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)

The pathogenesis of the degenerative vascular disease and myocardial infarction that develop in mice with lupus-like disease was studied by immunofluorescence, light microscopy, and electron microscopy. Medium and small coronary arteries and arterioles of both infarcted and noninfarcted hearts had focal degenerative lesions consisting of deposits of periodic-acid--Schiff (PAS)-positive or eosinophilic material in the intima and to a lesser extent in the media, degenerative changes in the media without accompanying cellular inflammation, and occasional proliferation or swelling of intimal cells. These lesions often narrowed and, together with platelet aggregation, occasionally occluded the vascular lumens. Granular deposits of mouse immunoglobulin, C3, and occasionally gp70 were present in the walls of medium and small arteries, arterioles, and venules of both infarcted and noninfarcted myocardium. Dense deposits of foreign material were found by electron microscopy in areas corresponding to the immune deposits. These findings are consistent with the interpretation that these noninflammatory vascular lesions are caused by local deposition of antigen--antibody complexes. The immune-complex--mediated injury appears to lead to thrombotic and/or obliterative vascular changes that contribute to decrease of the coronary blood flow and to the development of myocardial infarction.
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PMID:Degenerative vascular disease and myocardial infarction in mice with lupus-like syndrome. 47 7

Serum FDPs were investigated in 30 healthy and 95 patients with pulmonary thrombembolia, not-stabilized angina pectoris, myocardial infarction, rheumatism, rheumatoid arthritis, lupus erythematodes and dermatomyositis. FDPs are determined by hemagglutination inhibition according to Merskey. They are found in the sera of the healthy in average values of 3.73 mkgr/ml. The highest average values in the first 24 h were found in case of pulmonary thrombembolia up to 106.64 mkgr/ml, followed by rheumatoid arthritis 26.3 mkgr/ml, myocardial infarction with complication 22.4 mkgr/ml, rheumatism +5.58 mkgr/ml, not-stabilized angina pectoris 5.5 mkgr/ml; and noncomplicated myocardial infarction 4.3 mkgr/ml. By the third day of the disease FDP in pulmonary thrombembolia decreased, whereas a negligible elevation was observed in case of non-complicated myocardial infarction. The results were interpreted as well as the cause for the presence of the mentioned products in those groups of diseases. FDP determination is recommended as a routine method in case of: diagnosis of pulmonary thrombembolia, differentiation of myocardial infarction with or without complications, differentiation of pulmonary thrombembolia from myocardial infarction in emergency states, progressing with chest pain, collapse phenomena, dyspnea and establishment of the activity of the process of rheumatoid arthritis. FDP determination in stenocardia and rheumatism is not expedient.
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PMID:[Level of fibrinogen/fibrin degradation products (F/FDP) in certain internal diseases]. 49 29

An unusual case of systemic lupus erythematosus (SLE) in a young child is reported with sudden death from myocardial infarction. The diagnosis of lupus erythematosus in this patient was made by renal biopsy at the age of 3 years. Atherosclerosis of the coronary arteries and aorta was found at autopsy with occlusion of the anterior descending branch of the left coronary artery. It is suggested that the vascular changes in this case were related to hypertriglyceridemia and prolonged prednisone therapy superimposed on a hypersensitivity vasculitis related to SLE.
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PMID:Myocardial infarct in a child with systemic lupus erythematosus. 66 98

A syndrome that resembles Systemic Lupus Erythematosus both clinically and on laboratory studies may be induced by procainamide. It is associated with multisystemic involvement, positive Antinuclear Antibody titers (ANA), and positive LE cell preparations. In patients on procainamide therapy the syndrome must be differentiated from osteoarthritis, myocardial infarction, and pulmonary embolism. When procainamide is discontinued, this Lupus-like syndrome is usually reversible. Other drugs, including hydralazine and isoniazid have also been implicated in provoking this Lupus-like syndrome.
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PMID:A systemic lupus erythematosus-like syndrome induced by procainamide. 72 56

