Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Soluble interleukin 2 receptor (sIL2R) may be used as an index of immune perturbation. We report on the correlation between the serum levels of sIL2R, as assessed with a sandwich-ELISA, and disease activity in 61 patients with Systemic Lupus Erythematosus (SLE) and in 15 with systemic idiopathic vasculitis (SIV). The mean levels of sIL2R in SLE and SIV patients were significantly higher than in healthy controls and higher values were detected in patients with active disease or severe organ involvement or infection. We also studied patients with clinically silent SLE, characterized by the presence of several immunologic abnormalities. The sIL2R mean level in this group did not differ from that of quiescent SLE patients, suggesting that immunologic alterations are present even in inactive SLE. Finally, the sIL2R assay showed higher sensitivity and specificity than most of the common immunologic parameters.
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PMID:Serum levels of soluble interleukin-2 receptor in patients with systemic lupus erythematosus and systemic idiopathic vasculitis. 823 90

Two TNF binding proteins have been characterized as soluble fragments of TNF receptors. We measured the plasma concentrations of soluble type A (p75) and type B (p55) TNF receptors in patients with systemic lupus erythematodes (SLE), progressive systemic sclerosis (PSS), and mixed connective tissue disease (MCTD). In SLE and PSS patients plasma concentrations of both types of TNF receptors and in MCTD patients type A TNF receptors were significantly elevated compared to controls. Plasma concentrations of both soluble TNF receptors were highly correlated in SLE, PSS, and MCTD patients, indicating a possible coregulation of both TNF receptors. In contrast, soluble interleukin 2 receptor (sCD 25) plasma concentrations were not correlated and seem to be an independent parameter. The soluble forms of the TNF receptors neutralize TNF in cytotoxicity assays and are functionally active as TNF antagonists. In one patient with SLE, autoantibodies against type A TNF receptors were detected, TNF alpha, and TNF beta did not interfere with the autoantibody binding to the receptor.
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PMID:Evaluation of soluble tumor necrosis factor (TNF) receptors and TNF receptor antibodies in patients with systemic lupus erythematodes, progressive systemic sclerosis, and mixed connective tissue disease. 824 78

Soluble interleukin 2 receptor (SIL-2R) levels in serum appear to reflect the status of lymphocytic activation and proliferation. We examined the levels of serum SIL-2R in 65 patients with diffuse connective tissue diseases by using ELISA method. The mean levels of serum SIL-2R were respectively 0.46 U/L, 0.53 U/L, 0.46 U/L in systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and dermatomyositis during disease activity and were significantly higher than those in healthy controls (0.25 U/L). The levels of serum SIL-2R were 0.62 U/L and 0.60 U/L respectively in a patient with mixed connective tissue disease and a patient with systemic sclerosis. The levels of SIL-2R were respectively 0.24 U/L and 0.29 U/L in SLE and RA patients during clinical remission, being significantly lower than during disease activity. SLE patients with high SIL-2R levels were associated with high levels of 125I-DNA rate and erythrocyte sedimentation rate and lower levels of C3 complement components. The measurement of SIL-2R levels may be an useful indicator for monitoring disease activity in SLE and RA patients. Moreover it is a noninvasive method.
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PMID:[Serum soluble interleukin 2 receptor levels in patients with diffuse connective tissue diseases]. 826 81

