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)

A radioimmunoassay for fibrinopeptide A (FPA) has been developed. This assay uses rabbit antibodies induced by injection of native FPA-human serum albumin conjugates and 125I introduced into tyrosine-FPA synthesized in out laboratory. Plasma FPA is separated from fibrinogen by TCA extraction. The assay is capable of detecting as little as 50 pg/ml of FPA. In 20 normal donors this assay revealed a mean concentration of 0.9 ng/ml (0.3 SD). In five patients with disseminated intravascular coagulation, FPA concentrations ranged from 13.0 to 346 ng/ml. Two groups of patients with systemic lupus erythematosus (SLE) whose disease had achieved complete remission were studied; one consisted of four patients with no history of lupus nephritis and another with a history of nephritis. Mean FPA concentrations of 1.5 ng/ml (range, 0.7-1.8 ng/ml) and 2.7 ng/ml (range, 1.1-5.6 ng/ml) were found in these two groups, respectively. Another group of nine patients with active SLE, but without evidence of lupus nephritis, had a mean FPA concentration of 4.5 ng/ml (range, 2.4-7.8 ng/ml). Finally, a group of seven patients with active SLE, including active nephritis, had a mean FPA concentration of 10.2 ng/ml (range, 5.3-17.0 ng/ml). A positive correlation was found between the concentration of plasma FPA and serum DNA-binding activity and an inverse correlation was found between plasma FPA and the concentration of serum C3. No correlation existed between plasma FPA and concentration of serum creatinine. Several possibilities for the origin of plasma FPA in patients with SLE were considered; at present it seems most likely that FPA arises through the action of thrombin on fibrinogen.
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PMID:Fibrinopeptide A in plasma of normal subjects and patients with disseminated intravascular coagulation and systemic lupus erythematosus. 93 2

Anasarca with pronounced hypoalbuminemia developed in a young woman 15 months after the onset of a mild, arthralgic type of systemic lupus erythematosus (SLE) without evidence of active nephritis. Investigation indicated a gastrointestinal rather than a renal site for protein loss. A full clinical remission was achieved with low-dose corticosteroid therapy.
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PMID:Systemic lupus erythematosus with a protein-losing enteropathy. 94 33

Serial complement component (C3 and C4) determinations were performed in 26 children with systemic lupus erythematosus. Twenty-one children with SLE had 52 episodes of C3 depression (mean duration 25 weeks); only 11 of these children had active nephritis when serum concentrations of complement were depressed. Fourteen children had active rash associated with low C3; in seven of these children rash was the only clinical evidence of disease activity. Ten children had active CNS disease; in seven children the CNS involvement correlated with low C3. In general, variations in serum concentrations of C4 did not reflect changes in SLE activity which were not reflected by changes in serum concentrations of C3. Serum C4 occasionally remained depressed longer than C3, perhaps reflecting continuing subclinical disease activity. Increased C3 occurred in 18 of 26 children as doses of corticosteroid were increased, in six of 14 when cyclophosphamide was added, and in two children when hydroxychloroquine was added. Our findings suggest that a wide variety of manifestations of childhood SLE may produce hypocomplementemia. In addition to renal disease, variations in serum concentrations of C3 and C4 can reflect, or occasionally predict, changes in rash and CNS disease.
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PMID:Systemic lupus erythematosus in childhood correlations between changes in disease activity and serum complement levels. 95 59

A patient population admitted to the hospital for either SLE or RA was surveyed for the subsequent development of neoplasms. The frequency of neoplasm in SLE patients appeared to be exaggerated, whereas the frequency of subsequent neoplasm in rheumatoid patients was unexpectedly low. A paucity of nephritis in the SLE group was noted. Further reports are encouraged so that the magnitude of the risk of malignancy developing with immunosuppressive therapy can be more precisely ascertained.
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PMID:Frequency of neoplasia in systemic lupus erythematosus and rheumatoid arthritis. 99 36

Extractable nuclear antigen (ENA) is composed of at least two components, one a ribonucleo-protein sensitive to ribonuclease or heat and the other a protein. Antibodies to ENA are associated with a relatively benign clinical course in patients with systemic lupus erythematosus (SLE) in which DNA anti DNA complexes are thought pathogenic. The effect of ENA and anti-ENA on DNA anti-DNA reactions in vitro was studied. ENA effectively inhibited an anti-DNA hemagglutination reaction but no effect was found on binding of radioactive DNA or on the anti-hemocyanin hemagglutination reaction. The inhibitory effect was not abolished by yeast ribonuclease (RNase), heating, or DNase. Anti-ENA HAD NO EFFECT ON ANTI-DNA hemagglutination. In vivo, ENA altered the NZB/NZW mouse nephritis thought to be a model for human SLE nephritis. These results suggest the possiblity of a role for ENA in alteration of diseases due to pathogenic DNA anti-DNA complexes.
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PMID:Extractable nuclear antigen effect on the DNA anti-DNA reaction and NZB/NZW mouse nephritis. 107 29

The incidence of autoantibodies to various nuclear antigens was studied in 64 patients with SLE, 137 patients with various connective tissue diseases, 63 other patients and 90 controls. A positive correlation was found between SLE, nephritis, and the presence of antibody against native DNA. Antibody to denatured DNA showed no specificity for SLE and was correlated with the absence of nephritis. Antibody to RNA-protein occurred mainly in SLE, regardless of the presence or absence of nephritis.
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PMID:[Antibodies against various nuclear antigens (especially DNA and RNA proteins) in disseminated lupus erythematosus with and without kidney involvement and in other collagen diseases. Preliminary report]. 108 42

