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 specific factors predisposing to thrombosis in patients with LAs have not been resolved. With extensive cross-reactivity, and several proposed sites of action, LAs and their effects may be heterogeneous. While the risk of thrombosis with phenothiazine-induced LAs is probably low, the incidence of thrombosis in association with procainamide-induced LAs is uncertain. Procainamide is a commonly used antiarrhythmic drug associated with the induction of autoantibodies, and occasionally with a lupus-like syndrome. Serologic and coagulation profile monitoring may be required to detect patients in whom LAs develop since these individuals may be at increased risk for thrombosis. Monitoring may be especially important in patients who are receiving procainamide and who have atherosclerosis and cardiac disease, since they may be at increased risk for thrombosis of coronary and other arteries. Future prospective studies are needed to investigate whether the development of lupus anticoagulants during procainamide therapy increases the risk of thrombosis.
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PMID:Procainamide-induced lupus anticoagulants and thrombosis. 312 75

Patients with systemic lupus erythematosus are at increased risk for premature atherosclerosis. We examined one possible etiologic factor, dyslipoproteinemia, both before and after corticosteroid therapy. We identified 2 distinct patterns of dyslipoproteinemia. One is attributable to active disease; the other is attributable, in part, to corticosteroid therapy. The dyslipoproteinemia of active disease consists of depressed high density lipoprotein cholesterol and apoprotein A-I with elevated very low density lipoprotein cholesterol and triglyceride, while the dyslipoproteinemia after corticosteroid therapy consists of increased total cholesterol, very low density lipoprotein cholesterol, and triglyceride. The possible pathophysiologic mechanisms responsible for these patterns, as well as the possible roles in premature atherosclerosis seen in systemic lupus erythematosus patients, are discussed.
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PMID:Dyslipoproteinemia in pediatric systemic lupus erythematosus. 313 97

Anatomical studies have demonstrated the high incidence of vasculitis in SLE, the appearances of which are variable and non-specific, ranging from necrotizing angiitis which is undistinguishable from periarteritis nodosa, to scarring lesions. Micro-angiitis is easily demonstrated in skin lesions and is also encountered to varying degrees in CNS, renal, cardiac, pulmonary and gastrointestinal localisations. Disease of large vessels is more rare and sometimes causes gangrene of the limbs. In SLE, vasculitis should be distinguished from thrombosis related to lupus anticoagulant and from atherosclerosis favoured by chronic steroid therapy but perhaps initiated by vascular deposits of immune complexes during the acute inflammatory stage. The treatment of lupic angiitis is mainly based on steroid therapy. The results are variable, probably due to the fibrous nature of some of the vascular lesions.
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PMID:[Lupus vasculitis]. 332 46

SLE is an inflammatory disease of unknown etiology with the potential of affecting virtually all organ systems. Cardiovascular involvement occurs frequently, although it is often mild enough not to cause clinical concern. Pericarditis is most commonly subclinical, noted only on echocardiogram. Pericardial fluid, which can accumulate rapidly enough to cause tamponade, is inflammatory in nature and can totally mimic infection. The occurrence of Libman-Sacks endocarditis, usually a pathological diagnosis of little clinical significance, has little if any correlation with the presence of audible murmurs. However, valve replacement is occasionally necessary secondary to sterile destruction. These valvular lesions can also embolize or become infected. The incidence of ischemic coronary disease is increased, both secondary to premature atherosclerosis and, rarely, coronary arteritis. Conduction disease and arrhythmias are infrequently reported in adult patients, but congenital CHB has been noted in children born to mothers who have circulating anti-Ro antibody. Evidence is accumulating that suggests there is a mild cardiomyopathy associated with SLE that may be due to thrombotic or inflammatory microvascular coronary disease. Acute clinical myocarditis also rarely occurs. Therapeutically, at present, a reasonable course would seem to be to limit all known possible contributing factors to premature coronary artery and myocardial disease (hypertension, hypercholesterolemia, smoking, steroid therapy, etc), to be vigilant about recognizing the rarer complications associated with SLE (infectious pericarditis and endocarditis, coronary arteritis, pericardial tamponade, clinical myocarditis), and to remember that these uncommon complications are indeed uncommon. The importance of vigorously treating systemic hypertension cannot be overstressed.
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PMID:Cardiovascular involvement in systemic lupus erythematosus. 333 84

