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PubMed2005

Association between physician volume and in-hospital mortality in patients with systemic lupus erythematosus.

OBJECTIVE: Systemic lupus erythematosus (SLE) is an uncommon, clinically complex disease for which prior experience treating similar patients may be particularly important. This study was undertaken to determine if physician volume is associated with the outcome of hospitalization of patients with SLE. METHODS: Data on in-hospital mortality in a population-based sample of 15,509 patients with SLE ages 18 years or older who were hospitalized in 2000, 2001, or 2002 in New York or Pennsylvania were obtained from state health planning agencies. Risks of in-hospital mortality were examined in relation to the average annual number of patients with SLE hospitalized by the admitting physician. RESULTS: Physician volume was inversely associated with mortality. Mortality was 4.1% among patients of physicians who treated <1 hospitalized patient with SLE per year, 3.5% among patients of physicians who treated 1-3 patients per year, and 2.5% among patients of physicians who treated >3 patients per year. After adjustment for demographic characteristics, severity of illness, and hospital characteristics, the mortality risk was 20% lower among patients in the middle category of physician volume (odds ratio 0.80, 95% confidence interval 0.66-0.96, P =0.02), and 42% lower among patients in the highest category of physician volume (odds ratio 0.58, 95% confidence interval 0.42-0.82, P = 0.002), compared with patients in the lowest category. The association was stronger among patients with nephritis (n = 2,673), for whom the adjusted odds of mortality were approximately 60% lower among those in the highest category of physician volume. CONCLUSION: Our findings indicate that higher disease-specific physician volume is associated with lower risks of in-hospital mortality in patients with SLE.

Female↗
PubMed2006

Rapamycin reduces disease activity and normalizes T cell activation-induced calcium fluxing in patients with systemic lupus erythematosus.

OBJECTIVE: Systemic lupus erythematosus (SLE) is an autoimmune disease of unknown origin. Current treatment options are often ineffective or poorly tolerated. Recent observations have revealed mitochondrial hyperpolarization and enhanced Ca2+ fluxing in T cells from SLE patients. Rapamycin, a lipophilic macrolide antibiotic that regulates mitochondrial transmembrane potential and Ca2+ fluxing, has been used safely and effectively to treat renal transplant rejection since 1999. In addition, rapamycin has been shown to ameliorate T cell function and to prolong survival in lupus-prone MRL/lpr mice. We therefore undertook the present study to investigate whether rapamycin is beneficial in patients with SLE. METHODS: Nine patients with clinically active SLE that had been treated unsuccessfully with other immunosuppressive medications began therapy with rapamycin, 2 mg/day orally. Disease activity was assessed with the British Isles Lupus Assessment Group (BILAG) score, SLE Disease Activity Index (SLEDAI), and requirement for prednisone therapy. Mitochondrial transmembrane potential and Ca2+ fluxing were assessed by flow cytometry. RESULTS: In patients treated with rapamycin, the BILAG score was reduced by a mean +/- SEM of 1.93 +/- 0.9 (P = 0.0218), the SLEDAI by 5.3 +/- 0.8 (P = 0.00002), and concurrent prednisone use by 26.4 +/- 6.7 mg/day (P = 0.0062) compared with pre-rapamycin treatment. While mitochondrial hyperpolarization persisted, pretreatment cytosolic and mitochondrial Ca2+ levels and T cell activation-induced rapid Ca2+ fluxing were normalized in rapamycin-treated patients. CONCLUSION: Rapamycin appears to be a safe and effective therapy for SLE that has been refractory to traditional medications. Mitochondrial dysfunction and Ca2+ fluxing could serve as biomarkers to guide decisions regarding future therapeutic interventions in SLE.

Adolescent↗
PubMed1996

Evaluation of the BCL-2 gene locus as a susceptibility locus linked to the clinical expression of systemic lupus erythematosus (SLE).

