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 polyclonal IgM-RF-binding assay (pRF-BA) for the detection of circulating immune complexes (IC) is described. The method is based on the competitive binding of heat-treated iodinated IgG (deltaIgG) and naturally occurring IC to solid phase IgM-RF. The sensitivity limit of the assay was 300--400 ng deltaIgG/ml dilute serum. The coefficient of variation for the assay varied from 6 to 12% of the total binding when deltaIgG concentrations up to 1 microgram/ml were measured. One hundred and six patient sera were examined for IC occurrence and significant differences (p less than 0.01) were observed between 30 normal control sera and sera from SLE, sarcoidosis and glomerulonephritis patients. About 40% of patients suffering from acute myocardial infarction (AMI) gave IC-positive reactions with samples taken 5 to 10 days after the infarction. The kinetics of IC appearance was studied in AMI patients by the pRF-BA and three complement-dependent assays. IC appearance was registered in the RF assay 5 to 12 days after the rise in ASAT enzyme values and the IC reactivity corresponded to complexes ranging from 2 to 5 x 10(6) in molecular weight.
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PMID:A solid-phase, polyclonal IgM-RF binding assay for circulating immune complexes. 10 21

The serum level of myoglobin, an LMW constituent of striated and myocardial muscle, has been studied in various clinical situations in order to obtain information about factors influencing myoglobin turnover. The myoglobin level was significantly correlated to different variables of GFR such as serum beta2-microglobulin, serum creatinine, and 51Cr-EDTA clearance. Following a successful renal transplantation rapid decrease in serum myoglobin was found parallel to increase in GFR's. In patients with advanced long-standing uremia, comparatively small elevations of serum myoglobin were seen when correlated to the degree of GFR reduction, demonstrating an influence of extrarenal factors on the myoglobin levels. The importance of extrarenal factors on the actual serum level of LMW proteins was also illustrated by serial studies on SLE patients receiving corticosteroid therapy. In these patients, elevations of serum myoglobin levels were found, but serum beta2-microglobulin levels gradually decreased during therapy. Finally, calculations based on curves of serum disappearance of myoglobin in patients with acute myocardial infarction indicate that only about 0.3 mg of myoglobin per day is released from the muscle pool during normal conditions, which suggests that myoglobin catabolism mainly occurs within the muscle tissue.
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PMID:Myoglobin turnover--influence of renal and extrarenal factors. 34 Jun 2

An autoimmune response to certain nuclear antigens frequently develops in patients receiving prolonged therapy with procainamide. In order to define events involved in the initiation of this immune response, patients with myocardial infarction were studied early after starting procainamide and at later times. Polynucleotide antibodies and circulating polynucleotide antigens were sought by sensitive assay techniques in the sera of these patients. Very high titers of antiribonucleoprotein developed selectively in the majority of these patients after short-term therapy with procainamide. Such antibodies were infrequent in the long-term therapy group, most of whose members exhibited anti-single-strand DNA and were symptomatic with overt procainamide-induced lupus. Patients with acute myocardial infarction who did not receive procainamide did not develop anti-polynucleotide antibodies, but rather had high levels of free ribonucleoprotein antigen in their serum. Various interpretations of these data are discussed.
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PMID:Development of antibodies to ribonucleoprotein following short-term therapy with procainamide. 120 Nov 4

Acute myocardial infarction in systemic lupus erythematosus may be due to an atheromatous or arteritic process. Confirmation of the latter etiology has previously been made only at postmortem examination. A 45-year-old white woman with known systemic lupus erythematosus developed anginal pain and multiple episodes of acute myocardial infarction. During this period, there was serologic but no other clinical evidence of active systemic lupus erythematosus. Serial coronary angiographic studies were strongly suggestive of an arteritic process based upon (1) a saccular aneurysm with no obstructive lesions in a coronary artery supplying an area of recent transmural myocardial infarction and (2) the development of significant obstructive lesions in a previously normal coronary artery over a period of 18 days. This case illustrates the difficulties in distinguishing between atherosclerosis and arteritis using a single coronary angiographic study. The distinction is significant because of the different therapeutic interventions required.
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PMID:Coronary arteritis in systemic lupus erythematosus. 126 86

