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PubMed2001

The great pretender. Systemic lupus erythematosus.

BACKGROUND: Systemic lupus erythematosus (SLE) is a multisystem disorder with a multitude of clinical symptoms and a wide variety of presentations. OBJECTIVE: To outline the variety of possible clinical presentations of SLE. DISCUSSION: Although joint symptoms and a rash are common at onset it may present as a neurological, cardiovascular or obstetric problem without more obvious clues to the diagnosis and lupus should be considered in the differential diagnosis of a wide variety of clinical problems. The prevalence of lupus, however, is low and over-reliance on a positive antinuclear antibody, especially at low titre, can lead to error, especially in the context of musculoskeletal symptoms.

Adolescent↗

PubMedDate not supplied

[Peripheral neuropathy in systemic lupus erythematosus].

INTRODUCTION: Systemic lupus erythematosus (SLE) is the connective tissue disorder in which neuropsychiatric complications are most often seen. The prevalence of peripheral neuropathy varies from 5 to 27% depending on the series of cases described, with subclinical forms being most frequent. OBJECTIVES: To determine the prevalence of subclinical peripheral neuropathy in a group of patients with SLE, define their characteristics, and investigate any possible associations with clinico analytical parameters of the disease. PATIENTS AND METHODS. 32 patients with SLE were diagnosed in an Internal Medicine Outpatient Clinic and followed up for at least a year. They were studied prospectively and consecutively by clinical examination, laboratory test and neurophysiological studies (electroneurogram). RESULTS: Neurophysiological study showed peripheral neuropathy to be present in 50% of the patients, who were mainly asymptomatic (75%) and found to be normal on neurological examination (81.2%). The most frequent type of neuropathy was polyneuropathy (37.5%) which was predominantly axonal symmetrical and sensomotor followed by isolated mono neuropathy (6.2%) and multiple mononeuritis (6.2%). No clinical or analytical parameter was significantly associated with the development of peripheral neuropathy. CONCLUSIONS: The considerable frequency of subclinical peripheral neuropathy in patients with SLE and the absence of associated clinical or analytical parameters makes it necessary to carry out neurophysiological studies in these patients to detect its presence and establish the precise extent of the disorder.

Adolescent↗

PubMedDate not supplied

Acetylation genotype and phenotype in patients with systemic lupus erythematosus.

UNLABELLED: Systemic lupus erythematosus (SLE) is a chronic autoimmune disease affecting various tissues and organs. In the studies on SLE etiopathogenesis, a potential role of genetically determined impairment of xenobiotic metabolism has been emphasized. N-acetyltransferase 2 enzyme (NAT2) exhibits gene polymorphism and the acetylation rate with NAT2 involvement varies from person to person. The study on acetylation phenotype was carried out using isonicotinic acid hydrazide (isoniazid) as a model drug, while NAT2 alleles were determined by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assays. Among patients with SLE, NAT2*4/NAT2*6 and NAT2*5/NAT2*5 genotypes occurred most frequently, while NAT2*4/NAT2*6 and NAT2*5/NAT2*6 prevailed in the control group. The concordance of 96.8% was achieved between acetylation phenotype and NAT2 genotype in the group of SLE patients studied. CONCLUSION: Acetylation polymorphism appears not to be an important risk factor in SLE.

Acetylation↗

PubMed2006

Differential expression of estrogen receptors in women with systemic lupus erythematosus.

OBJECTIVE: Systemic lupus erythematosus (SLE) is an autoimmune disease primarily affecting women. T cell activation markers (calcineurin, CD154) increase in SLE T cells cultured with estradiol 17-beta. Biological effects of estradiol are mediated through 2 receptor proteins, estrogen receptor-alpha (ER-alpha) and estrogen receptor-beta (ER-beta). We compared the amount of estrogen receptor subtypes in T cells and measured the ability of receptor agonist-specific ligands to activate marker gene expression. METHODS: T cells were isolated from 22 female patients with SLE and 17 control women. The amount of ER subtypes was measured by immunoblotting. Some T cells were cultured with ER-alpha or ER-beta-specific agonists. Receptor activation was measured by increased expression of the T cell activation markers CD154 and calcineurin. RESULTS: Although the amount of ER-alpha appeared to be less in SLE T cells than in control T cells, the difference was not statistically significant (p = 0.081). The quantity of ER-beta was similar in SLE and control T cells. The expression of ER-alpha or ER-beta was independent of menstrual cycle phase, age, or SLE disease activity. Calcineurin and CD154 expression increased in SLE T cells cultured in medium containing ER-alpha and ER-beta agonists. CONCLUSION: These data indicate that both ER subtypes activate calcineurin and CD154 in SLE but not in normal T cells. Variation in the amount of ER-alpha in SLE T cells suggests this receptor subtype participates in the sensitivity of SLE T cells to estrogen.