Patients treated with corticosteroids often have a dyslipoproteinemia characterized by elevated plasma levels of triglyceride and low density lipoprotein cholesterol and/or decreased levels of the high density lipoprotein2 fraction of high density lipoprotein cholesterol. This study was undertaken to determine if such patients also have elevated apolipoprotein-B (apoB) levels and/or abnormalities of the activities of the triglyceride lipases in postheparin plasma. Plasma lipoprotein levels and the postheparin activities of hepatic lipase and lipoprotein lipase were measured in 28 women with systemic lupus erythematosus (SLE) who were treated with prednisone, 10 women with SLE not treated with prednisone, and 15 normal women. The prednisone-treated group had higher mean plasma levels of triglyceride [2.06 +/- 1.3 (+/- SD) vs. 1.15 +/- 0.35 and 0.95 +/- 0.46 mmol/L; P less than 0.01], low density lipoprotein cholesterol [3.41 +/- 1.4 (+/- SD) vs. 2.79 +/- 0.67 and 2.84 +/- 0.70 mmol/L; P less than 0.01], and apoB [1.16 +/- 0.35 (+/- SD) vs. 0.82 +/- 0.13 and 0.76 +/- 0.22 g/L] than the other 2 groups. Forty-three percent of the prednisone-treated group had apoB levels of 1.20 g/L or more compared to 7% of normal subjects and none of the untreated SLE group (P less than 0.05). However, of the 12 prednisone-treated patients with elevated plasma apoB levels 5 had normal plasma lipid levels. There were no differences in the postheparin lipase activities among the 3 groups. These data indicate that corticosteroid-treated patients have elevations in apoB as well as hyperlipidemia. The lipoprotein abnormalities may explain the increased risk of atherosclerosis reported in these patients.
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PMID:Elevated apolipoprotein-B levels in corticosteroid-treated patients with systemic lupus erythematosus. 341 Sep 32

Using a computed image analyser, coronary arteries from 50 autopsied patients with systemic lupus erythematosus (SLE) were examined on the three vessels (RCA, LAD, LCX) and compared with those of age-matched controls. The intima of coronary artery was significantly thickened much more in the case of SLE than in the case of age-matched controls. This was statistically significant (p less than 0.01). Hypertension and glomerulonephritis did not but corticosteroid therapy had an influence on the development of intimal thickening ratio of the coronary arteries in SLE patients. The mean intimal thickening ratio of the coronary arteries in the patients with SLE and without corticosteroid therapy was larger than that of patients with corticosteroid therapy (p less than 0.1). It appears possible to conclude that inflammatory change of SLE itself is one of the promoting factors of coronary atherosclerosis.
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PMID:Coronary atherosclerosis in patients with systemic lupus erythematosus at autopsy. 357 64

Over the past 30 years there has been an increase in the survival rate in systemic lupus erythematosus (SLE). As patients with SLE live longer, clinicians involved in their care are confronted with the longterm morbid complications that result either from previous SLE disease itself or as a complication of therapy. Our paper deals with the changing pattern of morbidity in SLE and specifically highlights 3 aspects: atherosclerosis, avascular necrosis and neuropsychological dysfunction. These must be considered as added features in the disease spectrum of SLE.
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PMID:Morbidity in systemic lupus erythematosus. 361 50

