios did not differ between patients with or without kidney involvement. This concluded the authors to measure the concentration of lipoprotein (a) in SLE patients, as Lp(a) is known to be an independent risk factor of atherosclerosis. Results indicated a significantly increased Lp(a) concentration in patients with lupus nephritis as compared to the LN- group. All but 2 patients without kidney involvement had lower than 100 mg/L Lp(a) concentration, while 27% of patients with lupus nephritis has an Lp(a) level between 100-300 mg/L. Further more, Lp(a) concentration was higher than 300 mg/L in 13% of the LN+ group. In a good correlation of these observations patients with nephritis suffered more frequently from deep venous thrombosis and ischaemic heart disease. The frequencies of hypertension and non-insulin dependent diabetes mellitus were slightly elevated in patients with nephritis. Present results suggest the importance of elevated lipoprotein (a) concentration in patients with lupus nephritis, further increasing the risk of athero-thrombotic cardiovascular complications.

Adult↗
PubMedDate not supplied

Posture in systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a connective autoimmune disease that may involve many organ systems and neural function impairment. Postural apparatus dysfunction in SLE may develop in the case of central and peripheral neural involvement. We studied the presence of postural abnormalities in SLE patients with different degrees of disease activity. Twenty-eight subjects (18 SLE patients and 10 normal controls) underwent postural evaluation by means of Static Computerised Posturography. Disease severity or specific clinical problems did not form selection criteria. Lupus activity was assessed using the Systemic Lupus Activity Measure (SLAM). A statistically significant (p < 0.05) increase in the parameters of trace length, trace surface, trace velocity, standard deviation in velocity, and Fast Fourier trX and Y (FET), were found in both the closed and opened eyes tests, when lupus patients were compared to controls subjects. No significant pattern variation in posture was observed between more active and less active SLE patients. Postural control alterations in SLE may be considered a complication of the chronic autoimmune inflammatory process, independent of disease activity as evaluated by the SLAM index. The site of the neuropathy remains uncertain, although we believe it to be peripheral rather than central in origin due to the absence of symptoms or clinical signs of CNS involvement or vascular degeneration.

Adult↗
PubMed1996

[Nephrotic syndrome in systemic lupus erythematosus].

Systemic lupus erythematosus as one of the most important connective tissue diseases represents an outstanding disease commonly associated with nephrotic syndrome. The author reviews important facts relating to ethology and pathogenesis of the disease emphasising the renal involvement. Personal observations concerning systemic lupus erythematosus as an ethological factor of nephrotic syndrome as well as relevant diagnostic and therapeutic procedures are presented.

Humans↗
PubMed2005

Systemic lupus erythematosus due to Epstein-Barr virus or Epstein-Barr virus infection provocating acute exacerbation of systemic lupus erythematosus?

Systemic lupus erythematosus (SLE) is a rheumatologic disease characterized by an inflammatory destruction of the target organ systems of the body in an unknown way by autoantibodies formed against self-antigens. Infectious agents like Epstein-Barr virus (EBV), cytomegalovirus and parvovirus B19 may have a role in the occurrence or the exacerbation of the SLE. In this report, the clinical follow-up of a 14-year-old girl diagnosed with SLE following an EBV infection with bicytopenia, lymphadenomegaly and hepatomegaly is discussed. This case could support the role of viral infections in the etiology of SLE.

Adolescent↗
PubMed2005

Association analysis of the R620W polymorphism of protein tyrosine phosphatase PTPN22 in systemic lupus erythematosus families: increased T allele frequency in systemic lupus erythematosus patients with autoimmune thyroid disease.

