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)

Whole sera and serum fractions from 24 patients with Felty's syndrome, 42 patients with systemic lupus erythematosus (SLE), and 48 patients with rheumatoid arthritis (RA), as well as 30 patients with miscellaneous acute and chronic disease states, were studied for their effect on numbers of mouse bone marrow colonies grown on soft agar in the presence of human colony stimulating factor. Significant early retardation of mouse bone marrow colony counts was recorded in 87.5 percent of Felty's sera, 43 percent of SLE sera, and 12.5 percent of sera from patients with uncomplicated RA. Forty percent of 30 other control patients with acute or chronic inflammatory diseases also showed this activity. No diminution was noted with any of 40 normal control sera. Degree of marrow colony retardation could be directly correlated to amounts of test serum added. No single serum fraction isolated by ion exchange chromatography, gel filtration, or electrophoresis was identified as solely responsible for marrow growth retardation; however lipoprotein fractions including chylomicrons, LDL and HDL showed inhibiting activity in various sera.
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PMID:Retardation of colony growth of in vitro bone marrow culture using sera from patients with Felty's syndrome, disseminated lupus erythematosus (SLE), rheumatoid arthritis, and other disease states. 16 5

Men with ankylosing spondylitis (AS) and females with systemic lupus erythematosus (SLE) were found to have low total serum lipid concentrations similar to results previously obtained in patients with rheumatoid arthritis (RA). In AS men total serum TG was about 50% of control values and in AS men and SLE women total serum cholesterol was 78% of control values but close to corresponding RA concentrations. This was explained mainly by low LDL concentrations. There was a marked difference between RA patients and AS and SLE patients in that the two latter groups had normal HDL cholesterol concentrations whereas in RA patients the HDL cholesterol concentration was only 70% of control values. Thus in spite of similar and low total serum lipid concentrations, differences in lipoprotein composition were found in the three different rheumatic diseases, underlining the importance of lipoprotein analyses in the study of dyslipoproteinaemia.
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PMID:Further studies on serum lipoproteins in connective tissue diseases. 21 90

The effect of dietary fish oil (Omega-3 fatty acids--eicosapentenoic acid [EPA] and docosahexaenoic acid [DHA] on several mechanisms involved in immune, inflammatory and atherosclerotic vascular disease was determined in 12 subjects with systemic lupus erythematosus (SLE) and nephritis. These out-patients supplemented their usual diet for five weeks with daily doses of 6 g of fish oil, followed by a five-week washout period, then five weeks of 18 g of fish oil daily. The platelet EPA content rose six-fold with the lower and 15-fold with the higher dose of fish oil, and similar changes occurred to the platelet DHA content. The platelet arachidonic acid incorporation was reduced by 16 and 20%, respectively. These changes were associated with a reduction in collagen-induced platelet aggregation and an increase in red cell flexibility and a decrease in whole blood viscosity. Prostacyclin (PGI2) production was unaffected by the fish oil, but PGI3 formation correlated with its administration and dosage. Neutrophil leukotriene B4 release was reduced 78 and 42%, respectively, by the low and higher doses of fish oil. The higher fish oil dose induced a 38% decrease in triglyceride and a 39% reduction in VLDL cholesterol associated with a 28% rise in HDL, cholesterol. The fish oil had no effect on immune complex or anti-DNA antibody titer, albuminuria, intraplatelet serotonin or [14C]-serotonin release from platelets. We conclude that in patients with lupus nephritis, dietary supplementation with fish oil affects the mechanisms involved in inflammatory and atherosclerotic vascular disease.
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PMID:Omega-3 fatty acid dietary supplementation in systemic lupus erythematosus. 281 Oct 63

Serum was examined for a cytotoxic effect on cultured human fibroblasts, using 8 normal controls and 4 patients. Three of the patients had secondary lipidoses associated with monoclonal gammapathies of IgA kappa, IgG kappa and IgG lambda types. The fourth had systemic lupus erythematosus (SLE) with hyperlipidemia. Only serum containing the monoclonal IgG lambda was found to be cytotoxic. This circulating IgG lambda was strongly bound to HDL and behaved like an antilipoprotein antibody. The circulating immune complexes may be the serum factor responsible for the cytotoxicity and the cutaneous plane xanthomas, thus giving another example of 'antibody-dependent' cellular cytotoxicity previously described for endothelial cells in other diseases.
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PMID:Cytotoxic effect of serum on fibroblasts in one case of normolipidemic plane xanthoma and myeloma IgG lambda. 309 2

