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)

An anti-membrane antibody was present in the sera of systemic lupus erythematosus patients in immunoelectrosyneresis with sodium dodecyl sulfate (SDS) solubilized erythrocyte membrane as antigen. The SDS bound to protein was detected by chromatography at 10(-3)M concentration under U.V. light, at 10(-5)M concentration by the distilled water spray method and at 10(-6)M concentration by using rosaniline hydrochloride colorimetry. SDS was removed from the membrane protein at a concentration of 10(-3)M by the first gel filtration of Sephadex G-25 column and at a concentration of 10(-6)M by rechromatography of the same column. More than 99% of SDS in the solubilized erythrocyte membrane was removed by gel filtration. The antigenicity was still positive in the refiltrated fractions of systemic lupus erythematosus patients. Therefore, all precipitates in the gels were antigen-antibody aggregates.
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PMID:Effect of sodium dodecyl sulfate on immuno-electrosyneresis between normal human erythrocyte membrane and sera of systemic lupus erythematosus patients. 13 42

Electrophoresis in polyacrylamide gels in the presence of sodium dodecyl sulfate was used to separate and quantitate the components of a washed immune precipitate. Serum was from patients with systemic lupus erythematosus known to have antibodies to soluble nuclear ribonucleoprotein (RNP) or to a soluble nuclear non-nucleic acid protein (Sm). Amounts of antibody that was predominantly IgG ranged from 0.2 to 8 mg/ml of patients' serum, and in some cases accounted for over 20% of the total serum IgG. Results demonstrate that some patients respond to the disease by producing large amounts of a specific antibody, and that these antibodies can contribute significantly to hypergammaglobulinemia.
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PMID:Quantitation of precipitating antibodies to certain soluble nuclear antigens in SLE. 30 Oct 28

Qualitative analysis of urinary proteins is contrasted with histological findings of 45 renal biopsies performed in patients with chronic glomerulonephritis. Compared to electrophoresis on cellulose acetate and immunoelectrophoresis, a method using polyacrylamide gel after sodium dodecylsulfate treatment makes for more refined and objective differentiation of protein abnormalities. On the whole, proteinuria of the selective glomerular or physiological type predominates in the event of minimal change or membranous lesions. The non-selective type is found more frequently with diffuse proliferative or membranoproliferative glomerulonephritis (p less than 0.025). There are, however, too many exceptions to this rule to allow certainty, and a precise diagnosis of the particular type of glomerulonephritis is thus only possible histologically. Each type of histological involvement may cause almost any of the qualitative abnormalities of proteinuria. On the other hand, qualitative analysis of urinary proteins is useful for the detection of glomerulonephritis. A glomerular type of proteinuria may sometimes reveal involvement of kidneys at a time when, quantitatively, there is no proteinuria. In cases of orthostatic proteinuria a persistent glomerular type of tracing in recumbency suggests an organic kidney ailment. All patients in this series had a glomerular type of proteinuria when excretion was pathological, thus allowing a distinction from pure tubular involvement. 10 patients of the group, however, although they clearly had glomerular lesions (3 were diffuse proliferative glomerulonephritis) showed perfectly normal proteinuria both quantitatively and qualitatively. This was the case in systemic lupus erythematosus where kidney biopsy was performed without clinical suspicion of renal involvement. In summary, qualitative abnormalities of proteinuria call attention to underlying glomerulonephritis, although no distinction can be made between the various forms and there may be no detectable abnormality even in the event of major kidney involvement.
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PMID:[Value and limits of urinary protein electrophoresis with sodium dodecyl sulfate in the evaluation of glomerular nephropathies]. 45 9

This study investigated the effects of prolonged corticosteroid therapy on the course of spontaneous autoimmune disease and oncogenesis in NZB/NZW mice, an animal model of systemic lupus erythematosus. Twenty young female NZB/NZW mice were treated until death with low-dose hydrocortisone sodium succinate (3.3 mg/kg/day), and 21 mice received high-dose hydrocortisone (10 mg/kg/day). Fifteen control mice were injected with saline. Long-term therapy with either dose of hydrocortisone effectively prevented renal disease and prolonged lifespans in NZB/NZW mice. Fifty-six percent of low-dose treated animals developed neoplasms, and 38% of mice in this treatment group died with renal disease. Neoplasms caused death in 76% of mice receiving high-dose treatment. Long-term hydrocortisone therapy was associated with a predominance of sarcomas, which appeared in aged mice after a long period of treatment. In earlier studies conducted in this laboratory, cyclophosphamide treatment prolonged life in NZB/NZW mice. Ninety-seven percent of cyclophosphamide-treated mice developed neoplasms; most tumors were lymphomas or carcinomas. It was concluded that neoplasms occur commonly in old NZB/NZW mice with lives prolonged by immunosuppressive or antiinflammatory drugs. Nevertheless, the specific therapeutic agent used in each study influenced the types of neoplasms appearing in treated mice.
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PMID:Prolonged lifespan and high incidence of neoplasms in NZB/NZW mice treated with hydrocortisone sodium succinate. 69 74

