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)

Since immunological events were found to be pathogenetically involved in various forms of glomerulonephritis, corticosteroids and immunosuppressive drugs were introduced in the treatment of nephritis. However, as opposed to the findings in the paediatric nephrotic syndrome, controlled and multicentric trials with immunosuppressive therapy revealed disappointing results in the management of renal disease in adults. Significantly better results under immunosuppressive therapy, were seen only in the nephrotic syndrome based on the so-called "no changes" or "minimal changes" nephritis. In chronic membranous and proliferative glomerulonephritis the clinical course in the treated group was not statistically different from that of the untreated group. In some disorders of connective tissues, such as systemic lupus erythematosus, polyarteritis nodosa and Wegener's granulomatosis, corticosteroids and immunosuppressive agents seem to exert a favourable effect on the course of renal disease. Encouraging results concerning the combined use of immunosuppressive drugs, anticoagulants and platelet aggregation inhibitors in mesangiocapillary (membrano-proliferative) glomerulonephritis and rapidly progressive nephritis have also been presented. Several factors such as incomplete immunosuppression, druginduced antigen tolerance and increased immune complex formation as a consequence of inhibited antibody production may contribute to the fact that many patients with different forms of nephritis do not benefit from long-term immunosuppressive therapy.
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PMID:[Immunosuppressive therapy in renal disease (author's transl)]. 0 14

NZB/NZW F1 female mice received levamisole in an attempt to increase suppressor T cell function. Responses varied with dosage of drug and age of mice. When treatment with 25 microgram/gm doses (intermittent or daily) was begun at 12 weeks of age, nephritis was accelerated in spite of transient reduction of anti-DNA antibodies. When treatment was begun at 4 weeks, or when doses of 250 microgram/gm were given, no clinical effects were observed. In the mice with accelerated disease, delayed hypersensitivity and antibody responses to sheep erythrocytes increased; antibody responses to pneumococcal polysaccharide were unaffected. It is possible that some increased immune responses associated with levamisole are undesirable in murine lupus.
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PMID:Alteration of lymphocyte function in NZB/NZW mice. IV. Response to levamisole. 3 81

Although it is generally accepted that DNA:anti-DNA immune complexes play a significant role in the pathogenesis of tissue injury in systemic lupus erythematosus, their presence in the circulation is still a matter of controversy. In this study, we detected DNA:anti-DNA compexes by identification of both the antigen and(or) the antibody, the necessary requisites for immune complex definition, in 14 of 24 plasmas (7 of 11 patients). These antibodies were specific for native DNA and could be adsorbed by anti-immunoglobulin (Ig)G antisera. The DNA recovered was, at least in part, of low molecular weight. The presence of DNA:anti-DNA compexes was not related to high molecular weight IgG, cryoprecipitins, positive polyethylene glycol precipitation, or low plasma C3 levels. It was related significantly to low plasma C4 levels and to the presence of diffuse proliferative nephritis. The lack of correlation with other methods of detection of immune complexes and with the presence of heavy IgG (above 13 S) is in favor of the existence of other antigen-antibody systems (or aggregated immunoglobulins) in systemic lupus erythematosus plasmas. From the results, it appears that methods directed towards the demonstration of specific immune complexes are more informative than those detecting heavy or altered immunoglobulins.
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PMID:Circulating DNA:anti-DNA complexes in systemic lupus erythematosus. Detection and characterization by ultracentrifugation. 3 10

In a comparative study the hemolytic activity of C3, C5, C6, C7, C8, C9 and the C3 proactivator (C3PA) were measured in sera of 22 patients with chronic membrano-proliferative glomerulonephritis (CMPGN), 15 patients with idiopathic nephrotic syndrome, 10 patients with systemic lupus erythematosus, 7 patients with anaphylactoid purpura and 10 patients with acute poststreptococcal nephritis. In CMPGN, C3, C5, C6, C7 and C8 were low in the majority of the patients, whereas C9 and C3PA were depressed only in 21% and 11% of the patients, respectively. By contrast, C3PA and C8 showed striking depressions in the idiopathic nephrotic syndrome. In lupus erythematosus, all the C factors, including C3PA were found to be low with the exception of C9, which was normal in 80% of the patients studied. C3, C5, C6 and C7 were found to be depressed in acute glomerulonephritis; C8 and C9 titers were normal. In all patients studied with anaphylactoid purpura, CH50 and C3 titers were elevated markedly.
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PMID:A study of complement components C3, C5, C6, C7, C8 and C9 in chronic membranoproliferative glomerulonephritis, systemic lupus erythematosus, poststreptococcal nephritis, idiopathic nephrotic syndrome and anaphylactoid purpura. 4 34