Estrogen replacement therapy has been demonstrated to shift the lipoprotein profile toward a less atherogenic one with concomitant increases in HDL and reductions in LDL cholesterol and serum triglycerides. Estrogen, however, has also been implicated in playing a significant role in autoimmune disease and may be involved with disease incidence and progression. The MRL/lpr mouse strain represents an autoimmune disease model with features resembling systemic lupus erythematosus including high-titer autoantibodies, glomerulonephritis, and vasculitis. In the present study, the effects of estrogen treatment on serum lipoprotein profiles were investigated by fast protein liquid chromatography in female MRL/lpr mice, in the MRL/++ strain with a milder form of disease, and in control Balb/c mice. Treatment of MRL/lpr mice for periods of 1 week or longer with pharmacologic doses of estrogen resulted in a significant increase in the amount of cholesterol carried on LDL particles. The up to eightfold increase in LDL cholesterol was less significant in the MRL/++ or Balb/c mice. Maximal increases were observed at 1 to 2 mg/kg of estrogen agonists, and the effect on LDL cholesterol increases was inhibited by tamoxifen. The HDL-to-LDL shift in cholesterol observed in estrogen-treated autoimmune mice correlated with an increase in apolipoprotein E, primarily on larger HDL particles. In addition to the increase in LDL cholesterol, hormonal treatment also resulted in a shift in triglycerides from the VLDL to the LDL fraction in both normal and autoimmune mice. These results suggest that pharmacologic doses of estrogen may contribute to cardiovascular disease progression by shifting the relative distribution of cholesterol from HDL to LDL in this murine model of lupus.
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PMID:Estrogen-induced alterations in lipoprotein metabolism in autoimmune MRL/lpr mice. 758 27

Lipid, lipoprotein, and apolipoprotein effects of hydroxychloroquine were studied in 18 female patients with systemic lupus erythematosus (SLE) with mild or inactive disease. Patients were case matched (200-400 mg hydroxychloroquine daily vs no hydroxychloroquine) on several factors including daily corticosteroid dose in this cross sectional study. All had normal menstrual cycles; none smoked, used alcohol, were taking lipid altering medications or had other concurrent diseases. Patients taking hydroxychloroquine had 35-54% lower total triglyceride, VLDL-triglyceride, LDL-triglyceride, HDL-triglyceride, VLDL-cholesterol, and apolipoprotein CIII levels (p < 0.03). These results are encouraging in that hydroxychloroquine, in addition to being useful for alleviating the primary symptoms of SLE, may also be useful for ameliorating the adverse effects of corticosteroid therapy on triglyceride-rich lipoprotein metabolism.
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PMID:The lipid, lipoprotein, and apolipoprotein effects of hydroxychloroquine in patients with systemic lupus erythematosus. 849 61

Kidney involvement in immuno-mediated diseases is a life threatening complication to be early detected. Glomerulo-tubular functional indices, kidney-released enzymes and metabolic profiles were assessed in 21 patients with systemic lupus erythematosus, progressive systemic sclerosis and mixed cryoglobulinaemia, without overt nephropathy at a current laboratory examination, and in 31 age-sex-matched healthy controls. All patients had a urinary total protein excretion rate higher than controls (353.6 +/- 182.4 vs 243.0 +/- 108.2 mg/24 h, p < 0.01); 12 of them resulted albuminuric (775.5 +/- 1192.4 mg/24 h), while 9 were normoalbuminuric (16.6 +/- 7.6 mg/24 h). Urinary enzyme excretion rates (GGT and NAG) were significantly heightened compared to healthy subjects, both in albuminuric and in normoalbuminuric patients. Serum albumin resulted significantly lower in all patients, independent of their urinary albumin leakage. Finally, all subjects with connective tissue diseases had significantly higher triglycerides, lower HDL cholesterol and double serum fasting insulin than normals. In conclusion, all patients with collagen diseases show signs of subclinical nephropathy, not always detectable by albuminuria. They also provide evidence of insulin-resistance, a conceivable forerunner of cardiovascular complications.
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PMID:An early diagnosis of kidney involvement in immunologically-mediated multisystem diseases. 892 70