Actins↗

PubMed1989

Circulating colony-forming units of granulocytes and monocytes/macrophages in systemic lupus erythematosus.

In systemic lupus erythematosus (SLE) patients, in vitro bone marrow (BM) colony-forming units of granulocytes and monocytes/macrophages (CFU-GM) are decreased, suggesting that granulomonopoietic failure may play an important role in the mechanism of peripheral blood (PB) depletion of neutrophils and monocytes. No information concerning CFU-GM in PB of patients with SLE is available. The present study was undertaken in order to determine whether SLE itself and the inactive or active stage of disease would modify the number of GFU-GM in PB samples from 20 treatment-free SLE women, 12 inactive and eight active. CFU-GM growth was significantly decreased in both inactive (P = 0.018) and active (P = 0.008) SLE patients as compared with controls (n = 8). The difference in CFU-GM growth between SLE groups was not significant. These results indicate that the number of circulating CFU-GM is significantly reduced in patients with SLE regardless of disease activity or remission.

Female↗

PubMed1985

Decrease in the reaction of DNA repair synthesis in response to nicotinamide or 3-aminobenzamide in ultraviolet irradiated systemic lupus erythematosus lymphocytes.

Systemic lupus erythematosus (SLE) lymphocytes failed to accelerate ultraviolet (UV) induced DNA repair synthesis normally observed following inhibition of poly(adenosine diphosphoribose) polymerization. Without inhibitors of poly(adenosine diphosphoribose) polymerase such as nicotinamide or 3-aminobenzamide, DNA repair synthesis following UV irradiation was found to occur normally in the cells of patients. These data suggest that DNA repair is disturbed under special conditions in the lymphocytes of SLE patients.

Benzamides↗

PubMedDate not supplied

Lack of type C virus antibodies in systemic lupus erythematosus.

Twelve systemic lupus erythematosus (SLE) and 10 normal sera were similarly reactive in an assay for cytotoxic antibody to type C virus-infected and uninfected cells, but both were less cytotoxic for infected cells. Thus antibodies to type C viruses were not detected in SLE or normal sera, but type C infection may interfere with antibody recognition of other cell membrane antigens.

Animals↗

PubMed1984

Exophthalmos in systemic lupus erythematosus.

In systemic lupus erythematosus (SLE) exophthalmos is distinctly rare. This article describes the first patients with SLE in whom exophthalmos was preceded by pseudotumor cerebri. The apparent lack of resolution of the exophthalmos with corticosteroids in our case emphasizes the potential need for therapeutic alternatives such as immunosuppressive agents, orbital irradiation, and/or plasmapheresis.

Adult↗

PubMed1984

[Cytophotometric study of the change in DNA content in the nuclei of human blood lymphocytes in systemic lupus erythematosus].

During systemic lupus erythematosus, a correlation between the nuclear DNA contents in lymphocytes and their tendency to proliferate, on the one hand, and the activity of disease, on the other hand, has been revealed. At the high activity and acute run of disease, a negative tendency of lymphocyte proliferation and negative figures of the index of proliferation prevailed, the findings reflecting the extent of diminution of the lymphocyte DNA amounts. With a decline in the activity of disease and its transition to a phase of remission, a positive proliferative tendency starts to predominate in lymphocytes.

Acute Disease↗

PubMed1996

[Cytokines in systemic lupus erythematosus].