OBJECTIVE: Recent case-control studies show associations of the minor T allele (of the C1858T single-nucleotide polymorphism corresponding to the R620W amino acid substitution) of PTPN22 with multiple autoimmune diseases, including systemic lupus erythematosus (SLE). We performed family-based association studies of this polymorphism in 4 independent cohorts containing SLE patients and their parents and/or other family members. METHODS: A total of 2,689 individuals from 902 independent Caucasian families with SLE were genotyped using polymerase chain reaction pyrosequencing (cohorts 1 and 2) and the Sequenom MassArray system (cohorts 3 and 4). The transmission disequilibrium test (TDT) and the pedigree disequilibrium test (PDT) were conducted to assess the evidence of association. RESULTS: The 1858 C > T allele frequencies of the parents showed no deviation from Hardy-Weinberg equilibrium within each cohort. No evidence of preferential transmission of the T allele from heterozygous parents to their affected offspring was observed in each of the 4 cohorts or in the combined sample. Consistent with the TDT result, the PDT analysis revealed no significant association between the T allele and SLE. In 54 of the 661 SLE patients (cohorts 1 and 3) with documented autoimmune thyroid disease, the T allele frequency was higher than in individuals with SLE alone (16.7% versus 8.5%; P = 0.008, odds ratio 2.16 [95% confidence interval 1.25-3.72]). CONCLUSION: The R620W polymorphism of the PTPN22 gene is not a major risk allele for SLE susceptibility in our sample of Caucasian individuals from northern America, the UK, or Finland, but it appears to be a risk factor for the concurrent autoimmune diseases of autoimmune thyroid disease and SLE.

Arginine↗
PubMed1997

The reliability of the Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index in patients with systemic lupus erythematosus.

OBJECTIVE: To test the reliability of the Systemic Lupus International Collaborating Clinics/American College of Rheumatology (SLICC/ACR) Damage Index and the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) in the assessment of patients with SLE. METHODS: Ten patients with SLE, representing a spectrum of damage and activity, were included. Each patient was examined by 6 of 10 physicians from 5 countries, representing 10 lupus clinics. The SLICC/ACR Damage Index was used to assess accumulated damage, and the SLEDAI was used to assess disease activity. The order of the patients and physicians was randomized according to a Youden square design. RESULTS: The SLICC/ACR Damage Index detected differences among patients (P < 0.001). There was no detectable observer difference (P = 0.933), and there was no order effect (P = 0.261). Similar results were obtained with the SLEDAI. There was concordance in the SLICC/ACR Damage Index among observers, despite a wide spectrum of disease activity detected by the SLEDAI. CONCLUSION: Physicians from different centers are able to assess patients with SLE in a reproducible way, using the SLEDAI to assess disease activity and the SLICC/ACR Damage Index to assess accumulated damage.

Adult↗
PubMed1991

Systemic lupus erythematosus after renal transplantation: patient and graft survival and disease activity. The Dutch Working Party on Systemic Lupus Erythematosus.

OBJECTIVE: To determine the outcome of renal transplantation in patients with systemic lupus erythematosus and end-stage renal failure and to compare disease activity after transplantation with disease activity before transplantation. DESIGN: Retrospective case finding using data for an 8-year period from the central registry for renal replacement therapy in The Netherlands. SETTING: Tertiary care hospitals with facilities for renal transplantation in the Netherlands. PATIENTS: Twenty-eight patients who fulfilled at least four of the American Rheumatology Association's criteria for the classification of systemic lupus erythematosus and who received a renal transplant. MEASUREMENTS: Actuarial survival rates for grafts and patients after transplantation, maximal nonrenal scores on the Systemic Lupus Erythematosus Disease Activity Index, and time-adjusted disease exacerbation rates in all patients before and after transplantation. RESULTS: The actuarial graft survival rate at 1 year and 5 years was 68% (95% CI, 47% to 82%) and 54% (CI, 25% to 77%), respectively, whereas the actuarial patient survival rate was 87% (CI, 69% to 96%) at 1 and 5 years. High disease activity was not found to affect graft survival adversely before the start of renal replacement therapy or during dialysis. After transplantation, disease activity per patient and the overall incidence of disease exacerbations decreased. One case of recurrent lupus nephritis was seen. CONCLUSIONS: Patients with systemic lupus erythematosus and end-stage renal failure are excellent candidates for renal transplantation; disease activity after transplantation is sporadic and low, and the recurrence of lupus nephritis is rare.

Actuarial Analysis↗