Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As autoantibodies are thought to participate in the pathogenesis of renal inflammation in systemic lupus erythematosis (SLE) we investigated associations between serological markers of disease activity in SLE and the activity of renal histopathological lesions in thirty-five patients with lupus nephritis (LN). We found the following prevalence of serum auto-antibodies in LN: IgG antinuclear antibodies (ANA) 100%, IgM ANA 69%, IgA ANA 60%, IgG anti-dsDNA 60%, IgM anti-dsDNA 71%, IgA anti-dsDNA 60%, anti-RNP 20%, anti-Sm 14%, anti-SSA 31%, anti-SSB 14%, anti-histone 37%, anti-cardiolipin 80% and antibody to ribosomal protein (anti-P) 6%. No correlation was found between serological parameters and the WHO-classification of biopsies. The activity-index of histological lesion, assessed according to the NIH-renal histology scoring system, correlated with IgM ANA and IgM anti-dsDNA titers. Of all the specific features of histological renal inflammation, glomerular proliferation showed the best overall correlation with serological parameters of disease activity. Anticardiolipin antibodies were correlated with overall disease activity, but not with renal histological activity. Thus, serological markers of disease activity did not adequately reflect the amount of renal inflammation in LN and cannot replace renal biopsy as a diagnostic tool.
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PMID:Relation between serological data at the time of biopsy and renal histology in lupus nephritis. 194 73

Polyclonal B cell activation (PBA) and autoimmune disease can be induced in immunologically normal mice, or enhanced in lupus-prone mice, by bacterial lipopolysaccharide (LPS). Because immune defects are common in autoimmune diseases and IgA deficiency is prevalent in patients with systemic lupus erythematosus, we investigated: (i) whether LPS might induce IgA deficiency in normal mice; (ii) whether IgA deficiency might be a feature in lupus-prone mice; (iii) whether, if present in lupus-prone mice, IgA deficiency could be further accentuated by LPS; and (iv) whether the effects of LPS on IgA concentrations of normal and lupus-prone mice might be reversible upon withdrawal of LPS. We injected normal (C57BL/6) and lupus-prone (NZB/W) mice with 50 micrograms of LPS from Salmonella minnesota Re595 twice a week for 5 weeks and then discontinued LPS for 6 weeks. We determined the concentrations of plasma immunoglobulins, DNA antibodies, and circulating immune complexes before, during, and after mice were exposed to LPS. Our results indicate that: (i) LPS induces IgA deficiency in normal mice concurrently with PBA; (ii) IgA deficiency is a feature of lupus-prone mice; (iii) LPS accentuates naturally occurring PBA and IgA deficiency in lupus-prone mice; and (iv) LPS induced, or LPS enhanced, IgA deficiency and PBA in normal and lupus-prone mice persist long after withdrawal of LPS. Thus, LPS triggers or enhances autoimmune disease by a mechanism that involves in part PBA with selective increase (IgG, IgM) and concurrent decrease (IgA) of specific isotypes.
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PMID:Bacterial lipopolysaccharide induces long-lasting IgA deficiency concurrently with features of polyclonal B cell activation in normal and in lupus-prone mice. 201 4

We studied the effects of difluoromethylornithine (DFMO), an experimental drug that inhibits the biosynthesis of natural polyamines, on anti-DNA antibody production, immunoglobulin synthesis, proteinuria, and blood urea nitrogen (BUN) in lupus-prone female NZB/W mice. Administration of 1% of the drug in drinking water reduced anti-DNA antibody levels by about 80% of that of untreated mice of the same strain. There was a reduction of IgG and IgA levels in older DFMO treated mice, whereas IgM level was not affected. Proteinuria and BUN were also significantly reduced in treated mice. Moreover, DFMO treatment reduced the concentration of putrescine and spermidine in spleen cells. Our results suggest that polyamine biosynthesis inhibition by DFMO may provide a new approach to the treatment of lupus.
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PMID:Difluoromethylornithine therapy of female NZB/W mice. 202 14