The risk factors of stroke in young adults and in the whole population are the same in general, but there are some special risk factors in young adults. They are congenital or early acquired diseases which are complicating with early stroke. We studied the risk factors of cerebrovascular insults in 150 patients, 20-49 years old (Table 1). This was 26.04 percent of all patients that were hospitally treated in the urgent neurological department over one year. However, twenty years ago, this percent was 20.20 [2]. We found that arterial hypertension was dominant both among young adults (47.99 percent) and in the whole population (Table 2) [1-3]. Essential hypertension was the most frequent, and renal and thyreotoxical hypertensions were rare. The atherogenic level of low density and high density lipoproteins (LDL/HDL) was present in 14.66 percent of young adult patients [3]. Diabetes mellitus, a known risk factor of stroke, was found in 5.33 percent of our studied patients, especially in the juvenile form [1-3]. Besides juvenile diabetes mellitus, we found other risk factors that were characteristic of young adults: systemic lupus erythematosus (3.33 percent), which began at an early vital age, and numerous cerebrovascular complications appeared during the first five years of illness [7]. In this group of young adults, we found no other type of vasculitis, which also can be a risk factor of stroke. Great risk factors of stroke in young adults were arterial-venous malformation, brain aneurysm and congenital muscular hypoplasia of the carotide and middle caliber cerebral arteries-multiple progressive intracranial arterial occlusion or Nishimoto Takeuchi disease or Moya Moya disease, which were found in 3.99 percent of our patients. These diseases were complicated by cerebrovascular haemorrhagic or ischaemic insults over the young vital period [9]. The similar was with congenital or early acquired (rheumatic fever) heart valve defects (3.99 percent in our group), with early cerebrovascular complications due to cardiogenic thromboembolism mechanisms [10]. In 2 percent of patients the stroke was the consequence of anticoagulant therapy. These were the patients with operated heart valve defects (haemodynamic risk factor was eliminated, but haemorrheological risk factor was evident) [2, 3]. Also, disturbances of cardiac rhythm were risk factors of stroke in 2 percent of our patients. The mechanism of stroke originated is cardiogenic thromboembolism or global hypotension and the following ischaemia in the border brain zone [11]. All these risk factors were present in a relatively small number of patients, but they were "strong" risk factors of stroke, especially in young adults. On the other hand, there were nicotinism, alcoholism and obesity. They were present in a greater percent (25.33; 15.66; 18.66 percent), but their influence was slow and indirect by haemorrheologic mechanism (the increasing aggregation of platelets, reduced flexibility of red and white blood cells, changed prostacycline-prostaglandin relation in endothelial and blood cells, viscosity of blood, LDL/HDL) [2, 3, 12, 13]. A prolonged psychogenic stress (8.66 percent in our group) was, also, a risk factor of stroke. It induced increase in catecholamine level, arterial hypertension, constriction of blood vessels, endothelial cell damages, increased aggregation of platelets, changed prostacycline-prostaglandin relation, metabolism of lipids and polysaccharides) [2, 3]. We found no abuse of ephedrine [16] or cocaine [15] as risk factors of stroke in our group, although it was described in litterature. Also, we found no postoperative thromboemolism (foramen ovale apertum). Ischaemic cerebrovascular insults dominated (77.34 percent) in our group of patients. In one article (Canada) [17] haemorrhagic insults were dominant in young adults. In our opinion, the number of our patients was not adequated, as haemorrhagic stroke is also treated in neurosurgical departments. The mor
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PMID:[Risk factors for stroke in young people]. 910 54

