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)

Heart disease responsive to steroids is well described in many disorders, including sarcoidosis, systemic lupus erythematosus, polyarteritis nodosa, myocarditis and Churg-Strauss syndrome. The underlying disorder is often obvious and the response is usually slow. We describe a woman who had severe left ventricular failure, cardiac dilatation and pericardial effusion which were rapidly rectified by steroid therapy. Steroid withdrawal led to recurrence of signs, which were reversed by recommencing steroids. The aetiology was not determined.
Int J Cardiol 1990 Aug
PMID:Steroid responsive cardiomyopathy. 239 29

An autopsy case of congenital atrioventricular (AV) heart block is described. A newborn infant of a mother with systemic lupus erythematosus died 10 h after birth. Autopsy revealed hematoxylin bodies in the AV node, central fibrous body, and fibrous annulus of the heart. Also, immunoglobulin G (IgG) localization in the hematoxylin bodies was demonstrated by an immunoperoxidase technique. It is suggested that IgG or immune complexes crossed the placenta and that the immune deposition directly injured the cardiac conduction system, causing AV block.
Pediatr Cardiol 1988
PMID:An autopsy case of congenital complete heart block in a newly born of a mother with systemic lupus erythematosus. 246 Aug 45

Regarding two cases of idiopathic lupus valvulopathy, the authors review the various mechanisms responsible for the endocardial lesions in disseminated lupus erythematosus. In addition to the classic Libman-Sachs endocarditis, there are sclerous forms, ruptures of the chords, thromboses and bacterial superinfections. The role of steroid therapy in the genesis of valvular stenosis is not always determined. A surgical treatment, effective and without major risk, must be advocated at an early stage in the presence of poorly tolerated forms.
Ann Cardiol Angeiol (Paris) 1989 Nov
PMID:[Heart valve involvement in lupus erythematosus disseminatus. Apropos of 2 cases. Review of the literature]. 269 Jul 25

Beginning in the early 1950s, when a ganglioplegic agent and a vasodilator were used in combination to provide long-term control of severe hypertension, which neither drug alone could control, much has been learned about the management of hypertension from the use of new antihypertensive agents in man and from clinical trials of antihypertensive regimens. Some of this information includes: the unexpected yet very real hazards as well as benefits associated with the long-term use of powerful drugs, in particular the original description of hydralazine-induced lupus, its relation to genetic markers and its association with control of hypertension; the apparently decreasing need for antihypertensive drugs in subjects with well-controlled severe and moderate hypertension; the identification of risk factors for the complications of hypertension and the quantitation of their effects; the decrease in the incidence of hypertensive complications associated with the pharmacologic treatment of severe, moderate and, at least, the upper ranges of mild hypertension; the possibility of designing a chemical to block a specific reaction and the realization that it would have broader than expected effects; and the primary prevention of myocardial infarction in very high risk subjects.
Am J Cardiol 1985 Dec 06
PMID:The evolution of antihypertensive therapy. 286 8

Cardiac manifestations of the mucopolysaccharidoses often include valvular regurgitation, but stenotic lesions are quite rare. This report describes a 30-year-old man with mucopolysaccharidosis type II (Hunter's syndrome) and systemic lupus erythematosus who developed severe progressive aortic stenosis and died. Autopsy examination revealed evidence of various cardiac mucopolysaccharide disease including valvular leaflets thickened and distorted with fibrocalcific nodules. A brief review of previously reported valvular disease in Hunter's syndrome and other mucopolysaccharidoses is presented. This is also the first report of a patient with both systemic lupus and a mucopolysaccharidosis.
Clin Cardiol 1988 Oct
PMID:Severe aortic stenosis in systemic lupus erythematosus and mucopolysaccharidosis type II (Hunter's syndrome). 314 55

A 40-year-old man who presented with exertional angina had had two myocardial infarctions within the same myocardial distribution several years earlier. Coronary arteriography revealed a large intramural thrombus in the right coronary artery and minimal atherosclerotic disease. Special coagulation studies detected a circulating lupus anticoagulant. The association of repeated episodes of thrombosis and lupus anticoagulant is important. In patients with repeated thrombotic events, the lupus anticoagulant should be sought, particularly in those less than 40 years of age.
Int J Cardiol 1988 Nov
PMID:Myocardial infarction, persistent coronary artery thrombosis and lupus anticoagulant. 314 43

A case is presented where the distinction between rheumatic fever and systemic lupus as a cause of mitral valvar disease was made by cross-sectional echocardiography. This showed an unusual appearance, consistent with descriptions of Libman-Sachs endocarditis from the presteroid era.
Int J Cardiol 1988 Sep
PMID:Cross-sectional echocardiography in the diagnosis of Libman-Sachs endocarditis. 317 43

Few such observations of beta-blocker-induced lupus have been published in the medical literature. In the index case, the usual criteria were present. Acebutolol withdrawal resulted in rapid clinical improvement. Antinuclear antibodies are still present after nine months follow up. Pathogenic hypotheses are discussed.
Ann Cardiol Angeiol (Paris) 1985 Jun
PMID:[A new case of lupus induced by acebutolol]. 387 7

A case of aortic infective endocarditis due to Hemophilus paraphrophilus in a patient with previous Libman-Sacks endocarditis is presented. Suggestions regarding antibiotic prophylaxis are made concerning patients with systemic lupus erythematosus.
Int J Cardiol 1985 Apr
PMID:Clinical considerations regarding infective Libman-Sacks endocarditis. 398 75

The antiarrhythmic efficacy and pharmacokinetics of N-acetylprocainamide (NAPA), the major metabolite of procainamide, were investigated in 23 patients with chronic, high frequency ventricular ectopic depolarizations. An extensive trial design incorporated the approaches of (1) generation of dose-response relations, (2) randomized crossover, and (3) prolonged electrocardiographic monitoring. Seven patients with reproducible suppression of arrhythmias (70 percent or greater reduction in frequency) were thus identified. The mean plasma concentration of acecainide associated with efficacy was 14.3 micrograms/ml (range 9.4 to 19.5) and with side effects (primarily gastrointestinal) was 22.5 micrograms/ml (10.6 to 37.9). The antiarrhythmic response to procainamide did not predict response to acecainide; this finding implies that estimates of the antiarrhythmic contribution of acecainide concentrations achieved during long-term procainamide therapy are unlikely to be meaningful in a given person. The mean half-life of elimination after a single 500 mg dose of acecainide was 7.5 hours; this had prolonged significantly (p < 0.05) to 10.3 hours after higher dosages. No variable examined (including acetylator phenotype) was found to be a predictor of responsiveness to acecainide. Outpatient therapy (2 to 20 months) was not associated with the development of antinculear antibodies or the lupus syndrome; one patient's procainamide-induced arthritis resolved during therapy. Acecainide, unlike procainamide, is an agent whose pharmacokinetics allow long-term therapy on a practical schedule. It is effective in a subset of patients with ventricular arrhythmias yet appears much less likely to induce the lupus syndrome seen with the parent compound.
Am J Cardiol 1980 Sep
PMID:Antiarrhythmic efficacy, pharmacokinetics and safety of N-acetylprocainamide in human subjects: comparison with procainamide. 615 63


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