The methods currently used for the detection of ANA have been analyzed, with emphasis on their practical application to the diagnosis of the CTD. The use of the indirect IF-ANA test was recommended as a screening procedure to detect ANA. The need to standardize the technique using a single substrate and fluorescent conjugates with uniform F/P ratios was stressed. Most importantly, the value of titrating ANA for the diagnosis of the CTD was discussed. ANA titers higher than 1/500 are usually very significant clinically, often found in spontaneous or drug-induced SLE and few other CTD. The immunologic aspects of ANA and their potential value as aids in the diagnosis and management of the CTD were discussed. Anti-nDNA antibodies have been found to have a high degree of specificity for SLE and high titers of these antibodies correlate well with low levels of serum complement and severity of kidney involvement. The spectrum of ANA in the sera from patients with SLE has been expanded with the finding of anti-Sm antibodies which, when detected by gel precipitation with prototype serum, have been found so far only in SLE. Some of these antibodies have been found to have prognostic significance. Patients with MCTD and a group of patients with SLE have high titers of serum ANA with specificity for an RNase-sensitive component of ENA. The group of SLE patients defined by the presence of these antibodies (anti-Mo) have a better prognosis and in general develop only mild nephritis or have no kidney involvement at all. High titers of pure antinucleolar antibodies probably are found almost exclusively in the sera of patients with scleroderma. Some ANA have organ specificity, and GS-ANA have been found in all patients with Felty's syndrome and in a large proportion of patients with RA. One of the great advances in the field has been the recognition that ANA can be induced in the human and in experimental animals by the use of a number of therapeutic agents. Some of these agents can also induce a clinical picture resembling spontaneous SLE, though kidney involvement does not occur or is extremely mild. It is interesting that the whole spectrum of ANA can be found in drug-induced LE except anti-nDNA antibodies which have been associated to the pathogenesis of immune complex nephritis in spontaneous SLE. There is no doubt that research on ANA has contributed a great deal to the understanding of the CTD and will continue to be a valuable tool for the clinician and the investigator.
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PMID:Antinuclear antibodies (ANA): immunologic and clinical significance. 6 98

Main components of kinin system, the arginine-esterase activity and proteinase inhibitors were estimated in blood serum of patients with nephrotic syndrome of various etiology (glomerulonephritis, amyloidosis, systemic lupus erythematous) and also in patients with latent nephritis and in healthy donors. Content of all the kinin system components (kallikreinogen, kininogen and kininase 1) proved to be increased in all the forms of nephropathy studied. Free kallikrein was found in blood serum of patients with nephrotic syndrome as distinct from healthy persons and patients with latent nephritis. The arginine-esterase activity, which shows the level of trypsin-like proteinases, was altered dissimilarly, depending on the nephrotic syndrome etiology: it was maximally increased in nephrotic syndrome of amyloid genesis and decreased in patient with systemic lupus erythematosus. High content of kallikrein and kininase I with simultaneous decrease in kininogen was typical for patients with severe form of nephrotic syndrome. Impairment of kidney in nephrotic syndrome was also characterized by an increase in alpha1-antitrypsin and in the total antitryptic activity, which reached the maximal value in nephrotic syndrome of the I degree and decreased at the II degree of the disease. In nephrotic syndrome content of alpha2-macroglobulin was maximally increased at the II degree of nephrotic syndrome and decreased in severe form of the disease. The primary alteration in content of proteinase inhibitors and high level of kinin system components were assumed to determine the conditions for activation of kinin system in blood serum and to impair the nephrotic syndrome pathogenesis, which was complicated by systemic manifestations. High content of kinin system components was apparently determined by the increased synthesis in liver tissue in response to inflammation and massive proteinuria; kininase I and alpha2-macrolgobulin, as proteins with high molecular weight, were likely to be selectively retained in blood circulation when the capillary penetration was increased.
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PMID:[State of the kinin system and level of serum proteinase inhibitors in latent nephritis and the nephrotic syndrome of different etiology]. 7 Jan 11

Two complement-dependent assays for circulating immune complexes, the C1q-binding assay and the conglutinin binding, were used to study patients with suspected immune-complex disease. Complexes were detected most frequently in multisystem disease such as infective endocarditis (69%) and systemic lupus erythematosus (60%), and less frequently in isolated nephritis (26% of membrano-proliferative nephritis). Sequential estimations in 32 patients showed that concentrations of circulating immune complexes correlated with disease activity and were useful in monitoring therapy.
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PMID:Value of immune-complex assays in diagnosis and management. 7 21