In systemic lupus erythematosus (SLE) is a disease characterized by B cell hyperactivity, autoantibody production and immune complex deposition in vital organs. To explain the mechanisms responsible for immune dysregulation in SLE cytokines have received increasing attention. This review has discussed a number of cytokines which appear to be involved in lupus pathogenesis. Recent studies have shown that disease activity and the main symptoms of SLE are associated with increasing serum levels of cytokines such as interleukin-(IL)-1, IL-2, IL-6, interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (THF-alpha). Constitutive expression and in vitro induction of specific cytokines are also aberrant in SLE. The presence of IL-1, IL-6 and IFN-gamma in involved kidneys suggests that they have local pathogenic effects. Moreover IFN-gamma, IL-6 and IL-1 modulate spontaneous IgG production by SLE mononuclear cells. During the next several years, the exact role of these cytokine in the pathogenesis of lupus become more fully elucidated.

Animals↗

PubMed1998

Increased risk of malignancy in patients with systemic lupus erythematosus.

BACKGROUND: Systemic lupus erythematosus is a chronic, multisystem, autoimmune disorder that primarily affects women. Morbidity and mortality have improved for lupus patients during the last 15 years. An increased risk of malignancy in patients with lupus has been shown in some, but not all studies. The purpose of this study was to ascertain cancer risk in lupus patients by linking two disease registries. METHODS: Participants in the Chicago Lupus Cohort included 616 women with lupus who were residents of Cook County, Illinois. They were seen during 1985-1995 at 4 University, inner city, and suburban inpatient and outpatient clinics in Chicago. Malignancies occurring in these subjects during the study interval, 1985-1995, were identified from the Illinois State Cancer Registry by matching name, birthdate, and social security number. Standardized incidence ratios (SIRs) were estimated for all malignancies in this cohort of lupus patients using age, gender, and all race or race-stratified specific cancer incidence data from Cook County, Illinois. RESULTS: The registry linkage study with the Illinois State Cancer Registry documented that 30 women with lupus had a malignancy. The expected number of malignancies for women in the lupus cohort was 15.0. There were 8 cases of breast cancer and 4 each of lung and cervical cancer. In the remaining 14 women, 12 different types of cancers were noted. The SIR and 95% confidence interval (CI) for malignancy for all women with lupus in the study were 2.0 (1.4, 2.9) and lung cancer was the only individual cancer increased in all women--SIR and 95% CI were 3.1 (1.3, 7.9). In the analysis stratified by race, the risk of malignancy (SIR and 95% CI) was increased in Caucasian women, 2.3 (1.4, 3.9). Breast cancer was the only individual cancer increased in Caucasian women with lupus with an SIR and 95% CI of 2.9 (1.4, 6.4). CONCLUSIONS: Lupus patients have an increased risk of malignancy. Breast, lung, and gynecological malignancies were the most common malignancies observed in the cohort and breast cancer was significantly increased in Caucasian women.

Adult↗

PubMed2006

Elevated serum levels of interferon-regulated chemokines are biomarkers for active human systemic lupus erythematosus.

BACKGROUND: Systemic lupus erythematosus (SLE) is a serious systemic autoimmune disorder that affects multiple organ systems and is characterized by unpredictable flares of disease. Recent evidence indicates a role for type I interferon (IFN) in SLE pathogenesis; however, the downstream effects of IFN pathway activation are not well understood. Here we test the hypothesis that type I IFN-regulated proteins are present in the serum of SLE patients and correlate with disease activity. METHODS AND FINDINGS: We performed a comprehensive survey of the serologic proteome in human SLE and identified dysregulated levels of 30 cytokines, chemokines, growth factors, and soluble receptors. Particularly striking was the highly coordinated up-regulation of 12 inflammatory and/or homeostatic chemokines, molecules that direct the movement of leukocytes in the body. Most of the identified chemokines were inducible by type I IFN, and their levels correlated strongly with clinical and laboratory measures of disease activity. CONCLUSIONS: These data suggest that severely disrupted chemokine gradients may contribute to the systemic autoimmunity observed in human SLE. Furthermore, the levels of serum chemokines may serve as convenient biomarkers for disease activity in lupus.

