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)

Although sunlight is known to induce generalized manifestation in systemic lupus erythematosus (SLE) patients, its underlying mechanism remains obscure. In the present study we have investigated whether UVA (320-400 nm), the most predominant UV component in solar radiation, induces enhanced accumulation of reactive oxygen species in murine SLE-derived cells (MRL/l) in comparison to normal cells (Balb/c), as measured by oxygen (O2) consumption, by means of a Clark-type electrode. Our data show enhanced O2 consumption by MRL/1 cells (which correlates with the formation of reactive oxygen species), accompanied by decreased viability, in comparison to irradiated normal cells. This finding suggests that increased accumulation of reactive oxygen species contributes to the enhanced photosensitivity observed in SLE patients.
Lupus 1994 Apr
PMID:Solar ultraviolet radiation induces enhanced accumulation of oxygen radicals in murine SLE-derived splenocytes in vitro. 792 Jun 8

8-Hydroxydeoxyguanosine (80HDG) is a specific marker of oxidative damage to DNA. We have observed that patients with SLE (systemic lupus erythematosus), have undetectable levels of urinary 80HDG by HPLC. Further analysis by GC-MS confirmed that levels of 80HDG in SLE urine were 10(3)-fold lower than in an age- and sex-matched control group. Experiments utilising cultures of SLE and normal lymphocytes exposed to H2O2 confirmed the impaired ability of SLE lymphocytes to repair 80HDG. We subsequently observed in SLE patients that 80HDG had accumulated in low molecular weight DNA associated with circulating immune complexes. We suggest that oxygen radicals may induce pathology in SLE by maintaining the presence of an antigenic form of DNA in the circulation.
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PMID:8-Hydroxydeoxyguanosine. A marker of oxidative DNA damage in systemic lupus erythematosus. 803 28

Enrichment of diet with omega-3 lipid rich-menhaden fish oil (FO) when fed ad libitum to autoimmune lupus-prone NZB/NZW F1 (B/W) female mice delayed the onset and slowed progression of renal disease while significantly extending life-span compared to omega-6 lipid rich-corn oil (CO)-fed mice. Northern blot analysis of kidneys from FO-fed mice revealed no detectable levels of IL-1 beta, IL-6 and TNF alpha mRNA contrasted to levels that were easily detected in CO-fed mice. In contrast to the cytokines, FO-fed mice showed higher renal levels of the antioxidant enzymes-catalase, glutathione peroxidase (GSH-Px), superoxide dismutase (SOD)-mRNAs compared to CO-fed mice. The results suggest that dietary supplementation with FO, as compared to CO, inhibits the production of pro-inflammatory cytokines and ameliorates immune-complex-mediated kidney injury possibly by enhancing the ability of cells to dispose of harmful reactive oxygen intermediates.
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PMID:Decreased pro-inflammatory cytokines and increased antioxidant enzyme gene expression by omega-3 lipids in murine lupus nephritis. 817 24

Gel-filtered sera of patients with various inflammatory and autoimmune rheumatic diseases (N = 354) were screened for the presence of the inflammation marker Cu-thionein. The concentrations of Cu-thionein were significantly diminished in patients with connective tissue diseases (P < 0.001). Sera of patients suffering from inflammatory rheumatic diseases were almost totally depleted of this low-molecular-weight copper protein that exerts pronounced superoxide dismutase activity and scavenges effectively hydroxyl radicals and singlet oxygen. Cortisone treatment of patients with rheumatoid arthritis, systemic lupus erythematosus, and polymyalgia rheumatica replenished impressively the serum concentration of Cu-thionein. The partial oxidation of the EPR-silent Cu(I)-chromophore to Cu(II)/Cu(I)-thionein, which is essential for the catalytic dismutation of superoxide, was monitored by electron paramagnetic resonance in the presence of activated neutrophils and monocytes. Release of Cu-thionein during the oxidative burst of peripheral blood monocytes was demonstrated in vitro. The role of prooxidant-antioxidant imbalances in the pathogenesis of rheumatic diseases is discussed.
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PMID:Copper-dependent antioxidase defenses in inflammatory and autoimmune rheumatic diseases. 807 Sep 7