Systemic lupus erythematosus (SLE) is an autoimmune disease characterised by the production of a large number of autoantibodies. It has been postulated that this may be the result of prolonged longevity of auto-reactive B cells due to defective regulation of programmed cell death (apoptosis). The proto-oncogene bcl-2 is involved in the control of apoptosis in immunocompetent cells, and its over-expression is noted in T and B cells from SLE patients. This study examined the genetic linkage between the bcl-2 gene locus and SLE susceptibility using the affected sib-pair method in SLE families. Seventeen caucasian multiplex families were evaluated. A polymorphic microsatellite marker closely linked to the bcl-2 gene on 18q21.3 was used to determine the bcl-2 genotype. We demonstrated that haplotype sharing among the affected sibling pairs was not statistically different from random (P > 0.5). This suggests that the bcl-2 gene locus does not confer a genetic susceptibility to SLE expression.

Alleles↗
PubMed2002

Initial presentation of hemolytic uremic syndrome in a boy with systemic lupus erythematosus.

Associating systemic lupus erythematosus (SLE) with an initial presentation of hemolytic uremic syndrome (HUS) is rare. We report on a 13-year-old boy admitted to our hospital with an initial complaint of bilateral knee pain and multiple petechiae on both lower extremities. Diagnosis of atypical HUS was established according to the clinical triad of HUS without a veriotoxin-producing organism in his stool and the pathological finding compatible to thrombotic microangiopathy. In addition, his symptoms fulfilled the 1982 revised criteria for the classification of SLE. After methylprednisolone and cyclophosphamide pulse therapies, his laboratory findings and general condition improved. No plasmapheresis or any plasma infusion was required.

Adolescent↗
PubMed2006

Novel cardiovascular risk factors and cardiac event predictors in female inactive systemic lupus erythematosus patients.

Systemic lupus erythematosus (SLE) is associated with severe and premature cardiovascular disease, which cannot be explained by traditional risk factors alone. This study aims to investigate novel cardiovascular risk factors and cardiac event predictors in inactive SLE female patients who do not have any major cardiovascular risk factors. Twenty-five inactive (SLE disease activity index score <4) SLE female patients and 22 healthy control women were studied. SLE patients with a history of diabetes mellitus, hypertension, hyperlipidemia, smoking, or coronary artery disease (CAD) were excluded. Venous blood samples were analyzed for lipid subfractions and novel cardiovascular risk factors such as lipoprotein (a), homocysteine, fibrinogen, high-sensitivity C-reactive protein (hs-CRP), and serum amyloid A (SAA) levels. Endothelial dysfunction was assessed by flow-mediated dilatation (FMD) from the brachial artery at baseline and during reactive hyperemia. SLE patients and controls were similar in terms of age (40+/-10 years vs 38+/-10 years, p = NS). No significant difference was found between the groups regarding family history of premature CAD, blood pressure, body mass index, lipoprotein (a), homocysteine, fibrinogen, SAA, apoprotein A-1 and B levels. Compared with the controls, SLE patients had higher levels of hs-CRP [median (range): 1.82 (0.02-0.98) vs 0.68 (0.02-0.35), p=0.04]. FMD was lower in SLE patients than controls (7.1+/-2.1 vs 11.4+/-1.2%, p<0.001). Increased levels of hs-CRP and decreased FMD were found in inactive SLE patients. Increased hs-CRP levels may reflect ongoing low-grade inflammation that could be a cause of impaired FMD in SLE patients. These findings suggest that SLE patients without traditional major cardiovascular risk factors may have increased risk of cardiovascular disease and future cardiac events.

Adult↗
PubMed1992

Insoluble DNA-like phosphorylated polystyrene: specific interactions with anti-DNA antibodies from systemic lupus erythematosus patients.