Platelet activation may contribute to the increased risk of thrombotic complications in patients with antiphospholipid antibodies (aPL). The increased urinary excretion of 11-dehydro-thromboxane B2 (11-DH-TXB2) reported in patients with lupus anticoagulant (LA) and/or anticardiolipin antibodies (aCL) reflects in vivo platelet activation. However the majority of autoimmune aPL are directed to beta2 glycoprotein I (beta2GPI) or prothrombin (II). We investigated the relationship of these antibodies with 11-DH-TXB2 urinary excretion in 34 patients with aPL. The urinary 11-DH-TXB2 was measured by EIA after extraction on octadecyl columns and purification on silica gel columns, which was validated by thin-layer chromatography/EIA procedure. A significantly increased excretion of 11-DH-TXB2 was found in aPL patients as compared to 18 normal controls (p <0.01). But no differences were seen in the excretion of 11-DH-TXB2 between patients with or without LA, or aCL. The number of patients with anti-II antibodies was too small to draw any conclusion. In contrast, patients with anti-beta2GPI antibodies IgG at moderate/high titre (group A, n = 14) had higher levels of urinary 11-DH-TXB2 than those at low titre or negative (group B, n = 20) (p = 0.01). The group A of patients presented an increase in 11-DH-TXB2 compared to controls (p <0.001), but no statistically significant difference was found between patients from the group B and normal controls. A correlation between levels of urinary 11-DH-TXB2 and titre of antibodies was only found for anti-beta2GPI-IgG (r(s) = 0.51, p <0.005). Our data show that the observed platelet activation in aPL patients is related to the presence of antibodies reacting with beta2GPI.
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PMID:Anti-beta2 glycoprotein I antibodies and platelet activation in patients with antiphospholipid antibodies: association with increased excretion of platelet-derived thromboxane urinary metabolites. 945 20

The autoimmune MRL/lpr mouse strain, a model for systemic lupus erythematosus, exhibited an unusual plasma lipoprotein profile, suggesting a possible interaction of autoimmune disease and lipoprotein metabolism. In an effort to examine the genetic basis of such interactions, and to study their relationship to atherogenesis, we performed a quantitative trait locus analysis using a total of 272 (MRL/lprxBALB/cJ) second generation (F2) intercross mice. These mice were examined for levels of total plasma cholesterol, HDL cholesterol, VLDL and LDL cholesterol, unesterified cholesterol, autoantibodies, and aortic fatty streak lesions. Using a genome scan approach, we identified 4 quantitative trait loci controlling plasma lipoprotein levels on chromosomes (Chrs) 5, 8, 15, and 19. The locus on Chr 15 exhibited lod scores of 11.1 for total cholesterol and 6.7 for VLDL and LDL cholesterol in mice fed an atherogenic diet, and it contains a candidate gene, the sterol regulatory element binding protein-2. The locus on Chr 5 exhibited lod scores of 3.8 for total cholesterol and 4.1 for unesterified cholesterol in mice fed an atherogenic diet, and this locus has been observed in 2 previous studies. The locus on Chr 8 exhibited a lod score of 3.1 for unesterified cholesterol in mice fed a chow diet. This locus contains the lecithin-cholesterol acyltransferase gene, and decreased activity of the enzyme in the MRL strain suggests that this gene underlies the quantitative-trait locus. The locus on Chr 19 exhibited a lod score of 8.4 for HDL cholesterol and includes the Fas gene, which is mutated in MRL/lpr mice and is primarily responsible for the autoimmune phenotype in this cross. That the Fas gene is responsible for the HDL quantitative-trait loci is supported by the finding that autoantibody levels were strongly correlated with HDL cholesterol levels (rho=-0.37, P<0.0001) among the F2 mice. HDL cholesterol levels were in turn significantly associated with aortic fatty streak lesions among the F2 mice (rho=-0.17, P=0.006). Further, there was a threshold effect of autoantibody levels on the development of fatty streak lesions (rho=0.45, P=0.004 for 42 F2 mice with anti-dsDNA Ab over 0.5 OD). Our results support the concept that the high prevalence of coronary artery disease in systemic lupus erythematosus is due in part to a reduction of HDL cholesterol levels resulting from the autoimmune disease.
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PMID:Quantitative trait locus analysis of plasma lipoprotein levels in an autoimmune mouse model : interactions between lipoprotein metabolism, autoimmune disease, and atherogenesis. 997 30


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