We examined the relationship between peripheral blood and bronchoalveolar lavage (BAL) lymphocyte phenotypes and lung function in 19 patients with SLE, and evaluated their association with disease activity. Lung function assessment showed a mildly restrictive pattern with frequent impairment of transfer factor for carbon monoxide (T1,co) and diffusing capacity of the alveolocapillary membrane (Dm), of late-expiratory airflow rates and with a high prevalence of increased airway resistance. T1,co, Kco and Dm correlated inversely with the numbers of CD8+ cells and CD56+/CD16+/CD3- (NK) cells in BAL. Oxygen radical production, both by stimulated and unstimulated BAL cells and blood polymorphonuclear leucocytes (PMN) was significantly increased in SLE. In comparison with healthy controls, patients with SLE had a lower percentage of CD19+ B cells in the BAL versus an increased percentage of these cells in peripheral blood. HLA-DR expression on CD4+ and CD8+ lung lymphocytes was markedly increased in SLE. Current SLE disease activity was not associated with changes in BAL or peripheral blood lymphocyte phenotypes. Our data suggest that an ongoing cell-mediated immune response is present in the lungs in SLE, particularly involving activated CD8+ T cells and CD56+/CD16+/CD3- NK cells. It is associated with up-regulated local production of oxygen radicals and with impaired pulmonary diffusing capacity. This inflammatory process seems to be independent of general SLE disease activity.
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PMID:Bronchoalveolar lavage cell analysis and lung function impairment in patients with systemic lupus erythematosus (SLE). 840 94

Hydrogen peroxide in the presence of short wavelength UV light was able to induce alterations in native DNA fragments of 300 bp (ROS-DNA), thereby rendering it immunogenic in experimental animals. The specificity of induced antibodies was investigated by direct binding and competition ELISA. Inhibition studies revealed nearly 89% inhibition in the antibody binding by the immunogen and recognition of native B-, A- and allied conformations presented by various synthetic polynucleotides. Gel retardation assay reiterated the formation of immune complexes between induced antibodies and native and ROS-DNA fragments. It was observed that naturally occurring anti-DNA autoantibodies from systemic lupus erythematosus (SLE) sera recognize ROS-DNA. The comparison of the specificities of anti-DNA autoantibodies from 10 SLE patients showed a 20-50-fold preference for ROS-DNA over native DNA. These results demonstrate that anti-DNA antibodies can be induced by ROS-DNA, and that some of the autoimmune DNA binding antibodies found in SLE may result from response to reactive oxygen species.
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PMID:Polynucleotide specificity of anti-reactive oxygen species (ROS) DNA antibodies. 840 95

In the past 10 years, there have been multiple published reports associating silicone breast implants with scleroderma, morphea, SLE, rheumatoid arthritis, CREST syndrome and "human adjuvant disease." The alleged offending material, silicone, is a synthetic polymer containing a silicon-oxygen backbone. Beginning with the heating of SiO2 in the presence of carbon, elemental silicon is produced. Methylchloride is added and the resulting product is hydrolyzed to form low molecular weight prepolymers which are linked to form linear silicone polymers and cross-linked to yield silicone rubbers or elastomers. The polymeric and hydrophobic characteristics of silicone and the presence of electrostatic charges and organic sidegroups make silicone a potentially ideal immunogen, leading to cross-reactivity with autoantigens. Silicon is an essential constituent of proteoglycans which theoretically could result in immunological cross-reactions between silicone and connective tissues. Although the literature contains numerous examples of silicone-associated autoimmune disease, there is no consistent pattern of immunological abnormalities observed. There are, however, some intriguing and interesting observations. Further large-scale studies are needed to determine if a link between silicone exposure and autoimmunity exists. Also, since the inducing events of autoimmune diseases are unknown, studies on silicone could provide a model for autoimmune diseases associated with toxicological factors.
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PMID:Silicon and silicone: theoretical and clinical implications of breast implants. 844 26