Systemic lupus erythematosus (SLE) is an autoimmune disease. Antibodies directed mainly against DNA and/or phospholipids are present in the serum of SLE patients. Therefore phosphorylated polystyrene derivatives acting as DNA-like polymers should be able to interact with the SLE anti-DNA antibodies. Such functional polymers were synthesized and subsequently their interactions with the anti-DNA antibodies studied. Adsorption experiments performed with both anti-DNA antibodies and normal immunoglobulins showed high affinity constants of the phosphorylated polymer for anti-DNA antibodies (4 x 10(9) M-1) whereas for normal IgG the affinity was low (2 x 10(5) M-1). Moreover, the interaction was specific involving the idiotypic moiety of the anti-DNA antibodies and an array of phosphoester groups at the surface of this biomaterial.

Adsorption↗
PubMed2005

Attempt to correct abnormal signal transduction in T lymphocytes from systemic lupus erythematosus patients.

Systemic lupus erythematosus (SLE) is an autoimmune disease, which predominantly affects females, and causes multiple organ dysfunctions. Recent studies have revealed the underlying immunological abnormalities, especially in lymphocytes from SLE patients. T lymphocytes from SLE patients present abnormalities in T cell receptor (TCR) signaling, for example, decreased expression of TCR zeta chain, PKC theta, and NF-kB p65, decreased PKC dependent protein phosphorylation, impaired translocation of NF-kB p65, decreased production of IL-2 etc. Recently, it is known that reconstitution of deficient TCR zeta chain in T lymphocytes from SLE patients leads to restoration of impaired IL-2 production upon CD3/CD28 stimulation. This time, analysis of abnormal TCR signaling in SLE patients and attempt to correct the impaired IL-2 production by replenishing missing signaling molecules are to be discussed.

Genetic Therapy↗
PubMed2005

Increased prevalence of transfusion-transmitted virus and cross-reactivity with immunodominant epitopes of the HRES-1/p28 endogenous retroviral autoantigen in patients with systemic lupus erythematosus.

OBJECTIVE: Systemic lupus erythematosus (SLE) patients produce autoantibodies to HRES-1/p28, a human endogenous retrovirus-encoded nuclear protein. To identify cross-reactive viral antigens capable of triggering autoreactivity, HRES-1/p28 epitopes were mapped by SLE antibodies. METHODS: Forty-four peptides overlapping HRES-1/p28 and 13 viral peptides were synthesized on cellulose membrane and tested for recognition by antibodies from 16 HRES-1 Western blot seropositive SLE patients. Transfusion-transmitted virus (TTV) was detected by gene amplification in sera of 211 SLE patients, 78 healthy SLE family members, 199 unrelated healthy donors, and 91 rheumatoid arthritis (RA) patients. RESULTS: HRES-1/p28 residues 41-55, 121-135, and 156-170 were recognized by 12/16 (75.0%), 11/16 (68.8%), and 9/16 lupus sera (56.25%) and considered immunodominant. HRES-1/p28 residues 121-135 harbor cross-reactive epitope with retroviral peptides and the 70 K U1snRNP lupus autoantigen. HRES-1/p28 residues 41-55 and 156-170 exhibited the highest prevalence of cross-reactivity with TTV peptide ORF2a (14/16, 87%). Prevalence of TTV DNA was increased in lupus patients (120/211) with respect to healthy (66/199; P < 0.0001) or RA controls (23/91; P < 0.0001). TTV prevalence in healthy lupus relatives (40/78) was decreased with respect to lupus patients (80/121; P = 0.0184) and increased with respect to unrelated healthy donors (66/199; P = 0.0026). HRES-1/p28 Western blot reactivity was observed in 12/23 TTV PCR-negative donors and 43/58 TTV PCR-positive donors (P < 0.0281). CONCLUSIONS: Increased prevalence of TTV and molecular mimicry with HRES-1/p28 may contribute to generation of antinuclear antibodies and pathogenesis of SLE.

Adult↗
PubMed2004

HLA class II haplotypes in Mexican systemic lupus erythematosus patients.