Drug-induced systemic lupus erythematosus (SLE)-like syndromes in children are most commonly associated with the administration of ethosuximide, diphenylhydantoin, and trimethadione. Five children receiving ethosuximide who presented with syndromes suggestive of SLE were studied. Each and fever, malar rash, arthritis, and lymphadenopathy. Two children had pleural effusions and another developed myocarditis and pericarditis. Three patients had anti-DNA antibodies associated with low serum C3. In four of five children symptoms disappeared with the discontinuation of ethosuximide; two of these continue to have antinuclear antibodies (ANA). One child continues to have active SLE with nephritis. A group of 101 children from a seizure clinic were tested for the presence of ANA. ANA were found in 14 of 70 children receiving ethosuximide and/or diphenylhydantoin; 2 of 14 had anti-DNA antibodies. Serum ANA titers in the drug-induced SLE group did not differ significantly from those of the asymptomatic seizure patients. ANA were also present in 5 of 23 children receiving phenobarbital only. The induction of ANA by phenobarbital is a possible hypothesis. Quantitative immunoglobulins and C3 were not significantly altered in the asymptomatic children with ANA. Follow-up studies at ten months showed no asymptomatic child with ANA to have developed clinical with ANA to have developed clinical evidence of SLE. This study suggests that asymptomatic children who develop ANA should have careful observation, but need not have their anticonvulsants discontinued.
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PMID:Antinuclear antibodies and lupus-like syndromes in children receiving anticonvulsants. 108 1

Forty-four patients with antibodies to ribonuclease-sensitive extractable nuclear antigen (ENA), ribonuclease-resistant ENA, or both, are described. Most patients with antiribonucleoprotein (anti-RNP) antibodies have overlapping features of systemic lupus erythematosus (SLE), progressive systemic sclerosis (PSS), and polymyositis, and have a low incidence of nephritis. Most patients with antibody solely to ribonuclease-insensitive ENA have SLE; these patients with SLE are typical of the general SLE population, except that they demonstrate an increased incidence of Raynaud phenomenon. Furthermore, it is shown that antibody to ENA may occur in other rheumatic and nonrheumatic diseases, and that not all patients who have a clinical overlap of SLE and PSS that is suggestive of mixed connective tissue disease have anti-RNP antibody.
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PMID:Antibodies to components of extractable nuclear antigen. Clinical characteristics of patients. 108 22

Serum C4 and C3 concentration and binding of double-stranded-DNA (ds-DNA) were measured in sera from ninety-nine patients with systemic lupus erythematosus and clinical evidence of nephritis. C3 and C4 concentrations correlated poorly with ds-DNA binding. In sera from fifty-three patients, precipitating antibody was sought using the counterimmunoelectrophoretic technique. Precipitating antibody was detected on at least one occasion in 44% of the patients, and these sera with precipitating antibody showed higher binding of ds-DNA and lower C4 concentrations than those without precipitating antibody. In thirty-two patients, serial assessments of the activity of the renal disease were made using decline or improvement in glomerular filtration rate, degree of proteinuria, oedema and hypertension as indices of "activity". All patients were receiving immunosuppressive drugs. Active nephritis was rarely found in patients showing, at that time, a normal serum C4 or normal ds-DNA binding; but a raised ds-DNA binding or lowered serum C4 were found in both active and inactive nephritis. There was no correlation of activity with serum concentrations of C3, or the presence or absence of precipitating antibody. We conclude that measurements of serum-complement concentrations and binding of ds-DNA are of most use in the diagnosis of systemic lupus erythematosus, and that in patients with nephritis and taking immunosuppressive drugs, these tests are of limited use in guiding treatment.
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PMID:Disease activity in the nephritis of systemic lupus erythematosus in relation to serum complement concentrations. DNA-binding capacity and precipitating anti-DNA antibody. 108 78

Interstitial immune complex nephritis in patients with systemic lupus erythematosus (SLE). Renal tissues from 45 patients with SLE nephritis, 34 patients with idiopathic membranous nephropathy (IMN) and 77 patients with minimal glomerular disease (MGD) were studied by light, immunofluorescence and electron microscopy. Interstitial nephritis characterized by focal or diffuse infiltration of inflammatory cells, tubular damage and interstitial fibrosis was observed in 66% of SLE patients. Fluorescein-conjugated antibodies to immunoglobulins or complement or both were bound to peritubular capillaries, interstitium and tubular basement membranes (TBM) in 53% of patients with a granular pattern corresponding to opaque deposits seen by light or electron microscopy or both. Antibodies reactive with thymidine or cytosine or both were bound to interstitial structures in 19% of patients tested and showed the same granular distribution. Interstitial cellular infiltration was rare and deposits of immunoglobulins and complement were rare or absent in IMN and MGD, whereas deposits of DNA products were never observed. The findings are consistent with the interpretation that in patients with SLE nephritis immune deposits, presumably containing DNA-anti-DNA complexes, localize in peritublular capillaries, TBM and interstitum, thereby producing an inflammatory reaction which contributes to development and evolution of renal diseases.
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PMID:Interstitial immune complex nephritis in patients with systemic lupus erythematosus. 109 62


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