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)

Several studies have provided evidence suggesting that "placebo effects" represent conditioning phenomena and that learning processes influence the response to placebo medication. This case report describes an adolescent with severe lupus erythematosus who received cyclophosphamide (CY) paired with taste (cod liver oil) and smell (rose perfume) as conditioned stimuli. The regimen was based on conditioning experiments with animals who had lupuslike autoimmune disease. After the initial pairings, the taste alone was offered between CY treatments. Over 12 months, the patient received six rather than 12 CY treatments, half the cumulative dose that might have been administered. The patient improved clinically, and 5 years later continues to do well.
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PMID:Conditioning as an adjunct in the pharmacotherapy of lupus erythematosus. 157 57

Antibodies against ENA (Extractable Nuclear Antigens), SSA/Ro and SSB/La were investigated in parallel in the serum and the immune complex precipitates of 41 patients with autoimmune disease (10 systemic lupus erythematosus, 23 discoid lupus erythematosus, 3 subacute cutaneous lupus erythematosus, and 5 progressive systemic sclerosis). It was demonstrated that in some cases the autoantibody spectrum of the serum did not coincide with that of the immune complex precipitate. In the majority of patients the protein content of isolated immune complexes was increased and the increase was attributed to IgG solely. In some patients antibodies appeared not only in the serum but also in immune complex, even in 4 patients (2 systemic lupus erythematosus, 1 subacute cutaneous lupus erythematosus, and 1 progressive systemic sclerosis) antibodies were detected only in the immune complex precipitate.
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PMID:[Detection of circulating antibodies in the blood and immune complex precipitates of patients with autoimmune diseases (preliminary report)]. 157 50

A 17-year old-male presented with a 6-week history of weight loss, lassitude and calf pains. On examination he was very pale. Laboratory tests showed a very high erythrocyte sedimentation rate (155 mm in the first hour), anaemia (haemoglobin 10.1 g/dl), and a raised serum creatinine of 1.54 mg/dl. Microhaematuria (5-10 erythrocytes/microliter) and pronounced pyuria (500 leucocytes/microliter) were present, but the urine was sterile and there was no increase in albumin excretion. The serum IgG was raised to 75.7 g/l, suggesting an autoimmune disorder. Anti-nuclear antibodies (titre 1 : 1920) and anti-double-stranded DNA antibodies (31 U/ml) were present, while the serum complement C4 was decreased to 0.11 g/l. Renal histology showed an interstitial nephritis without glomerular involvement, while the bone marrow showed vasculitis accompanied by a prominent plasma-cell infiltrate. A diagnosis of interstitial nephritis associated with systemic lupus erythematosus was made, with asymptomatic cardiac and hepatic involvement. Renal function recovered rapidly with prednisolone therapy (initial dose 2 mg/kg.d). While glomerulonephritis is the most common lupus-associated renal disorder, isolated interstitial nephritis may occur in some cases, often with an absence of proteinuria.
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PMID:[Interstitial lupus nephritis]. 158 9

The significance of anti-cardiolipin antibodies (ACLA) in patients with a range of autoimmune and infective disorders was investigated in this study. Although lower levels of IgG and IgM ACLA were present in 77 of 400 patients' sera (19%), high antibody levels were found in less than 5% of patients. These latter patients belonged to three clinical categories: patients with connective tissue disease (CTD), infectious mononucleosis or biological false positive serology. An assay was developed to measure lupus anticoagulant (LA) activity in serum: significant LA activity was found in the CTD patients alone (in 6 of 15 tested) and all of these had high titre ACLA. Features of the antiphospholipid syndrome (APS) were present in these six patients but also in three additional CTD patients with normal LA results and high levels of ACLA. In two CTD patients with APS features, the high ACLA were of IgM isotype. These results stress the importance of measuring both ACLA and LA in an investigation of the APS: a high positive ACLA supports the diagnosis of APS, particularly in patients with autoimmune disease, whilst a high positive ACLA in association with LA activity is specific for this syndrome.
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PMID:Selection of patients with the antiphospholipid syndrome by serological measurement of lupus anticoagulant activity in conjunction with anticardiolipin antibodies. 160 Jun 90

Transgenic mice were generated that express both the H and L chain genes derived from a hybridoma secreting an IgG2a mAb specific for ds- and ssDNA. This hybridoma is derived from a lupus mouse and can accelerate nephritis in young NZB x NZW F1 female mice and induce clinical nephritis in BALB/c mice. Some transgenic B cells did not exhibit allelic exclusion; they expressed both transgene-derived IgG and endogenous IgM intracellularly. Most of the B cells in transgenic mice expressed endogenous IgM, some of them expressed low levels of IgG on cell membranes. The transgenic mice, created in a strain not prone to SLE, expressed elevated serum IgG anti-DNA, and some developed clinical nephritis. The affinity of the spontaneously secreted IgG antibodies for dsDNA were similar in nephritic NZB x NZW F1 and transgenic mice. In contrast to the nontransgenic littermates, immunization of transgenic mice with murine DNA further enhanced serum levels of IgG anti-DNA in transgenic mice. Therefore, expression of transgene-encoded IgG anti-DNA mainly in the secreted form does not provide the signals necessary for allelic exclusion or self-tolerance. Expression of this Ig is sufficient to induce a mild form of autoimmune disease.
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PMID:Failed self-tolerance and autoimmunity in IgG anti-DNA transgenic mice. 160 61