Systemic lupus erythematosus (SLE) is an autoimmune disease in which polymorphisms within the human leukocyte antigen (HLA) region have been associated to its etiology. For this study, HLA-DQB1, DQA1, and DRB1 genes were typed by polymerase chain reaction-sequence-specific primer in 237 individuals, taken from 74 families, who had a member with SLE, and who had their residence in the western region of Mexico; as well as in 159 ethnically matched healthy volunteers taken from 32 families. Genotype and allele frequency analysis was performed in 74 SLE patients and 54 unrelated controls. Precise three-loci identification of independent haplotypes was performed in 48 patients and 54 controls by familial segregation. Genotype distribution at each loci was concordant with Hardy-Weinberg's equilibrium in the control group. In general, no genotype effect was observed in SLE patients. Allele distribution comparison showed in the SLE group a significant increase of HLA-DQA1*0102, DQB1*0402, and DRB1*15; whereas alleles HLA-DQB1*0303 and *0501 were significantly decreased. SLE patients showed haplotype DQB1*0602-DQA1-*0102-DRB1*15 increased. As expected, patients with SLE have a reduced haplotype genetic diversity. The associations found in this study are related to an ancestral haplotype that has been observed in SLE populations of different origins.

Adolescent↗
PubMed1996

Necrotizing lymphadenitis associated with systemic lupus erythematosus.

OBJECTIVE: Systemic lupus erythematosus (SLE) may have protean manifestations, including necrotizing lymphadenitis. After describing an illustrative case, we discuss the incidence, clinical features, and pathologic findings of SLE-associated necrotizing lymphadenitis. METHODS: A case of SLE associated with necrotizing lymphadenitis is reported. The patient's clinical presentation, course, and response to therapy is detailed. The literature on lupus lymphadenitis is reviewed. RESULTS: A young man who presented with a febrile illness characterized by multifocal necrotizing lymphadenitis is described. Glomerulonephritis, meningo-encephalitis, pericarditis, and hemolytic anemia evolved. The diagnosis of SLE was based on the clinical features, positive antinuclear antibody (ANA), and characteristic renal biopsy. High dose corticosteroids and cyclophosphamide induced a complete remission. In recent series from the literature the prevalence of lymphadenopathy was 12% to 59% of patients with SLE. The most common nodal groups involved were cervical (43%), mesenteric (21%), axillary (18%), and inguinal (17%). Lymph node pathology was characterized by paracortical foci of necrosis and infiltration by histiocytes, lymphocytes, plasma cells, and immunoblasts. The hematoxylin body, an amorphic aggregate of basophilic material, was pathognomonic of lupus lymphadenitis. The necrotizing lymphadenitis of SLE is pathologically similar to Kikuchi-Fujumoto disease (KFD), a distinctive, self-limited form of necrotizing lymphadenitis. The pathologic and clinical literature support a close link between SLE and KFD. CONCLUSIONS: SLE can be complicated by necrotizing lymphadenitis, with distinctive pathologic features. Lupus lymphadenitis and KFD share some common clinical and pathologic features, supporting a relationship between the disorders.

Adult↗
PubMed1998

Anti-T-cell receptor therapy in murine experimental systemic lupus erythematosus.

Experimental systemic lupus erythematosus (SLE), similar to that observed after immunization with the human anti-DNA mAb 16/6 Id+, could be induced in mice by injection of 16/6 Id specific T-cell lines. The above T-cell lines were exclusively CD4+ CD8- and the majority of cells expressed the Vbeta8 T-cell receptor (TCR) gene products. Furthermore, lymph node cells of mice immunized with the 16/6 Id were enriched with CD4+ Vbeta8+ T-cells. The TCR used by 16/6 Id-specific T-cells showed a limited homology in their CDR3 junctional regions. Nevertheless, mice injected with the anti-Vbeta8 mAb developed autoantibody titers that were not significantly different from those found in the non-treated, 16/6 Id-injected group.

Amino Acid Sequence↗
PubMed2002

Pregnancy in women with systemic lupus erythematosus.

