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)

The relationship between renal morphology and clinical disease was analysed in 148 patients with SLE attending a lupus clinic. Patients were not selected for renal disease. Renal tissue was assessed according to the World Health Organization classification of lupus nephritis, the presence of active and chronic lesions was recorded and disease activity was measured according to a standard protocol. All sections of the classification were represented in this group of patients. Active and chronic lesions were more likely to occur among patients with Class III/IV (proliferative glomerulonephritis), than in any other category. Patients with Class III/IV biopsy were more likely to have evidence of clinical renal disease than patients in Class II (mesangial). However, almost half of the Class II patients had some evidence of renal disease, including elevated serum creatinine, as well as important non-glomerular lesions. Without biopsy they might have been thought to have proliferative lesions and been treated more aggressively. Two patients with proliferative glomerulonephritis had no clinical evidence of renal disease. Thus, at the time of biopsy results renal histological examination did not uniformly correlate with clinical renal disease.
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PMID:Kidney biopsy in SLE. I. A clinical-morphologic evaluation. 261 34

A 28 year-old female patient who has been diagnosed as having systemic lupus erythematosus (SLE) developed an acute dissecting aneurysm of the aorta (DeBakey type I). The long-term, large dose corticosteroid therapy (i.e., accumulative dose of about 60 g) administered for the treatment of lupus nephritis (WHO class III----IV) was considered to be responsible for a hypercholesterolemia (300-560 mg/dl) and a steroid-dependent hypertension (WHO class III) in this patient. The autopsy findings for the aorta were compatible with atherosclerotic changes but not with lupus arteritis. While atherosclerotic cardiovascular complications have been considered to be rare in patients with SLE, a growing body of evidence suggests that the incidence of such a complication may be increasing along with a dramatic improvement in the longevity of patients with SLE after an introduction of a large dose, long-term corticosteroid therapy.
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PMID:[A case of acute dissecting aneurysm of the aorta in systemic lupus erythematosus]. 262 44

Anti-DNA antibodies play a pathogenic role in the development of lupus nephritis. The role of extracellular DNA in the pathophysiology of lupus diseases is still controversial. It is possible that anti-DNA antibodies are elicited by antigens which cross-react with DNA and that they play their pathogenic role through direct binding on cell membrane or tissue components. Alternatively, experimental and clinical studies suggest that extracellular DNA might be involved in the induction of anti-DNA antibodies and that they might be pathogenic through the formation of immune complexes. Recent studies done on circulating DNA led to propose the hypothesis that cell death phenomena might play a major pathogenic role in the induction of auto-immune reactions and/or in the development of kidney lesions in lupus diseases.
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PMID:[Does extracellular DNA play a pathogenic role in the development of lupus glomerulonephritis?]. 269 9

The literature on the treatment of lupus nephritis is scattered, much of it in rheumatological rather than nephrological journals. Whatever our ignorance of the nature and genesis of lupus nephritis, under empirical treatment the prognosis, especially for severe forms, has improved dramatically during the past 20 years. For severe lupus nephritis, the evidence that the addition of cytotoxic agents to corticosteroids improves outcome is now secure, and discussion centres mainly on which drug to use and by what route. Intravenous methylprednisolone is at least as effective as high-dose tapering oral therapy for initial treatment, and carries fewer side-effects. The role of plasma exchange in lupus remains undefined: it may have a role in the treatment of cerebral manifestations or otherwise resistant patients, but controlled trials have failed to show benefit. Future developments will probably centre around the use of specific monoclonal antibodies which target specific groups and subgroups of cells, "humanised" by the splicing of human Fc piece to rodent (fab)2, perhaps bearing toxins. To use these agents to best advantage, however, we will have to understand better than we do today the nature of the cellular defects in the immune response which underlie the lupus syndrome.
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PMID:The treatment of lupus nephritis. 270 18