Experience of using an SLE 2000 neonatal trigger ventilator as the sole means of ventilation in 68 infants with respiratory distress syndrome was reviewed. No death or complication was seen in 22 infants with a birth weight above 1500 g. Forty five infants under 1500 g birth weight including 18 infants between 23 and 28 weeks' gestation were trigger ventilated throughout. Six infants died, four of whom were under 28 weeks' gestation. Two infants under 1500 g birth weight sustained a pneumothorax while being ventilated. Nine of 61 infants (15%) had radiological evidence of pulmonary interstitial emphysema, which was mild in seven infants. Intraventricular haemorrhage occurred in 10 babies under 1500 g, four of these being grade III or IV. Twenty two (48%) of the babies under 1500 g required added oxygen at 28 days. The preliminary clinical experience of this trigger ventilator suggests that it is capable of providing respiratory support from birth to extubation in even the most immature infants with respiratory distress syndrome. A controlled clinical trial is now required to compare the safety and efficacy of patient triggered ventilation with conventional neonatal ventilation.
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PMID:Long term trigger ventilation in neonatal respiratory distress syndrome. 846 68

Pneumatosis cystoides intestinalis (PCI) is a relatively rare, benign condition characterized by multiple subserosal or submucosal gas-filled cysts in the bowel wall. The cause and incidence of PCI are uncertain, but the condition is most commonly diagnosed in patients who have chronic obstructive pulmonary disease, gastrointestinal disease (e.g. Crohn's disease, peptic ulcer disease) or collagen disease (e.g. scleroderma, systemic lupus erythematosus). The report of PCI associated with nephrotic syndrome has not be known as far as we have referred. We first experienced a case of PCI with nephrotic syndrome. The patient was a 28-year-old female who had developed nephrotic syndrome in 1977. Although she had been treated by steroid since the onset of the nephrotic syndrome, she was a frequent relapser. She was hospitalized to our hospital on November 1988, due to fourth relapse of the disease. The increasing dosage of steroid (60mg/day) improved general edema and decreased urinary protein, but abdominal pain and fullness occurred seven weeks after the admission. The abdominal radiographs showed air accumulations in the wall of the intestine (probably right sided colon) and retroperitoneum. That finding was confirmed by Barium enema and abdominal computed tomography. We diagnosed the lesions as PCI from the above findings, and high flow oxygen and hyperbaric oxygen therapy improved the symptom of PCI. The etiology of PCI in this case was thought to be mainly a long term steroid treatment.
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PMID:[Pneumatosis cystoides intestinalis following steroid treatment in a nephrotic syndrome patient: report of a case]. 850 60

A 24-year-old woman was admitted to our hospital because of pulmonary hypertension. Five years earlier, she had been given a diagnosis of systemic lupus erythematosus. The pulmonary hypertension was believed to have been caused by pulmonary vasculitis, because pulmonary angiography, nuclear perfusion scans, and axial magnetic resonance imaging of the pulmonary artery showed no evidence of pulmonary thromboembolism. Steroids, a calcium antagonist, and home oxygen therapy did not reduce the patient's pulmonary hypertension. The level of thromboxane B2, a stable metabolite of thromboxane A2, in the pulmonary artery was abnormally high (140 pg/ml). This suggested that vasoconstriction of the pulmonary artery and microthrombosis would cause continuous pulmonary hypertension. Beraprost sodium (120 micrograms/day, p.o.) was administered. This analogue of prostaglandin I2 is a potent relaxer of vascular smooth muscle, and it inhibits platelet aggregation. The pulmonary artery pressure was normal eight months after the start of therapy with beraprost sodium.
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PMID:[Systemic lupus erythematosus with pulmonary hypertension--normalization of pulmonary artery pressure by long-term administration of beraprost sodium]. 858 27


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