BACKGROUND: Systemic lupus erythematosus (SLE) is an autoimmune disorder which may be affected by hormonal changes, such as those of pregnancy. Women with SLE have increased adverse pregnancy outcomes. STUDY DESIGN: A retrospective analysis of the gynecologic and immunologic case history of 140 women with SLE and the outcome of 263 pregnancies in 99 women with SLE. RESULTS: In patients diagnosed with SLE, the proportion of pregnancies ending with live birth at term decreased to one-third compared with three quarters in those without a diagnosis of SLE and the incidence of pre-term deliveries and spontaneous abortions increased by 6.8 and 4.7 times, respectively. When SLE was associated with secondary antiphospholipid (APL) syndrome, and lupus anticoagulant (LA) or beta2-glycoprotein antibodies were present, a further increase in the incidence of pregnancy loss was observed. Pregnancy did not cause a flare-up of SLE in all cases, the disease remained stable in about 30% of the patients. Lupus was mild in the majority of the women who carried out their pregnancy to term. We also observed mothers with active SLE who successfully carried out pregnancies to term. CONCLUSION: These findings accord with previous literature and should inform rheumatologists, obstetricians and neonatologists who guide patients in their reproductive decisions.

Adolescent↗
PubMed2004

Gender differences in systemic lupus erythematosus.

BACKGROUND: Systemic lupus erythematosus (SLE) is known to be much more prevalent in females than in males, but the cause of this sexual predilection is not established. In addition, much controversy surrounds the differences in manifestations of SLE in both sexes. OBJECTIVE: This article reviews the possible etiologies of the greater prevalence of SLE in females, as well as the differences in the clinical presentation of the disease in both sexes. METHODS: Relevant studies were identified through a PubMed search for articles published between 1960 and 2001; no language restrictions were applied. Search terms included lupus, SLE, and gender differences. Books and online resources were also consulted. RESULTS: Potential causes of the female predilection for SLE included the effects of estrogen and its hydroxylation, decreased androgen levels, hyperprolactinemia, and differences in gonadotropin-releasing hormone (GnRH) signaling. Clinical manifestations of SLE included females having more frequent relapses, but the incidence of severe relapses was the same in both sexes. Raynaud phenomenon, arthritis, and leukopenia were more common in women, whereas skin manifestations, serositis, and renal involvement were more common in men. For neurologic manifestations, females with SLE experienced more psychiatric symptoms and headaches, whereas males with SLE experienced more seizures and peripheral neuropathy. Males with SLE also tended to have more severe renal disease and cardiorespiratory involvement. CONCLUSIONS: The increased frequency of SLE among women may be attributed to differences in the metabolism of sex hormones and/or GnRH. Though less common in men, when it does occur SLE tends to run a more severe course-an important consideration in the diagnosis and follow-up of male patients with SLE.

Female↗
PubMed2002

Mizoribine as an effective combined maintenance therapy with prednisolone in child-onset systemic lupus erythematosus.

BACKGROUND: Systemic lupus erythematosus (SLE) is one of the major collagen diseases in childhood. However, the pathogenesis of this disease still remains unknown. The disease is known as a chronic inflammatory disease. Since oral and intravenous corticosteroid therapy has been introduced into the treatment of SLE, the prognosis of patients has improved significantly. However, it has now become clear that there are limitations in the effectiveness, as well as adverse reactions when corticosteroids therapy is administered for a long-term period. Therefore, we have been attempting to improve the maintenance therapy of child-onset SLE. METHODS: We have proposed and tested a new type of combination therapy using prednisolone (PSL) and mizoribine (MZR) in pediatric patients with SLE for maintenance therapy after the induction of remission. RESULTS: Our results showed that this combination therapy is more effective than the previous regimen. In addition, no significant side-effects were observed in our study. CONCLUSION: This combination therapy is still not perfect. Efforts should be continued to establish an optimal therapy regimen for child-onset SLE.

Adolescent↗
PubMed2003

Autoantibodies against mannose-binding lectin in systemic lupus erythematosus.

