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)

A two-stage electroimmunoassay was developed for measuring macromolecular C1 (C1qrs) and free C1q. The method was based on Ca2+ dependent fixation of C1qrs to agarose, followed by immune precipitation of dissociated C1s in the presence of EDTA. Free C1q was estimated from the increase in C1qrs resulting from saturation of C1q in the samples with purified C1r-C1s. The assay system was studied under various experimental conditions. Combined analysis by electroimmunoassay and crossed immunoelectrophoresis indicated that part of the free C1q in undiluted normal serum could be attributed to physiological C1 activation. Owing to concentration dependent C1qrs dissociation the proportion of free C1q increased with the dilution of serum. Results obtained with serum and with purified C1qrs were consistent with the formation of an equimolar C1q:C1r-C1s complex. However, the capacity for C1r-C1s binding appeared to be higher in the purified system than in serum. Serum concentrations of free C1q were high in some of the patients with disease conditions characterized by increased C1 activation, such as systemic lupus erythematosus or primary biliary cirrhosis.
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PMID:C1 dissociation in serum: estimation of free C1q by electroimmunoassay. 387 85

In this review, the cardiac lesions which develop in association with the various collagen-vascular diseases are described. In rheumatoid arthritis, the most frequent lesions are: fibrous obliterative pericarditis, with pericardial deposits of calcium, fibrin, cholesterol, and rheumatoid granulomas; granulomatous or nonspecific myocarditis; valvulitis, vasculitis, and amyloid deposits. In ankylosing spondylitis, the lesions involve mainly the valves (aortic and mitral valves) and the aorta. In systemic lupus erythematosus, the predominant cardiovascular lesions are: pericarditis, Libman-Sacks endocarditis, nonspecific myocarditis, vasculitis with fibrinoid necrosis, and acceleration of atherosclerosis. In scleroderma, the main cardiac lesion is fibrosis with only scanty inflammatory cells; pericarditis and nonbacterial thrombotic endocarditis also occur. In dermatomyositis/polymyositis, fibrous or fibrinous pericarditis can occur, as well as myocarditis with infiltrates of lymphocytes and plasma cells and with degeneration and necrosis of myocytes; valvulitis is uncommon except when the disease is related to mucinous adenocarcinoma. In polyarteritis nodosa, various stages of necrotizing vasculitis involve all layers of the arterial walls; foci of myocardial necrosis of various sizes can occur in association with these lesions; cardiac hypertrophy related to hypertension and pericarditis related to uremia, may also be found. In Wegener's granulomatosis, pericarditis, inflammatory infiltrates, necrotizing granulomas, and vasculitis have been observed in the heart.
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PMID:Cardiovascular lesions in collagen-vascular diseases. 391 76

A simple sensitive method for verification of lupus anticoagulants utilizing dilution of phospholipid in the activated partial thromboplastin time (APTT) system is described. Patient plasma, mixed with an equal volume of normal plasma, is activated with micronized silica. To this mixture are added different dilutions of Thrombofax and then calcium chloride. Clotting times are plotted linearly against the logarithm of the phospholipid dilutions and slopes are calculated by regression analysis. In this assay the mean negative slope of 19 plasmas that contained anti-phospholipid activity was five times greater than those of normal plasma or those obtained from patients having single or multiple coagulation factor deficiencies such as those induced by warfarin. The assay can be modified to test heparinized plasmas. Thus, it is a sensitive means by which to verify the presence of lupus anticoagulants in patients who have congenital or acquired factor deficiencies or who are receiving anticoagulant therapy.
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PMID:The dilute phospholipid APTT: a sensitive assay for verification of lupus anticoagulants. 393 68

The deposition of calcium and phosphorous salts in the soft tissues can be classified into three categories: metastatic calcification, dystrophic calcification, and calcinosis. Metastatic calcification occurs when the calcium-phosphorous levels are elevated. The calcifications involve normal tissues. Associated disease include hyperparathyroidism, neoplasms, milk-alkali syndrome, hypervitaminosis D, and tumoral calcinosis. Dystrophic calcification occurs in the presence of normal metabolism in damaged or devitalized tissues. Disorders included in this classification are: Ehlers-Danlos syndrome, pseudoxanthoma elasticum, arteriosclerosis obliterans, venous calcifications, crystal deposition disorders, and calcification resulting from neurologic disorders. Calcinosis is also found in persons with normal metabolism. It occurs most often in subcutaneous tissues, skin, and related connective tissues. Associated disorders include: calcinosis universalis, calcinosis circumscripta, scleroderma, dermatomyositis, and systemic lupus erythematosus.
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PMID:A review of soft tissue calcifications. 404 12

A new method for differentiation of specific DNA-binding by human sera from non-specific binding was evaluated with sera from patients with systemic lupus erythematosus in different stages of the disease. An addition of dextran sulfate or calcium chloride to Farr's radioimmunoassay mixture reduced non-specific binding of thermally denatured [3H]DNA of the patient sera without much effect on the specific binding. The measurement of DNA-binding value by the sera in these addition systems provides accurate information with regard to the pathophysiological state of the disease.
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PMID:Differentiation of specific DNA binding activity of SLE sera from non-specific binding by an addition of dextran sulfate and calcium chloride to the Farr assay system. 617 85