Treatment with total lymphoid irradiation (TLI) and corticosteroids markedly reduced activity of systemic lupus erythematosis in 10 patients with diffuse proliferative lupus nephritis (DPLN) complicated by a nephrotic syndrome. Physiologic and morphometric techniques were used serially before, and 12 and 36 mo post-TLI to characterize the course of glomerular injury. Judged by a progressive reduction in the density of glomerular cells and immune deposits, glomerular inflammation subsided. A sustained reduction in the fractional clearance of albumin, IgG and uncharged dextrans of radius greater than 50 A, pointed to a parallel improvement in glomerular barrier size-selectivity. Corresponding changes in GFR were modest, however. A trend towards higher GFR at 12 mo was associated with a marked increase in the fraction of glomerular tuft area occupied by patent capillary loops as inflammatory changes receded. A late trend toward declining GFR beyond 12 mo was associated with progressive glomerulosclerosis, which affected 57% of all glomeruli globally by 36 mo post-TLI. Judged by a parallel increase in volume by 59%, remaining, patent glomeruli had undergone a process of adaptive enlargement. We propose that an increasing fraction of glomeruli continues to undergo progressive sclerosis after DPLN has become quiescent, and that the prevailing GFR depends on the extent to which hypertrophied remnant glomeruli can compensate for the ensuing loss of filtration surface area.
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PMID:Outcome of the acute glomerular injury in proliferative lupus nephritis. 276 Feb 19

Spontaneous idiotype shift of anti-DNA antibodies in systemic lupus erythematosus was shown to be associated with changes in the clinical manifestations of the disease. Characterization of two anti-DNA antibody preparations from the same lupus patient showed that lupus nephritis was associated with antibodies showing higher specific antigen-binding activity and avidity to DNA and presenting more cationic quality upon isoelectric focusing and Western blot analysis than the ones found in patients without renal involvement. Lupus cerebritis was associated with anti-DNA antibodies with different idiotypic characteristics not shared by anti-DNA antibodies present in lupus nephritis. Lupus cerebritis anti-DNA antibodies had less specific antigen-binding activity and avidity to DNA and did not show cationic quality. Idiotypic and immunochemical changes of anti-DNA antibodies in lupus may be associated with various clinical manifestations.
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PMID:Characterization of two anti-DNA antibodies bearing distinct idiotypes. Correlation with clinical manifestations. 276

As a result of a careful study of 150 patients with systemic lupus erythematosus (SLE) they could be distributed in 8 clinico-immunologic groups of the disease. Group I included patients with lupus nephritis manifesting by the nephrotic syndrome, group II patients with systemic vasculitis, group III patients with CNS injuries, group IV was made up of patients with discoid lupus, group V of patients with the prevailing damage to the respiratory organs, group VI of patients with hematologic disorders, group VII of patients with generalized visceral SLE, and group VIII included patients with generalized "peripheral" SLE. It was established on HLA typing that on the whole the patients with SLE manifested the increased frequency of HLAA11, B7, B35, DR2 and DR3 antigens. The patients' groups differed in primary carriership of certain antigens. Group I demonstrated a significant increase of the frequency of HLAA9, B13 and DR3, group II of HLADR2, group III of HLAB7, B12 and DR2, group IV of HLAB12, B13 and DR3, group V of HLAA1 and B8, group VII of HLADR1, and group VIII of HLAB35 and DR3. Group VI which was not numerous did not show any clinicogenetic association. The clinicoimmunologic polymorphism can be partially due to the genetic heterogeneity of certain patients' groups with SLE.
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PMID:[Subgroups of patients with systemic lupus erythematosus]. 278 84