The role of TNF-alpha and IFN-gamma in various models of autoimmune disease were analyzed. These include murine models of lupus, type 1 diabetes in NOD mice and the adjuvant arthritis model in rats. Rather than being involved mainly in the effector arm of the inflammatory process of autoimmune organ destruction, our data suggest a primary involvement of these cytokines in some of the basic mechanisms of the autoimmune process. Evidence has been presented that emphasizes the possibility of the involvement of TNF-alpha in the genetic predisposition to SLE. Based on the data presented, one should be cautious in extrapolating the effects of these cytokines in various in vitro systems to the in vivo situation.
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PMID:Tumor necrosis factor and interferon gamma: relevance for immune regulation and genetic predisposition to autoimmune disease. 162 86

A long-term side effect of therapy with a variety of drugs is a syndrome resembling the idiopathic autoimmune disease, systemic lupus erythematosus. Essentially all patients with drug-induced lupus display autoantibodies to nuclear histone components whose specificity appears to be related to the higher order structure of histones existing in chromatin. IgG antibodies to H1 and the (H2A-H2B)-DNA complex were observed in most patients with lupus induced by procainamide, hydralazine, and quinidine, whereas the H3-H4 tetramer, comprising half the mass of the nucleosome core particle, was largely nonantigenic. IgM antibodies to (H2A-H2B)-containing chromatin subunits were common also. IgM reactivity was observed with the DNA-free H3-H4 tetramer and with H1, especially in hydralazine-induced lupus. These results suggest that IgM antihistone antibodies may result from autoimmunization with a nonnative form of chromatin, whereas IgG antibodies may be selected for reactivity with H1 and a native form of the (H2A-H2B)-DNA subunit of the nucleosome. The chemical basis for induction of autoimmunity by drugs is unclear because lupus-inducing drugs do not have a common structural feature or biological activity nor are they capable of specific reactions with histones, the principal target antigen. However, in the presence of activated neutrophils, procainamide is transformed metabolically to the cytotoxic procainamide-hydroxylamine. Mixing experiments and cell-free studies demonstrated that procainamide was cooxidized with H2O2 by myeloperoxidase released when neutrophils undergo the respiratory burst and degranulation reactions. Preliminary results indicate other lupus-inducing drugs are also biotransformed by this mechanism suggesting that a common denominator linking these drugs may be the capacity to be oxidized to reactive metabolites by the action of activated phagocytic cells.
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PMID:Autoantibody specificity in drug-induced lupus and neutrophil-mediated metabolism of lupus-inducing drugs. 163 38

To evaluate effects of commonly used progestational estrogenic contraceptive steroids in a hormone-responsive model of lupus, we treated female NZB/W mice before clinical disease (6 wks of age) and after onset of lupus (24 wks of age) with doses of hormones titered to suppress reproduction. We report efficacy of norethindrone (NE) and norgestrel (NG), progestins derived from 19-nor-testosterone, in delaying expression of anti-DNA antibodies. Mice implanted with NG at 24 wks of age had prolonged lifespans. In contrast, the hydroxyprogesterone derivative, medroxyprogesterone acetate (MP), did not affect autoimmune disease. These observations suggest that prolonged administration of 19-nor-testosterone derivatives, in small doses adequate to suppress reproduction, may have ameliorative effects in systemic lupus erythematosus. Mice receiving ethinyl estradiol (EE) plus courses of tetracycline to suppress cystitis had active anti-DNA responses. In 60% of EE-treated mice, however, early deaths resulted from malignant lymphomas and complications of obstructive uropathy. Estrogen toxicity, rather than accelerated lupus, was the major cause of death in NZB/W mice treated with EE.
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PMID:Effects of prolonged administration of the 19-nor-testosterone derivatives norethindrone and norgestrel to female NZB/W mice: comparison with medroxyprogesterone and ethinyl estradiol. 166 44

MRL/MpJ-lpr/lpr mice spontaneously develop a lupus-like autoimmune disorder characterized by massive proliferation of T cells and rapidly fatal immune complex glomerulonephritis. We evaluated the therapeutic effect of 5-azacytidine (5AC), a cytidine analogue known as an inhibitor of DNA methylation, in MRL/MpJ-lpr/lpr mice. Intraperitoneal injection of 5AC (50 micrograms, twice a week) starting from 6 weeks of age retarded the development of lymphadenopathy and autoimmune syndrome. Its beneficial effects included: (a) increased life-span, (b) diminution of lymphadenopathy and splenomegaly, (c) reduction in circulating levels of autoantibodies such as anti-DNA and rheumatoid factors, and (d) suppression of lupus glomerulonephritis. However, similar treatment in BALB/c mice did not affect the development of IgG anti-human IgG antibody responses. These results suggest that the protective effect of 5AC is related to the inhibition of the lpr gene-induced T cell proliferation, thereby suppressing the autoimmunity-accelerating effect mediated by the lpr gene.
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PMID:5-Azacytidine inhibits the lpr gene-induced lymphadenopathy and acceleration of lupus-like syndrome in MRL/MpJ-lpr/lpr mice. 169 37

The authors report three cases of immunologic spontaneous abortions and fetal death. In the first patient there was lupus-like anticoagulant activity with a diagnosis of sub-clinical autoimmune disease; the second showed inadequate blocking factor activity, while the third subject presented excessive lymphocytotoxicity. In these cases three different therapeutic protocols were successfully used: flucortolone and salicylates, high-dose intravenous gammaglobulins and subcutaneous heparin.
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PMID:The use of three different therapeutic protocols according to the immunologic pathology present in three women with recurrent spontaneous abortion and fetal death for immunologic reasons: flucortolone and salicylates; high-dose intravenous gammaglobulins; subcutaneous heparin. 170 72


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