Apparently the incidence of coronary artery disease in systemic lupus erythematosus (SLE) has been increasing. However, most of the cases had been treated with corticosteroids, and had atherosclerotic lesions in the coronary arterial tree. A 21-year-old man with latent and untreated SLE had an attack of acute myocardial infarction. Coronary arteriography showed eccentric stenotic lesion at the proximal segment of the right coronary artery. One week later, in the 2nd coronary arteriography, this stenotic lesion was not able to be recognized. We supposed that the coronary artery occlusion was due to thrombus formation, and was not related to atherosclerosis, arteritis and embolus. He had no coronary risk factors. Laboratory data showed lymphocytopenia, proteinuria, positive antinuclear antibody, and positive LE cell, and the case was diagnosed as SLE. Subsequent investigations showed the presence of antibodies to cardiolipin. It was suggested that anticardiolipin antibody and other thrombogenic factors were the causes of the coronary occlusive thrombosis in this patient with SLE.
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PMID:[A case of myocardial infarction in a young man with systemic lupus erythematosus]. 158 50

Coronary artery disease has emerged as an important cause of death in young patients with SLE. We report three cases of acute myocardial infarction in young lupus patients who underwent emergent coronary angiography. One patient had a large coronary aneurysm and died five months later from myocarditis. The other two patients underwent coronary angioplasty. The difficulty in distinguishing coronary arteritis from premature atherosclerosis and its relevance to methods of treatment is discussed.
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PMID:Evaluation and treatment of acute myocardial infarction complicating systemic lupus erythematosus. 173 66

Acute myocardial infarction is a potentially fatal complication of SLE. Reported mechanisms include atherosclerosis, arteritis and coronary arterial spasm. The following case report presents a fourth possible cause; intracoronary thrombus with angiographically normal coronary arteries in a patient with active lupus and AMI.
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PMID:Myocardial infarction due to intracoronary thrombi without significant coronary artery disease in systemic lupus erythematosus. 186 45

Plasma concentrations of the recently isolated potent vasoconstrictory peptide endothelin were measured in 382 patients. The investigations were performed by means of a sensitive radioimmunoassay specific for Endothelin-1, 2. The results from 110 healthy volunteers displayed a normal range of 44.67 +/- 3.51 pg/ml. Significantly raised levels were found in 33 patients with chronic end-stage renal failure both before and after hemodialysis. In contrast, 35 patients with compensated renal insufficiency did not differ from the normals. Sixty-five patients after kidney transplantation revealed significantly elevated levels, as did 27 patients with acute myocardial infarction, 8 after coronary bypass surgery, and 5 with liver cirrhosis. The mean values of 27 patients with untreated hypertension, 22 with secondary hypertension, of various causes and 16 with coronary artery disease were comparable to the normal population. The values were significantly decreased in 9 pregnant women with hypertension and proteinuria. A marked decline was found in 5 patients with systemic lupus erythematodes, while 20 patients with rheumatoid arthritis demonstrated only a slight decrease. The pathophysiological role of endothelin as a local or circulating hormone in regulating systemic blood pressure or release of other hormones remains to be determined.
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PMID:[Plasma endothelin in normal probands and patients with nephrologic-rheumatologic and cardiovascular diseases]. 221 2

A young patient with systemic lupus erythematosus was admitted to our hospital because of acute myocardial infarction, and treated by thrombolysis. Coronary angiography revealed a significant stenosis of the left anterior descending artery, together with an intraluminal thrombus. Clotting studies demonstrated an anticoagulant factor suggestive of lupus erythematosus. We conclude that thrombolytic therapy can be useful in patients with systemic lupus erythematosus who present with acute myocardial infarction, although some caution is needed in treatment.
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PMID:Thrombolytic therapy for a patient with systemic lupus erythematosus and acute myocardial infarction. 226 45

Antiphospholipid antibodies--both the lupus anticoagulant and anticardiolipin antibodies--are closely associated with arterial and venous thrombosis. In this prospective trial the IgM- and IgG-anticardiolipin antibodies in serum were determined in acute and chronic coronary artery disease. Seventy-four unselected males (34-87 years, mean 60) were included in the study. All patients underwent coronary angiography; infectious and autoimmune diseases were exclusion criteria. Sixteen patients had coronary artery disease (group A), 34 showed coronary stenoses with prior infarction (B), and 14 had survived an acute myocardial infarction (C), whereas 10 patients revealed no significant coronary narrowing (D; controls). The major risk factors were the same for all groups. Neither the IgM- nor the IgG-anticardiolipin antibody levels showed any significant difference in the four groups. The severity of coronary artery disease did not correlate to these antibodies. Furthermore, no correlation was found between elevated anticardiolipin antibodies and thrombocyte levels. Thus, a higher anticardiolipin level does not appear to be a marker for recurrent cardiovascular events.
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PMID:Anticardiolipin antibodies are no marker for survived myocardial infarction. 237 55


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