Three patients, 24, 24 and 25 years of age, with systemic lupus erythematosus had signs of myocardial infarction. Two had serial electrocardiographic changes indicative of infarction without any cardiac symptoms. The third patient had clinical evidence of an acute massive myocardial infarction, which was proved at autopsy to be due to coronary atherosclerosis. This case is presented in detail and the association between systemic lupus erythematosus and myocardial infarction is reviewed. It is postulated that the relation between lupus erythematosus and coronary atherosclerosis is more than coincidental.
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PMID:Myocardial infarction due to coronary atherosclerosis in three young adults with systemic lupus erythematosus. 111 92

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

The changing pattern of mortality in systemic lupus erythematosus (SLE) led to an examination of the deaths in a long-term systematic analysis of 81 patients followed for five years at the University of Toronto Rheumatic Disease Unit. During the follow-up 11 patients died; six patients died within the first year after diagnosis (group I) and five patients died an average of 8.6 years (from 2.5 to 19.5 years) after diagnosis (group II). In those who died early, the SLE was active clinically and serologically, and nephritis was present in four. Their mean prednisone dose was 53.3 mg/day. In four patients a major septic episode contributed to their death. In those who died late in the course of the disease, only one patient had active lupus and none had active lupus nephritis. Their mean prednisone dose was 10.1 mg/day taken for a mean of 7.2 years. In none was sepsis a contributing factor to their death. All five of these patients had had a recent myocardial infarction at the time of death; in four, ti was the primary cause of death. Mortality in SLE follows a bimodal pattern. Patients who die early in the course of their disease, die with active lupus, receive large doses of steroids and have a remarkable incidence of infection. In those who die late in the course of the disease, death is associated with inactive lupus, long duration of steroid therapy and a striking incidence of myocardial infarction due to atherosclerotic heart disease.
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PMID:The bimodal mortality pattern of systemic lupus erythematosus. 125 49

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

A wide spectrum of cardiac involvement including valvular lesions, myocardial infarction and myocardial dysfunction has been reported in patients with antiphospholipid antibodies (aPL), suggesting that cardiac manifestations may be part of the antiphospholipid syndrome (APS). We describe 3 patients (2 with primary APS and one with APS and SLE) who were found to have right atrial masses by echocardiography (transthoracic and/or transesophageal) and/or angiography, which were felt preoperatively to be atrial myxomata. Pathological examination of resected material showed only organized thrombus with calcification. We describe outcome 12 months to 7 years after resection of thrombus and document possible recurrence in one patient after 7 years. Intracardiac mural thrombus may be an additional cardiac manifestation of the APS, and presents considerable diagnostic confusion in its differentiation from atrial myxomata.
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PMID:Intracardiac mural thrombus mimicking atrial myxoma in the antiphospholipid syndrome. 140 69

All patients with systemic lupus erythematosus in a prospective, epidemiologically based study within a defined area in southern Sweden were invited to participate in an investigation of cardiac function. From 1981 to 1988, 101 patients were included in the study, and 75 of them were investigated according to a fixed protocol by echocardiography, Doppler cardiography, electrocardiography (ECG) at rest and at exercise, and myocardial scintigraphy (in patients whose ECG became abnormal during exercise). IgG anticardiolipin antibodies (IgG aCL) were determined by ELISA. Twenty of the 75 patients (27%) had valvular disease and 12 of these (60%) had increased concentrations of IgG aCL, compared with 12 of 55 (22%) without valvular disease (p less than 0.01). Pericardial effusion was detected in 14 patients (19%) during the study period. Mild pulmonary hypertension was found in 11 patients (16%), who also had increased frequency of IgG aCL. Myocardial infarction had occurred in 7 patients, 3 of whom were women less than 40 years of age. Echocardiography revealed regional hypokinesis or akinesis in 5 of the patients with myocardial infarction. Exercise testing revealed low work capacity in 13 of 54 patients (24%), the limiting symptoms being mainly exhaustion or musculoskeletal pain. An abnormal resting ECG was found in 9 of the patients participating in the exercise test. During exercise, abnormal ST-depression was observed in 8 patients, 2 of whom developed angina. Myocardial scintigraphy was performed in 6 of these patients, revealing reversible uptake defects in all. Prolonged glucocorticoid treatment was associated with valvular abnormalities as well as myocardial infarction. Valvular abnormalities and IgG aCL appeared to be risk factors for cerebral infarction.
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PMID:Cardiovascular disease in systemic lupus erythematosus. A study of 75 patients form a defined population. 151 95


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