In systemic lupus erythematosus (SLE), autoantibodies directed against complement components of the classical pathway, especially against C1q, are associated with severe disease and are of prognostic value for flares of lupus nephritis. Mannose-binding lectin (MBL), the recognition unit of the MBL pathway of complement activation, has structural similarities to C1q. Deficiencies of MBL have been shown to predispose to the development of SLE and to influence the course of the disease. We hypothesized that the presence of autoantibodies to MBL, analogous to autoantibodies to C1q in patients with SLE, may contribute to disease development. The occurrence of anti-MBL autoantibodies was assessed by enzyme-linked immunosorbent assay (ELISA) of 68 serum samples from 20 patients with SLE and in serum from 70 healthy controls. Levels of antibodies directed against MBL were significantly higher in patients with SLE compared to healthy subjects. No significant difference was found between patients with active disease compared to those with inactive disease. While the occurrence of anti-C1q autoantibodies was associated with renal involvement, no such relationship was found for anti-MBL autoantibodies. A significant correlation was found between anti-MBL and anti-C1q antibody levels. The level of anti-MBL antibodies was negatively correlated with MBL-complex activity of circulating MBL. Anti-MBL autoantibodies were of the immunoglobulin G (IgG) isotype and the binding site of IgG anti-MBL was located in the F(ab')2 portion. We conclude that anti-MBL are present in sera from SLE patients and influence the functional activity of MBL.

Adult↗
PubMed2001

Evidence for a susceptibility gene, SLEV1, on chromosome 17p13 in families with vitiligo-related systemic lupus erythematosus.

Both systemic lupus erythematosus (SLE) and vitiligo are autoimmune disorders that have strong evidence of complex genetic contributions to their etiology, but, to date, efforts using genetic linkage to find the susceptibility genes for either phenotype have met with limited success. Since autoimmune diseases are thought to share at least some of their genetic origins, and since only a small minority (16 of 92) of the European-American pedigrees multiplex for SLE in our collection have one or more affected members with vitiligo, we hypothesized that these pedigrees might be more genetically homogeneous at loci important to both SLE and vitiligo and, hence, have increased power for detection of linkage. We therefore evaluated genomewide microsatellite-marker-scan data for markers at an average marker density of approximately 11 cM in these 16 European-American pedigrees and identified a significant linkage at 17p13, where the maximum multipoint parametric LOD score was 3.64 (P<4.3x10(-5)) and the nonparametric linkage score was 4.02 (P<2.8x10(-5)), respectively. The segregation behavior of this linkage suggests a recessive mode of inheritance with a virtually homogeneous genetic effect in these 16 pedigrees. These results support the hypotheses that SLE and vitiligo may share important genetic effects and that sampling on the basis of clinical covariates dramatically improves power to identify genetic effects.

Chromosome Mapping↗
PubMed1993

The role of the 16/6 idiotype network in the induction and manifestations of systemic lupus erythematosus.

Experimental systemic lupus erythematosus (SLE) has been induced in mice by immunization with either a human anti-DNA mAb bearing a common idiotype (Id) designated 16/6 Id (antibody 1, Ab1) or with a murine anti-16/6 Id mAb (Ab2). In the present study a murine mAb (5G12-4, Ab3) that bears the 16/6 Id and binds to DNA was produced and was found to bind rabbit anti-16/6 Id sera and murine anti-16/6 Id mAb similarly to the human mAb 16/6 Id (Ab1). Moreover, mAb 5G12-4 was shown to share T cell epitopes with the human 16/6 Id mAb, since lymph node cells of mice immunized with the mAb 5G12-4 proliferated significantly to the human 16/6 mAb and vice versa. Following immunization of mice with the murine mAb bearing the 16/6 Id, antibodies to dsDNA, ssDNA, 16/6 Id, anti-16/6 Id, and to HeLa nuclear extract proteins were detected, similarly to those observed previously upon immunization with Ab1 or Ab2. Six months following the immunization, the mice exhibited leukopenia, increased erythrocyte sedimentation rates, and proteinuria. Examination of the kidneys of the mice disclosed immune complex deposits, thickening of the Bowman's capsule and glomerular necrosis. These results show the importance of the 16/6 Id network in the induction and progression of SLE in mice.

Animals↗