OBJECTIVES--To investigate urine neopterin as a parameter of disease activity in an unselected group of patients with systemic lupus erythematosus (SLE) and to study the relation between urine neopterin and certain patterns of organ disease and differing drug regimens in the treatment of SLE. METHODS--Neopterin was determined by high performance liquid chromatography in 115 early morning urine samples from 68 patients with SLE. Serum soluble interleukin 2 receptor (sIL-2R) and antibodies to double stranded DNA (dsDNA) were determined by enzyme linked immunosorbent assay (ELISA), and the erythrocyte sedimentation rate (ESR), plasma C3, C4, and C3 degradation products (C3dg) were measured in corresponding blood samples. Disease activity was scored using the British Isles Lupus Assessment Group (BILAG) index. RESULTS--Urine neopterin was significantly increased in patients with active and inactive SLE compared with the control group and was significantly higher in patients with active than in those with inactive SLE. Urine neopterin did not distinguish between subsets of patients with SLE with particular patterns of organ disease, as defined by the BILAG index, nor was its level primarily influenced by differing drug regimens. Levels of serum sIL-2R, antibodies to dsDNA, the ESR, and plasma C3, C4, and C3dg were also significantly different between the patients with active and inactive SLE. Unlike urine neopterin there was considerable overlap in the values of these parameters between the two activity groups. Highly significant correlations found between urine neopterin and serum sIL-2R, ESR, and plasma C3, C4, and C3dg suggest the close association of neopterin with clinical activity in SLE. Multivariate logistic regression analysis showed that urine neopterin > 300 mumol/mol creatinine was a highly significant predictor of disease activity with an odds ratio of 3.51. CONCLUSIONS--Determination of urine neopterin, a non-invasive, relatively simple and inexpensive measurement, appears to be the best parameter for assessing and monitoring disease activity and treatment in patients with SLE.
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PMID:Urine neopterin as a parameter of disease activity in patients with systemic lupus erythematosus: comparisons with serum sIL-2R and antibodies to dsDNA, erythrocyte sedimentation rate, and plasma C3, C4, and C3 degradation products. 832 94

The correlation among the various markers of activated T cells (soluble interleukin 2 receptor (sIL-2R), HLA-DR+ and HLA-DP+ T cells, proliferating cell nuclear antigen (PCNA) positive lymphocytes) were examined in patients with systemic lupus erythematosus (SLE), and related to the cell cycle. The concentration of sIL-2R and the proportion of HLA-DR+ T cells, HLA-DP+ T cells or PCNA+ lymphocytes were increased significantly as compared to that in normal subjects. And, the concentrations of sIL-2R correlated with the proportions of PCNA+ lymphocytes, but not with the proportions of HLA-DR+ T cells, HLA-DP+ T cells. The correlation between sIL-2R and PCNA+ lymphocytes was attributed to both indicators being increased during the G1B or S phase in normal T cells upon stimulation by phytohemagglutinin (PHA). Upon cell cycle analysis it was learned that activated T cells could be found in the G1A and the S phases.
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PMID:Subsets of activated T cells in patients with systemic lupus erythematosus: the relation to cell cycle. 905

We describe a patient presenting with systemic lupus erythematosus (SLE) and concomitant low-grade (Ig) non-Hodgkin's lymphoma of the B cell type (B-NHL). Although the association of autoimmune disorder and lymphoma is well conceived, there is only scarce information available as to the simultaneous occurrence of both disease conditions in one patient. As in this patient diagnosis of Ig B-NHL was also based on the detection of a monoclonal population of CD5+ B lymphocytes, and given that the polyclonal expansion of CD5+ B cells has been previously reported in rheumatoid arthritis (RA), Sjogren's syndrome (SS) and single cases of SLE, the observations we made in this patient led us to discuss the role of the CD5+ population in the development of rheumatic disorders and concomitant lymphoid malignancy. Moreover, since impaired production rates of interleukin 3 (IL-3) and interleukin 4 (IL-4) have been associated with an abnormal expansion of CD5, lymphoma cells and seeing that soluble interleukin 2 receptor (sIL-2R) serum levels were found to be positively correlated with disease activity both in SLE and Ig B-NHL, these parameters were investigated and related to the patient's disease state throughout the entire clinical observation period.
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PMID:Concomitant manifestation of systemic lupus erythematosus and low-grade non-Hodgkin's lymphoma. 926 88

Graves disease (GD) is a common autoimmune thyroid disorder that is inherited as a complex multigenic trait. By using a single microsatellite marker at each locus, we screened the type 1 diabetes loci IDDM4, IDDM5, IDDM6, IDDM8, and IDDM10 and the fucosyltransferase-2 locus for linkage in sib pairs with GD. This showed a two-point nonparametric linkage (NPL) score of 1.57 (P=.06) at the IDDM6 marker D18S41, but NPL scores were <1.0 at the other five loci. Thus, the investigation of the IDDM6 locus was extended by genotyping 11 microsatellite markers spanning 48 cM across chromosome 18q12-q22 in 81 sib pairs affected with autoimmune thyroid disease (AITD). Multipoint analysis, designating all AITD sib pairs as affected, showed a peak NPL score of 3.46 (P=.0003), at the marker D18S487. Designation of only GD cases as affected (74 sib pairs) showed a peak NPL score of 3.09 (P=.001). Linkage to this region has been demonstrated in type 1 diabetes (IDDM6), rheumatoid arthritis, and systemic lupus erythematosus, which suggests that this locus may have a role in several forms of autoimmunity.
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PMID:Evidence for a new Graves disease susceptibility locus at chromosome 18q21. 1076 55