Systemic lupus erythematosus (SLE) is a well-known acute and/or chronic multisystem disease of complex autoimmune nature, having predilection for cardiovascular system. While its cardiac manifestations have been adequately studied, there is paucity of information on its vascular manifestations. Accordingly, we studied the incidence of vascular manifestations in 50 consecutive SLE patients seen at our institutions and in private practice during the past 12 years. Systemic hypertension (44%) was the most common vascular manifestation followed by vasculitis (30%), Raynaud's phenomenon (26%), telangiectasis (20%), premature coronary atherosclerosis (6%), digital ulceration (6%), thrombophlebitis (6%), pulmonary hypertension (4%) and portal hypertension (4%). Diffuse systemic vasculitis similar to polyarteritis nodosa was rare (2%). Often more than one lesion was found in the same patient. The clinical diagnosis of these vascular manifestations in the context of the primary disease (SLE) usually does not pose any difficulty except when they antedate it. We also studied the pathology and pathogenesis of some of these vascular lesions in both autopsy and biopsy specimens by both light microscopy and immunofluorescent techniques. Our results as well as those of others who also studied these lesions indicate that immune complex deposition and subsequent complement activation play an important role in the pathogenesis of vasculitis, coronary arteritis and premature coronary atherosclerosis. Corticosteroids and vasodilators remain the drugs of choice for the management of the majority of the symptoms arising from the vascular lesions of SLE.
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PMID:Vascular manifestations of systemic lupus erythematosus. 372 68

Acute myocardial infarction (AMI) is relatively rare in systemic lupus erythematosus (SLE), although other cardiac complications, such as pericarditis and myocarditis, occur frequently in this disease. A 20-year-old woman with documented SLE experienced a transmural anterior AMI due to thrombi in saccular aneurysms of the left main coronary artery and the proximal portion of the left anterior descending coronary artery. There were also saccular and fusiform aneurysms in the right coronary artery, but thrombi were not observed in them. Aorto-coronary bypass surgery was performed to salvage the viable myocardium and to prevent recurrent myocardial infarction and rupture or infection of these coronary aneurysms. Postoperative coronary angiography revealed a new small saccular aneurysm in the mid-portion of the right coronary artery. During this period, there was no immunological evidence of active SLE. It is important to ascertain whether such coronary aneurysms resulted from atherosclerosis or arteritis, because of the choice of the different therapeutic interventions. In this case, however, it was difficult to determine. It was speculated that these coronary aneurysms arose from an arteritic process, because the saccular aneurysm in the mid-portion of the right coronary artery was formed in less than three months, there were no coronary risk factors, and any microscopic evidence of atherosclerosis was not obtained in the aortic specimen during aortocoronary bypass surgery. Serial coronary angiographic studies are necessary for accurately diagnosing coronary artery disease. Anticoagulant therapy and antiinflammatory medication may be necessary to prevent myocardial infarction in patients with SLE, even if there is no immunological evidence of active SLE.
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PMID:[Myocardial infarction due to thrombi in coronary aneurysms in a young woman with systemic lupus erythematosus]. 378 87

SLE affects most aspects of cardiac function, and recent studies have reported increasing cardiovascular morbidity and mortality. Pathologically, SLE is characterized by a pancarditis involving pericardium, myocardium, endocardium, and coronary arteries. In autopsy series, pericarditis has been found in 43% to 100% (mean 62%, Table I), and myocarditis was found in 8% to 78% (mean 40%, Table II), but both have been underdiagnosed clinically. Libman-Sacks lesions have been noted in 25% to 100% (mean 43%) and infective endocarditis in 1.1% to 4.9% of clinical and autopsy studies (Table III). Coronary disease may be due to arteritis, which should be treated with high-dose steroids, or it may be due to atherosclerosis, which is amenable to medical or surgical therapy. Valvular disease has been treated surgically, but with a combined surgical mortality as high as 25%. Aortic insufficiency and mitral regurgitation are the most common valvular problems, although aortic and mitral stenosis have also been reported. Hypertension has been noted in 14% to 69%, and heart failure in 5% to 44%. Evidence for a lupus cardiomyopathy, which may be subclinical, is reviewed. While steroids may ameliorate SLE pancarditis, they have also been associated with hypertension, LV hypertrophy, purulent and constrictive pericarditis, mitral regurgitation, and perhaps accelerated atherosclerosis. It remains to be seen if improved diagnosis and treatment of the cardiovascular manifestations of SLE can enhance survival.
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PMID:Cardiovascular manifestations of systemic lupus erythematosus. 390 17


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