Adult↗

PubMedDate not supplied

[Spectral analysis of the electroencephalogram in children with systemic lupus erythematosus].

INTRODUCTION: Systemic lupus erythematosus (SLE) is an autoimmune disease that affects different systems and organs, including the central nervous system (CNS). It has been suggested that about 40% of the cases of neuropsychiatric lupus (NPSLE) develop before SLE is diagnosed or at the same time it is being carried out, and 63% appear during the first year following diagnosis. AIMS: The aim of this study was to check the hypothesis that the electroencephalogram (EEG) may be sensitive to the damage to the CNS in children with SLE in whom there is still no clinical evidence of NPSLE. PATIENTS AND METHODS: EEG recordings were performed in 30 children with a diagnosis of SLE with or without signs of a neuropsychiatric syndrome. The results of the EEG were evaluated visually and analysed quantitatively. RESULTS: The visual inspection of the EEG showed the presence of alterations in 44.5% of the children with SLE and in 76.9% of those with NPSLE. There were significant differences in Student's t test (p = 0.0055) between the two groups for the analysis of the broadband spectral measurements. The narrow band analysis revealed a significant increase in the theta and delta frequencies in children with SLE as compared to standard values, whereas in children with NPSLE significant differences were found in the fast bands in frontal regions. CONCLUSIONS: Spectral analysis of the narrow band could help to confirm diagnoses of NPSLE, while anomalies in the slow bands could be an early marker of damage to the CNS although there are still no symptoms of the disease.

Adolescent↗

PubMed1998

Mutations in T cell receptor zeta chain mRNA of peripheral T cells from systemic lupus erythematosus patients.

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease of unknown aetiology. Although it has been reported that T cells might be responsible for the pathogenesis of SLE, it remains unclear whether immune aberrations of SLE T cells are the primary event in this pathological process. We have recently reported that tyrosine phosphorylation and expression of the T cell receptor zeta chain (TCR zeta) was significantly decreased in SLE T cells and that two SLE patients exhibited a 36 bp, exon 7 deletion of the TCR zeta mRNA. To investigate further common mutations in TCR zeta mRNA among SLE patients, mRNA was isolated from the peripheral blood T cells of two normal controls, two systemic sclerosis (SSc) patients, and eight SLE patients. TCR zeta cDNA was amplified by RT-PCR. Five out of the eight SLE patients exhibited abnormal migration patterns of the TCR zeta cDNA in PCR single stranded conformational polymorphism analysis. PCR products were ligated into pUC18 and five clones obtained were sequenced. Analysis of the nucleotide sequences revealed that all of the five pUC18 clones from the normal controls and SSc patients had the normal nucleotide sequence, whereas all eight SLE patients had mutations in TCR zeta cDNA accompanied by predicted amino acid substitutions. Mutations found in six of these patients corresponded to those of the third immunoreceptor tyrosine-based activation motif (ITAM) domain or the GTP/GDP binding site in TCR zetaThus, these mutations in TCR zeta mRNA could be responsible for the decreased expression of the TCR zeta protein in SLE T cells.

Amino Acid Substitution↗

PubMed2006

Shrinking lungs syndrome, a rare manifestation of systemic lupus erythematosus.

In systemic lupus erythematosus (SLE), the respiratory system is frequently compromised. One of its uncommon manifestations is the shrinking lungs syndrome (SLS), characterised by dyspnoea, diaphragmatic elevation and a restrictive pattern in the spirometry. We report two cases affected with this rare entity. They presented with different degrees of respiratory involvement and responses to the therapy. At the same time, clinical, physiopathological, prognostic and therapeutic aspects of this syndrome are reviewed.

Adult↗

PubMed2006

TCRzeta mRNA splice variant forms observed in the peripheral blood T cells from systemic lupus erythematosus patients.