A 42-year-old woman was diagnosed as systemic lupus erythematosus (SLE), because of the findings of polyarthritis, leukopenia, positive antinuclear antibody, and positive anti DNA antibody. She was treated with predonisolone (PSL) at 10 mg per day. She was admitted to our hospital on October 2000 because of spiking high fever, skin eruption, and lymph node swelling. Since her illness of SLE was considered to be worsening, high dose of corticosteroids were given. However, high fever persisted and liver dysfunction was developed with increased serum ferritin. Her bone marrow smear showed hemophagocytosis. We made a diagnosis of hemophagocytic syndrome (HPS) complicated by disseminated intravascular coagulation (DIC). HPS was thought to be induced by viral infection, even though causative viral infection was not detected. Her general condition worsened with persistent high fever and liver dysfunction. Plasma exchange was carried for two consecutive days, followed by cyclosporine A and lipo-dexamethasone, which improved her fever rapidly. Her general condition gradually improved. Serum levels of ferritin, soluble interleukin 2 receptor (sIL 2-R), interferon-gamma and interleukin 6 decreased associated with improvements of her clinical condition. We thought plasma exchange could be effective to decrease serum levels of cytokine, which was suggested to be the pathogenic to HPS. However serum levels of IFN-gamma and IL 6 after plasma exchange did not change in this case. Further studies are required to confirm the effects of plasma exchange for HPS.
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PMID:[Case report of systemic lupus erythematosus patient with hemophagocytic syndrome, treated with plasma exchange, with specific reference to clinical profile and serum cytokine levels]. 1183 Oct 15

Synonymous with secondary hemophagocytic lymphohistiocytosis, macrophage activation syndrome (MAS) is a term used by rheumatologists to describe a potentially life-threatening complication of systemic inflammatory disorders, most commonly systemic juvenile idiopathic arthritis (sJIA) and systemic lupus erythematosus (SLE). Clinical and laboratory features of MAS include sustained fever, hyperferritinemia, pancytopenia, fibrinolytic coagulopathy, and liver dysfunction. Soluble interleukin-2 receptor alpha chain (sCD25) and sCD163 may be elevated, and histopathology often reveals characteristic increased hemophagocytic activity in the bone marrow (and other tissues), with positive CD163 (histiocyte) staining. A common hypothesis as to the pathophysiology of many cases of MAS proposes a defect in lymphocyte cytolytic activity. Specific heterozygous gene mutations in familial HLH-associated cytolytic pathway genes (e.g., PRF1, UNC13D) have been linked to a substantial subset of MAS patients. In addition, the pro-inflammatory cytokine environment, particularly IL-6, has been shown to decrease NK cell cytolytic function. The inability of NK cells and cytolytic CD8 T cells to lyse infected and otherwise activated antigen presenting cells results in prolonged cell-to-cell (innate and adaptive immune cells) interactions and amplification of a pro-inflammatory cytokine cascade. The cytokine storm results in activation of macrophages, causing hemophagocytosis, as well as contributing to multi-organ dysfunction. In addition to macrophages, dendritic cells likely play a critical role in antigen presentation to cytolytic lymphocytes, as well as contributing to cytokine expression. Several cytokines, including tumor necrosis factor, interferon-gamma, and numerous interleukins (i.e., IL-1, IL-6, IL-18, IL-33), have been implicated in the cytokine cascade. In addition to broadly immunosuppressive therapies, novel cytokine targeted treatments are being explored to dampen the overly active immune response that is responsible for much of the pathology seen in MAS.
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PMID:The Immunology of Macrophage Activation Syndrome. 3077 31


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