Central nervous system involvement of systemic lupus erythematosus was observed in 34 (36%) of the 94 patients studied between 1970-1990. A review of the diagnostic methods and therapy for central nervous system lupus is presented. The diagnosis of primary cerebral lupus was based on the history, physical examination and on the results of the cerebrospinal fluid analysis, CT-scan and EEG. Intractable headache (22/34), behavioural abnormalities (18/34), cranial neuropathy (16/34) occurred most frequently among neuropsychiatric symptoms. Immunoglobulin analysis of the cerebrospinal fluid proved to be the most sensitive method for detecting clinical activity (in 20/23). Central nervous system involvement was suggested by conventional serological test to a lesser degree. Alterations on CT scan and EEG were found in 17/27 and 14/26 of cases, respectively. IgM, IgA, and IgG indexes (indicators of intratechal immunglobulin synthesis) decreased when the central nervous system events subsided after successful treatment but the CT abnormalities (e. g. atrophy) were not altered.
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PMID:[The role of the central nervous system in lupus erythematosus]. 204 15

Fifty normal healthy adults, aged 18 to 41 years, without a history of systemic diseases, dermatoses, or photosensitivity and who were not receiving medication were studied. Paired 3-mm punch biopsy specimens were obtained from the sun-exposed and the non-sun-exposed skin. The data from the study revealed a bright continuous band of immunofluorescence (IF) along the dermoepidermal junction in 10 (20%) of 50 sun-exposed skin biopsy specimens, as compared with none from non-sun-exposed skin biopsy specimens with the use of polyvalent antisera. Fractionated monospecific immunoglobulin demonstrated a bright continuous band of IF composed of IgG alone in one patient, IgA alone in two patients, IgG and IgA in combination in two patients, and the combination of IgG, IgM, and IgA in five patients. There was a statistically significant increase in positive IF in men (seven of 15) vs women (three of 35). This information suggests that in the examination of a patient suspected of having lesions of cutaneous lupus erythematosus, positive IF from sun-exposed skin is nonspecific and adds little information to the clinical and histopathologic findings.
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PMID:Twenty percent of biopsy specimens from sun-exposed skin of normal young adults demonstrate positive immunofluorescence. 173 11

Measurement of the complement activation products C1s:C1-inh, C3bP and C5b-9 by ELISA in plasma samples from normals, rheumatoid arthritis (RA) and systemic lupus erythematosis (SLE) patients showed significantly elevated levels in the two patient groups (P less than 0.0001 for C1s:C1-inh, C3bP and C5b-9) compared to normals. In seropositive RA patients there were significant correlations between the levels of the three complement activation complexes and IgM-RF, IgG-RF and IgA-RF. However, IgM-RF did not interfere with any of the ELISA systems. Mean levels of C1s:C1-inh, C3bP and C5b-9 were the same in paired plasma and synovial fluids; however, C3bP levels in the paired samples did not correlate with one another by rank. Our conclusions are that: (a) elevated plasma levels of these complement activation products are detectable in rheumatic diseases; (b) plasma levels of these complement activation products are related to Rheumatoid factor (RF) levels in seropositive RA patients; and (c) IgM-RF does not influence these solid-phase ELISA procedures.
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PMID:Measurement of complement activation products in patients with chronic rheumatic diseases. 207 70

The survival rate of 68 patients with immunoglobulin A glomerulonephritis (IgA GN), 29 patients with membranous glomerulonephritis (MGN), 13 patients with membranous-proliferative glomerulonephritis (MPGN) and 40 patients with lupus glomerulonephritis (LGN) was assessed using the life registration tables. The patients with IgA GN were treated symptomatically, and the remaining patients were treated with a combination of corticosteroids, immunosuppressors and anticoagulants. At the 10th year from the onset of the disease the survival rate was as follows: for the patients with IgA GN--88%, with MGN--94.9%, with LGN--81.0% and with MPGN--61.6%. The comparison with the survival rate established for the respective types of glomerulonephritis without treatment or the presence of mixed groups of treated and nontreated patients shows that the combined pathogenetic treatment improves the prognosis of MGN, LGN and of a number of patients with MPGN and it nears that of the comparatively more benign IgA GN.
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PMID:[The effect of treatment on the survival rate in chronic glomerulonephritis]. 209 80