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease of unknown etiology. Tyrosine phosphorylation and protein expression of the T-cell receptor zeta chain (zeta) have been reported to be significantly decreased in SLE T cells. In addition, zeta mRNA with alternatively spliced 3' untranslated region (zetamRNA/as-3'UTR) is detected predominantly in SLE T cells, and aberrant zeta mRNA accompanied by the mutations in the open reading frame including zeta mRNA lacking exon7 (zetamRNA/exon7-) is observed in SLE T cells. These zeta mRNA splice variant forms exhibit a reduction in the expression of TCR/CD3 complex and zeta protein on their cell surface due to the instability of zeta mRNA splice variant forms as well as the reduction in interleukin (IL)-2 production after stimulating with anti-CD3 antibody. Data from cDNA microarray showed that 36 genes encoding cytokines and chemokines, including IL-2, IL-15, IL-18, and TGF-beta2, were down-regulated in the MA5.8 cells transfected with the zeta mRNA splice variant forms. Another 16 genes were up-regulated and included genes associated with membranous proteins and cell damage granules, including the genes encoding poliovirus-receptor-related 2, syndecan-1, and granzyme A.

3' Untranslated Regions↗

PubMed2003

Interferon and granulopoiesis signatures in systemic lupus erythematosus blood.

Systemic lupus erythematosus (SLE) is a prototype systemic autoimmune disease characterized by flares of high morbidity. Using oligonucleotide microarrays, we now show that active SLE can be distinguished by a remarkably homogeneous gene expression pattern with overexpression of granulopoiesis-related and interferon (IFN)-induced genes. Using the most stringent statistical analysis (Bonferroni correction), 15 genes were found highly up-regulated in SLE patients, 14 of which are targets of IFN and one, defensin DEFA-3, a major product of immature granulocytes. A more liberal correction (Benjamini and Hochberg correction) yielded 18 additional genes, 12 of which are IFN-regulated and 4 granulocyte-specific. Indeed immature neutrophils were identified in a large fraction of SLE patients white blood cells. High dose glucocorticoids, a standard treatment of disease flares, shuts down the interferon signature, further supporting the role of this cytokine in SLE. The expression of 10 genes correlated with disease activity according to the SLEDAI. The most striking correlation (P < 0.001, r = 0.55) was found with the formyl peptide receptor-like 1 protein that mediates chemotactic activities of defensins. Therefore, while the IFN signature confirms the central role of this cytokine in SLE, microarray analysis of blood cells reveals that immature granulocytes may be involved in SLE pathogenesis.

Child↗

PubMed1988

Clinical and immunologic effects of monthly administration of intravenous cyclophosphamide in severe systemic lupus erythematosus.

Severe systemic lupus erythematosus affecting the kidney or central nervous system may lead to organ failure or death despite treatment with high doses of corticosteroids. To evaluate the clinical and immunologic effects of intravenous cyclophosphamide in this setting, we treated nine patients with monthly intravenous infusions of cyclophosphamide for six months. A comparison of characteristics at entry and follow-up revealed improvements (by paired t-test) in creatinine clearance (66 vs. 96 ml per minute, P less than 0.001); 24-hour urinary protein level (4.11 vs. 0.90 g, P less than 0.05), Farr anti-DNA titer (43 vs. 8.5 percent, P less than 0.01); complement components C3 (894 vs. 1150 mg per liter, P less than 0.05), C4 (154 vs. 222 mg per liter, P less than 0.05), and total complement activity (CH50) (88.7 vs. 113.4 IU, P less than 0.05); and Westergren erythrocyte sedimentation rate (60.2 vs. 34.4 mm per hour, P less than 0.0005). Other manifestations of lupus improved markedly in most cases, despite a reduction in the mean daily dose of prednisone, from 45 mg at entry to 17 mg at follow-up (P less than 0.01). The numbers of lymphocytes positive for T3, T4, T8, and B1 declined progressively during treatment. At follow-up, persistent decreases were observed in the T-lymphocyte subsets, whereas the absolute number of B lymphocytes had returned to levels near base line. T-cell proliferative responses at follow-up were not significantly different from entry values, except that the response to mitogenic anti-T11 (CD2) antibodies was decreased (P less than 0.01). Our data indicate that monthly intravenous administration of cyclophosphamide was associated with a substantial amelioration of severe systemic lupus, in conjunction with discrete changes in T-lymphocyte markers and T-cell function. This was a preliminary, uncontrolled study, but the results warrant further investigation of this form of treatment.

Adult↗