Lipomodulin, purified to near homogeneity from rabbit peritoneal neutrophils, was phosphorylated by cyclic AMP-dependent protein kinase from bovine heart with concomitant loss of its ability to inhibit phospholipase A2 from porcine pancreas. Phosphorylation of lipomodulin was confirmed by the incorporation of 32P from [gamma-32P]ATP. To demonstrate that lipomodulin undergoes phosphorylation in vivo, rabbit peritoneal neutrophils were incubated with 32P and lipomoculin was isolated by immunoprecipitation with serum from a patient with systemic lupus erythematosus which has anti-lipomodulin antibody. Analysis of 32P-labeled immunoprecipitates by sodium dodecyl sulfate electrophoresis revealed a single peak of radioactivity that comigrated with [35S]methionine-labeled lipomodulin. The administration of a chemoattractant, N-formyl-methionyl-leucyl-phenylalanine to intact rabbit neutrophils, resulted in a marked increase in arachidonate release from the cells and an increase in 32P incorporation into lipomodulin. A close correlation was found between the extent of phosphorylation of lipomodulin and the rate of arachidonate release. Phosphorylation of lipomodulin in neutrophils gradually returned to the control level with corresponding cessation of arachidonate release. In contrast to the in vitro system, phosphorylation of lipomodulin and release of arachidonic acid from peptide-stimulated neutrophils required Ca2+ entry into the cells. These results suggest that the phosphorylation-dephosphorylation of lipomodulin, phospholipase inhibitory protein, is an important mechanism for chemotactic receptor-mediated regulation of arachidonic acid release in rabbit neutrophils.
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PMID:The regulation of lipomodulin, a phospholipase inhibitory protein, in rabbit neutrophils by phosphorylation. 626 23

In each of the 16 patients included in our first study [6 idiopathic Raynaud's phenomenon (I), 4 associated with systemic lupus erythematosus (SLE) and 6 with progressive systemic sclerosis (PSS)] digital vasospasm could be reproduced by immersion of both hands in cold water (4 degree C). Each patient received in a double-blind manner and random order on two consecutive days, the calcium-channel blocking agent nifedipine (20 mg) and placebo. Nifedipine protection against vasospasm provoked by cold water (4 degrees C) was considered good or excellent in 14 of the 16 patients (p less than 0.001 versus placebo). In the second study, 30 patients [12 I, 10 PSS, 5 SLE and 3 rheumatoid arthritis (RA)] received in a double blind manner and random order, on two consecutive weeks, nifedipine (20 mg 3 time daily) and placebo. The improvement with nifedipine (in percentage of the decrease of the number of vasospastic attacks) was 90.95 in the 1 group, 78.63 SLE and RA and 64.02 in PSS (p less than 0.01). An open study during 3 months has confirmed the effectiveness of nifedipine (10 mg 3 times daily). The improvement was 88.92 in the 1 group, 76.33 in SLE and RA and 59.16 in PSS, 7 out of 30 patients stopped the treatment because of side effects (headache, flush, nausea, oedema of the ankles). Thus nifedipine appears to be extremely useful in the treatment of Raynaud's phenomenon.
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PMID:[Controlled study of nifedipine in the treatment of Raynaud's phenomenon]. 628 45

We have evaluated the therapeutic effect of the calcium entry blocking agent nifedipine in Raynaud's phenomenon associated with connective tissue diseases and in idiopathic digital vasospasm. In a preliminary study 16 patients with a digital vasospasm that could be induced by hand-immersion in cold water (4 degrees C) were challenged a second time with cold water 1 and 6h after 20 mg oral nifedipine. Nifedipine provided an effective protection against this cold-induced vasospasm in 14 of the 16 patients. Thirty patients were included in a short-term ambulatory study: Raynaud's phenomenon was associated with progressive systemic sclerosis (PSS) in 10 patients, systemic lupus erythematosus (SLE) in five and rheumatoid arthritis (RA) in three; it was idiopathic (I) in 12 patients. Each patient received, in a double-blind manner and random order, on two consecutive weeks, nifedipine (20 mg three times daily) and placebo. Nifedipine proved to be effective: the mean number of digital vasospastic attacks per week decreased from 27.3 to 5.8 (P less than 0.01). The results in the SLE and RA groups were similar and were pooled. The improvement (in % decrease) was better in the idiopathic group (90.9) than in the SLE and RA group (78.6, P less than 0.02) and the PSS group (64.0, P less than 0.01).
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PMID:Calcium entry blocking agents in digital vasospasm (Raynaud's phenomenon). 635 67

Acquired abnormalities of platelet aggregation have been reported with increasing frequency. We studied five patients (including two with systemic lupus erythematosus and one with compensated chronic idiopathic thrombocytopenic purpura) in whom platelet aggregation responses to collagen, epinephrine and ADP are impaired; in all cases, we found that levels of platelet-associated immunoglobulin G (IgG) were increased. In all five patients substances stored in platelet-dense granules (ATP, ADP, serotonin and calcium) were diminished. The content of the alpha-granule substance, beta-thromboglobulin, was also decreased in most cases, whereas the levels of two secretable acid hydrolase enzymes (beta-glucuronidase and beta-N-acetyl glucosaminidase) were within normal limits. These findings are similar to those observed in subtypes of congenital storage pool deficiency. However, in contrast to the congenital disorder, a membrane-bound (nonsecretable) acid phosphatase was also decreased in the patients with acquired storage pool deficiency. These findings suggest that impaired platelet aggregation on an acquired basis may, in some patients, be due to immune platelet damage resulting in a distinctive type of platelet storage pool deficiency.
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PMID:Acquired storage pool deficiency with increased platelet-associated IgG. Report of five cases. 644 50

A 26-year-old white woman developed systemic lupus erythematosus (SLE) and extensive soft tissue calcification. Striking features of this patient related to severe complication of corticosteroids, including proximal muscle weakness and multiple areas of avascular necrosis. In addition to localized areas of erythematosus induration, the patient demonstrated yellowish papules on her legs. Biopsies of the former showed thickening of the dermis with extensive collagen deposition and focal deposits of calcium. The latter revealed eosinophilic degeneration of the subcutaneous fat.
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PMID:Systemic lupus erythematosus and diffuse soft tissue calcifications. 662 5


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