Circulating antibodies against certain nuclear acidic protein antigens have been shown to have diagnostic and prognostic importance in connective tissue disease. We describe a new precipitin system found in the sera of patients with systemic lupus erythematosus. The antigen, called MA, was prepared from calf thymus nuclei, and was shown to be distinct from other nuclear acidic protein antigens by physicochemical and immunologic techniques. MA antibodies were detected in the serum of 12 of 66 lupus patients and in none of 554 sera from normal controls or patients with other rheumatic diseases. Lupus patients having MA antibodies had more severe disease than did lupus patients with Sm or native DNA antibodies, manifested by recalcitrant skin rashes and a significantly greater incidence of hypocomplementemia, serious renal disease, hypertension, hepatosplenomegaly, lymphadenopathy, and neurological disease (P values range from 0.025 to 0.005). The presence of circulating MA antigen was demonstrated in three lupus patients immediately before a flare of nephritis. These data suggest that MA is a nuclear acidic protein antigen that may identify a subset of lupus patients with very severe disease. The presence of the antigen in the circulation before clinical flares suggests a possible biologic role for the MA system in an immune complex nephritis.
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PMID:Characterization of a distinct nuclear acidic protein antigen (MA) and clinical findings in systemic lupus erythematosus patients with MA antibodies. 8 19

In order to evaluate the incidence of extraglomerular immunoglobulin deposits and to correlate their presence with histopathologic abnormalities, we performed both prospective and retrospective immunofluorescence studies of renal biopsy specimens. Of 200 diagnostic biopsy specimens examined prospectively, 21 had extraglomerular deposits, 19 in association with presumed immunologically-mediated glomerulonephritis. Nine had linear immunoglobulin deposits on tubular basement membrane (antitubular basement membrane antibodies), in one case coexisting with granular deposits, and 13 had granular deposits on tubular basement membrane, in peritubular capillaries and/or arteries, or in tubular cytoplasm (probably immune complexes). Linear deposits on tubular basement membrane were usually associated with antiglomerular basement membrane nephritis or methicillin-associated interstitial nephritis; granular extraflomerular deposits were seen primarily in systemic lupus erythematosus, cryoglobulinemia or membranoproliferative glomerulonephritis.. The incidence of immunoglobulin deposits was high in the three groups of patients examined retrospectively being present in 37 or 47 patients with antiglomerular basement membrane mephritis, 22 or 32 patients with systemic lupus erythematosus of 24 of 130 renal allograft recipients. The contribution of antitubular basement membrane antibodies to renal damage was difficult to assess, although studies in experimental animals attest to their pathogenicity. The occurrence of granular extraglomerular deposits appeared to correlate roughly with the degree of tubulointerstitial injury in the patients with systemic lupus erythematosus.
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PMID:Extraglomerular immunoglobulin deposits in human nephritis. 12 32

Evidence for the presence of immune complexes in blood, synovial fluid, and tisues of patients with rheumatoid arthritis (RA) includes low complement levels in blood and effusions, deposition of immunoreactants in tissues and vessel walls, precipitate formation after addition of monoclonal rheumatoid factor (mRF) to serum or synovial fluid. To quantitate immune complex-like material in RA patients, we developed a radioimmunoassay based on inhibition by test samples of the interaction of (125I)aggregated IgG (agg IgG) and mRF coupled to cellulose. This method could measure immune complexes of human antibody with hemocyanine prepared in vitro. The assay was not influenced by presence of polyclonal RF in test samples, nor by freezing and thawing. Normal levels of immune complex-like material in serum were less than 25 mug agg IgG EQ/ML. 12 of 51 RA sera examined (26%) contained more than 25 mug/ml. The presence of this material in RA sera was found to correlate with severity of disease, as measured by anatomical stage and functional class. There was an inverse correlation of the material with serum C4 level. Rheumatoid synovial fluids generally contained higher levels than serum, and five of 23 contained very much higher levels. The frequency of elevated levels of immune complex-like material in sera of patients with systemic lupus erythematosus (2 of 29) and with miscellaneous vasculitides (2 of 21 was much lower than in RA, suggesting that mRF exhibits a specificity for only certain kinds of immune complexes. The reason for this apparent specificity may explain such distinctive features of RA as the high frequency of polyclonal RF, the lack of immune complex nephritis, and the generally normal levels of serum complement.
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PMID:Immune complexes in sera and synovial fluids of patients with rheumatoid arthritis. Radioimmunoassay with monocylonal rheumatoid factor. 12 89


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