High plasma renin activity (PRA) was found in 16 of 42 randomly selected nonuremic systemic lupus erythematosus (SLE) patients. Mild hypertension was present in 3 of the 16.6 high-PRA and 10 normal-PRA patients were admitted to a metabolic ward. Salt restriction produced a disproportionate rise in both PRA and aldosterone, a decrease in glomerular filtration rate (GFR) and a slightly greater negative sodium balance in the group with high PRA. Potassium excretion was less than intake in both groups. Balance studies were performed in 6 additional high-PRA patients before and during indomethacin administration (150 mg/24 h). PRA and aldosterone were markedly suppressed by indomethacin. UnaV was significantly greater than in the control period despite of the 28% reduction in GFR. These results suggest that high PRA is secondary to impaired distal tubular sodium reabsorption. Such a defect could be responsible for the relatively low frequency of hypertension in lupus nephritis.
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PMID:Normotensive hyperreninemia in systemic lupus erythematosus. An indicator of tubular dysfunction. 74 33

A modified 125I-labelled DNA-binding test was developed. By using an anionic detergent, 0-025% sodium dodecyl sulphate, the non-specific binding of DNA by basic proteins was completely eliminated, while the specific binding of DNA by anti-DNA antibodies was not interfered with. The level of DNA-binding activity in normal human sera was decreased in the modified DNA-binding test, while its sensitivity was similar to that of the Farr assay in presence of sera from SLE patients.
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PMID:Determination of anti-DNA antibodies by a modified 125I-labelled DNA-binding test. Elimination of non-specific binding of DNA to non-immunoglobulin basic proteins by using an anionic detergent. 79 75

Two patients with long-standing systemic lupus erythematosus were found to have persistent hyperkalemia. The hyperkalemia could not be explained by renal insufficiency, oliguria, diminished distal sodium delivery, acidemia, or hemolysis. After sodium depletion, urinary aldosterone excretion and plasma aldosterone concentration rose appropriately. No increase in urinary potassium excretion or decrease in serum potassium concentration was noted after fludrocortisone acetate, furosemide, or acetazolamide plus sodium bicarbonate. We conclude that these patients have a primary defect in renal tubular potassium secretion that may be related to an immune complex interstitial nephritis.
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PMID:Impaired renal tubular potassium secretion in systemic lupus erythematosus. 84 84

Polymorphonuclear (PMN) leucocytes from 4 patients with untreated systemic lupus erythematosus (SLE) showed defective random migration (P less than 0-05) and depressed chemotactic responses to C5a and kallikrein (P less than 0-01) compared to PMN leucocytes from normal subjects, or patients with rheumatoid arthritis (4) or Felty's syndrome (4) when examined at a standardized cell concentration with a micropore filter radioassay but not with a conventional Boyden technique. Normal in vitro enhancement of PMN leucocyte random and chemotactic migration by sodium ascorbate was absent in SLE and Felty's syndrome, but sodium ascorbate gave normal stimulation of hexose monophosphate shunt activity in the PMN leucocytes precluding a defect in ascorbate transport.
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PMID:Defective responsiveness to ascorbic acid of neutrophil random and chemotactic migration in Felty's syndrome and systemic lupus erythematosus. 100 18

HLA class I antigens (Bg) on red cells (RBCs) are expressed by some normal donors and by many patients with systemic lupus erythematosus (SLE). To identify the membrane components previously detected by hemagglutination with HLA class I-specific monoclonal antibodies (MoAbs), RBC membrane preparations were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotted with the HLA class I MoAbs. Two components were obtained that reacted with the MoAbs: a heavy chain of 45 kDa and a light chain termed beta2-microglobulin (beta2-M) of 11 kDa. The effect of chloroquine and acid elution in stripping HLA antigens is shown to be due to the removal of beta2-M, as only that component was detected in eluates from reactive RBCs. Neither antibody elution method affected the heavy chain expression assessed by immunoblotting. It is concluded that HLA class I antigens on RBCs are integral membrane components of the type normally found and wisely distributed on many nucleated cells. Platelets, which have stronger HLA class I antigen expression, were also studied, and their membrane preparations yielded heavy chain and beta2-M molecules; the effect of chloroquine treatment was harder to assess than that of acid elution, owing to the sensitivity with which both components are detected in immunoblotting. In eluates obtained from acid treatment only beta2-M is detected.
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PMID:A study of HLA (Bg) on red cells and platelets by immunoblotting with monoclonal antibodies. 168 15

The therapeutic history of sodium diethyldithiocarbamate (dithiocarb) is briefly reviewed. Dithiocarb was discovered serendipitously in our laboratory 35 years ago for the specific treatment of nickel carbonyl poisoning. Since that time, the therapeutic efficacy of dithiocarb has been reported for many disorders, including: nickel, cadmium, thallium, copper, and mercury poisonings, experimental nickel carcinogenesis, protection against radiation damage to bone marrow, treatment of candidiasis in experimental animals, hepatolenticular degeneration (Wilson's disease), systemic lupus erythematosis, and human immunodeficiency virus infection (HIV). It has been used as an antagonist to cisplatin and cyclophosphamide toxicities, and as an antidote to hepatotoxicity induced by chloroform, carbon tetrachloride, and halothane. Most recently, it has been observed that the progression of HIV-1 infection is inhibited by dithiocarb administered intravenously or orally to patients with acquired immunodeficiency syndrome (AIDS). Attention is directed to the interactions of divalent cations to viral infections and to metal chelators (e.g., dithiocarb) as potential antiviral agents.
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PMID:Therapeutic properties of sodium diethyldithiocarbamate: its role as an inhibitor in the progression of AIDS. 184 85


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