Spontaneous shift in Id expression of polyclonal anti-DNA antibodies in a patient, BS, with SLE was investigated. BS had active lupus nephritis in 1982 and developed central nervous system lupus in 1986 without evidence of active nephritis. Two rabbit polyclonal anti-Id (BS-82 and BS-86 R-anti-Id) were raised against affinity-purified anti-DNA antibodies prepared from 1982 serum (BS-82) and 1986 serum (BS-86), respectively. In addition, murine monoclonal anti-Id was prepared against BS-82 Id. Direct binding assays showed that all three anti-Id had preferential binding to the immunizing anti-DNA antibodies (the homologous Id) and poor binding to anti-DNA antibodies prepared from the different dated sample of BS. This was confirmed by inhibition assays of binding of anti-Id to the homologous Id by various Id. Moreover, inhibition assays of binding of various Id to DNA by the R-anti-Id showed that the R-anti-Id was the most effective inhibitor for the homologous Id. Testing for Id expression in serial (1982 to 1986) serum samples of BS with the R-anti-Id as probes showed that BS-82 Id declined and was undetectable after October, 1984, whereas BS-86 Id was first detectable in July, 1985, and increased by June, 1986. These results clearly demonstrate spontaneous shifts in Id expression of human anti-DNA antibodies. The phenomenon of Id shift should be considered in any future strategy for the diagnosis and therapy of human autoimmune disease by anti-Id.
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PMID:Spontaneous shift of anti-DNA antibody idiotypes in systemic lupus erythematosus. 283 39

This study focused on clinical subsets within systemic lupus erythematosus (SLE) in order to identify more homogeneous patient groups in which to define disease susceptibility gene(s). Analysis of the major histocompatibility complex gene products and genes with major histocompatibility complex class II and class III locus-specific probes and oligonucleotide probes for selected human leukocyte antigen DQ-beta alleles showed significant increases of human leukocyte antigen DR2 and the rare DQ-beta allele DR2-DQw1.AZH in the lupus nephritis patients compared with lupus patients without renal disease (relative risk = 8.3). C4A null was detected in one third of all of the SLE patients. In two thirds of the C4A null patients this was due to a DR3-associated C4A gene deletion. The remaining third may have a regulatory defect and this was DR2-associated. DR4 was significantly decreased in the nephritis patients in comparison with the non-renal SLE patients (relative risk = 0.3). A novel DQ-beta gene has been sequenced from two SLE patients that has not been observed in the normal population. Potential implications of these findings are discussed.
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PMID:Major histocompatibility complex associations with systemic lupus erythematosus. 290 62

We investigated the underlying mechanisms of systemic autoimmune disease in MRL-+/+, (NZB X NZW)F1, and (NZB X SWR)F1 mice, since these strains develop glomerulonephritis without the superimposition of any secondary lupus-accelerating genes. All three strains manifested a common immunoregulatory defect specific for the production of pathogenic anti-DNA autoantibodies that are of IgG class and cationic in charge. At or just before the age they began to develop lupus nephritis, spleen cells of the mice contained a subpopulation of Th cells that selectively induced their B cells in vitro to produce highly cationic IgG autoantibodies to both single-stranded DNA (ssDNA) and double-stranded DNA (dsDNA). By contrast, T cells from younger preautoimmune mice were incapable of providing this help. Moreover, only B cells of the older lupus mice could be induced to secrete cationic anti-DNA antibodies of IgG class. B cells of young lupus mice could not produce the cationic autoantibodies even with the help of T cells from the older mice, nor upon stimulation with mitogens. In the older lupus mice we found two sets of Th cells that spontaneously induced the cationic shift in autoantibodies; one set belonged to the classical Th category with L3T4+,Lyt-2- phenotype, whereas the other surprisingly belonged to a double-negative (L3T4-,Lyt-2-), Lyt-1+ subpopulation. The latter set of unusual Th cells were unexpected in these lupus mice since they lacked the lpr (lympho-proliferation) gene. Thus three apparently different murine models of systemic lupus erythematosus possess a common underlying mechanism specific for the spontaneous production of pathogenic anti-DNA autoantibodies.
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PMID:Induction of a cationic shift in IgG anti-DNA autoantibodies. Role of T helper cells with classical and novel phenotypes in three murine models of lupus nephritis. 295 49


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