Abnormal autoantibodies have recently been implicated in pregnancy wastage. The normal autoantibody profile of pregnancy has so far, however, not been established. We investigated the effect of pregnancy on autoantibody production prospectively and longitudinally. Forty-three healthy pregnant women were compared with 50 nonpregnant healthy controls matched for age, race, and various obstetric and medical indices. All sera were tested for total immunoglobulin (Ig) levels; IgG, IgM, and IgA isotypes of autoantibodies to six phospholipids; total histone and four histone subfractions; and four polynucleotides. Plasma samples were evaluated for the presence of lupus anticoagulant. Total IgG decreased significantly in pregnant patients. The majority of autoantibody levels in pregnant women were within normal nonpregnant ranges. Only a few autoantibodies were increased in early pregnancy, including IgG antiphosphatidylinositol and H 2B, IgM antiphosphatidylinositol and phosphatidic acid, and IgA antiphosphatidylinositol and H 4. Most autoantibodies, although increased at term, were still within the normal nonpregnant range. Normalizing the data for expanded plasma volume did not significantly alter these results. Adjustment regression analysis excluded age, race, and various medical and obstetric indicators as confounding variables for autoantibody levels. The expected and observed prevalence of positive autoantibody levels in pregnant women was not significantly different from that of nonpregnant controls. None of the pregnant women demonstrated positive lupus anticoagulant. We conclude that in normal pregnancy between 16 weeks' gestation and term, autoantibody levels are largely within the normal range. Alterations occur, if at all, at the time of delivery.
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PMID:The prevalence of autoantibodies and lupus anticoagulant in healthy pregnant women. 210 7

The patient is a 23 y.o. man with acute nephritis and bleeding at presentation. Laboratory data consistent with the diagnosis of systemic lupus erythematosus. A lupus anticoagulant was found: tissue thromboplastin inhibition test (TTIT) ratio 3.4; diluted Russell viper venom (DRVV) ratio 2.6. Hypoprothrombinemia (FII:C less than 1%; FIIR:Ag 5%) was present; prothrombin survival time (FII concentrate infusion 60 U/kg): t1/2 approximately to 9 hours. A prothrombin antibody was identified: it is not neutralizing but forms an immunecomplex with prothrombin. The antibody was characterized as IgG2, IgA, k, lambda. The prothrombin survival time indicates that the hypoprothrombinemia is due to the clearance of the prothrombin-antiprothrombin complex in vivo.
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PMID:Prothrombin-antibody coexistent with lupus anticoagulant (LA): clinical study and immunochemical characterization. 210 92

IgG immunoglobulin preparations have been increasingly utilized to treat a variety of diseases. Since disease response to this form of therapy in patients with abnormal autoimmune function is often evaluated through the subsequent investigation of autoantibody levels, it is possible that autoantibody positivities reflect autoantibody reactivity of circulating immunoglobulin preparations and not of the patient's inherent B-cell activity. We therefore investigated three commercially available IgG immunoglobulin preparations separately for IgG, IgM and IgA autoantibody reactivity to six phospholipid antigens, total histone and four histone subfractions, and four polynucleotides. Universally, all three preparations demonstrated considerable IgG antiphospholipid and antihistone reactivity at dilutions of up to 1:10(3) but not antipolynucleotide reactivity. Although no IgM reactivity was detected in any of the preparations, in all three preparations surprising IgA reactivity, especially with antihistone specificity, was detected. No autoantibody reactivity was detected at dilutions compatible with physiologic conditions in vivo. Identical observations were made for lupus anticoagulant reactivity, which was evaluated by activated partial thromboplastin time (APTT) and tissue thromboplastin inhibition (TTI). Since autoantibody reactivities and prolonged APTT assays are observed only at pharmacologic dilution levels, it is unlikely that the administration of IgG immunoglobulin preparation will affect the evaluation of autoantibody levels in patients undergoing such treatment.
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PMID:Commercial IgG immunoglobulin preparations exhibit IgG and IgA autoantibody reactivity at pharmacologic but not at physiologic concentrations. 212 97


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