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)

Cardiac involvement in patients with systemic lupus erythematosus (SLE) was assessed by full echocardiography and continuous wave Doppler in 50 consecutive patients and 50 age- and sex-matched control subjects in a prospective, blinded study. The left ventricular ejection fraction was decreased in patients compared to control subjects (61 +/- 9 vs 68 +/- 7%, p less than 0.001), whereas interventricular septum (12 +/- 3 vs 9 +/- 1 mm, p less than 0.001), and posterior wall dimension (9 +/- 2 vs 8 +/- 1 mm, p less than 0.001), left ventricular mass (186 +/- 54 vs 130 +/- 32 g, p less than 0.001) and mitral valve Doppler A:E ratio (0.8 +/- 0.2 vs 0.7 +/- 0.1, p less than 0.01) were increased. Pericardial effusion was detected in 27 patients and 5 control subjects, and valvular regurgitation was more frequent in the patients (aortic 2 vs 0; mitral 23 vs 5, p less than 0.001; tricuspid 34 vs 22, p less than 0.01 and pulmonary 28 vs 17, p less than 0.05). Mitral or aortic regurgitation was more common in patients with active SLE (60 vs 40%, difference not significant) but was not related to the duration of SLE (r = 0.02), duration of prednisone therapy (r = -0.13) or current dosage of prednisone (r = 0.01). This study demonstrates that pericardial effusion, valvular regurgitation and myocardial abnormalities are frequently present in patients with SLE.
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PMID:Cardiac involvement in systemic lupus erythematosus detected by echocardiography. 233 Sep 2

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.
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PMID:Severe aortic stenosis in systemic lupus erythematosus and mucopolysaccharidosis type II (Hunter's syndrome). 314 55

We performed echocardiography prospectively 4.9 +/- 0.7 years apart (mean +/- SD), in 74 patients with systemic lupus erythematosus. On the basis of the first study, the patients were distributed in four groups according to the type of valvular involvement: 7 patients had vegetations (Libman-Sacks endocarditis; group 1); 6 patients had rigid and thickened valves with stenosis, regurgitation, or both (group 2); 5 patients had miscellaneous forms of valvular involvement without valvular dysfunction (group 3), as did the 60 controls; and 56 patients had no valvular disease (group 4). The overall prevalence of clinically important valvular disease (groups 1 and 2) was 18 percent. Patients in group 1 were younger than those in group 2 (33.5 +/- 16.7 vs. 47.8 +/- 17.6 years; P less than 0.05), had a shorter mean duration of lupus (4.8 +/- 2.2 vs. 10.7 +/- 6.4 years; P less than 0.001), and had received a smaller cumulative dose of steroids (21.5 +/- 13.1 vs. 79.5 +/- 63.4 g of methylprednisolone or its equivalent; P less than 0.05). During the five-year follow-up, one patient in group 1 and five in group 2 required valve surgery, no patient in group 3 had valvular dysfunction, and five patients in group 4 had mild valvular lesions. We conclude that clinically important valvular involvement in systemic lupus is relatively frequent and sometimes requires surgery. Echocardiography can identify a subset of lesions (valvular thickening and dysfunction), other than verrucous (Libman-Sacks) endocarditis, that are prone to hemodynamic deterioration.
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PMID:Prevalence, morphologic types, and evolution of cardiac valvular disease in systemic lupus erythematosus. 341 13

Two patients had cardiac complications of childhood onset systemic lupus erythematosus (SLE). A 14-year-old boy had extramural and intramural coronary arteritis demonstrated by angiography. The signs and symptoms of myocardial ischemia improved dramatically when corticosteroid dose and immunosuppression were increased. A 20-year-old woman had had SLE for 18 years and had functionally significant mitral stenosis and regurgitation. Calcification of the mitral valve was observed on echocardiography. Corticosteroid treatment has controlled the renal manifestations of SLE. Cardiac complications of SLE are now a significant clinical problems.
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PMID:Cardiac complications in children with systemic lupus erythematosus. 663 79

We sought to correlate esophageal symptoms with esophageal motility abnormality in 17 patients with mixed connective tissue disease (MCTD) and in 14 patients with systemic lupus erythematosus (SLE). Heartburn and regurgitation were common symptoms (11/17) in patients with MCTD, and most of the (10/11) exhibited significant manometric abnormalities. Additionally, impairment of esophageal peristalsis was found in four of the remaining asymptomatic patients. Severe esophageal aperistalsis was noted in nine MCTD patients. Patients with SLE also frequently reported esophageal symptoms (8/14), but significant motility abnormalities were seen in only three cases. In both patient groups good correlation between Raynaud's phenomenon and esophageal aperistalsis was found. Our results reveal that, although esophageal symptoms are commonly present in patients with both MCTD and SLE, severe esophageal motility abnormalities are more often found in patients with MCTD than in those with SLE.
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PMID:Esophageal dysfunction in patients with mixed connective tissue diseases and systemic lupus erythematosus. 708 97

Unlike the Libman-Sacks vegetations of acute systemic lupus erythematosus (SLE), which are usually asymptomatic, valve involvement in chronic SLE and primary antiphospholipid antibody syndrome (APLAS) is similar to that of chronic rheumatic disease. Typical findings include valve thickening and nodularity, poor coaptation, and regurgitation. Elevated levels of antiphospholipid antibodies have been associated with the development of these valvular abnormalities in some but not all reported cases, and there are undoubtedly other etiologic cofactors. When cardiac valvular replacement is required, special attention must be given to preoperative reduction of elevated antibody levels, prevention of intraoperative thromboembolism, and prompt and aggressive postoperative anticoagulation.
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PMID:Etiology and management of chronic valve disease in antiphospholipid antibody syndrome and systemic lupus erythematosus. 777 77

This two-part article examines the histologic and morphologic basis for stenotic and purely regurgitant aortic valves. Part I discusses stenotic aortic valves and Part II will discuss causes of purely regurgitant aortic valves. In over 95% of stenotic aortic valves, the etiology is one of three types: congenital (primarily bicuspid), degenerative, or rheumatic. Other rare causes of stenotic aortic valves include active infective endocarditis, homozygous type II hyperlipoproteinemia, and systemic lupus erythematosis. The causes of pure aortic regurgitation are multiple but can be separated into diseases affecting the valve (normal aorta) (infective endocarditis, congenital bicuspid, rheumatic, floppy), diseases affecting the walls of aorta (normal valve) (syphilis, Marfan's, dissection), disease affecting both aorta and valve (abnormal aorta, abnormal valve) (ankylosing spondylitis), and diseases affecting neither aorta nor valve (normal aorta, normal valve) (ventricular septal defect, systemic hypertension). Diseases affecting the aortic valve alone are the most common subgroup of conditions producing pure aortic valve regurgitation.
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PMID:Pathology of aortic valve stenosis and pure aortic regurgitation. A clinical morphologic assessment--Part I. 816 31

An echocardiographic study was performed in 60 unselected patients affected with Systemic Lupus Erythematosus (SLE) and in 30 age- and sex-matched control subjects, to evaluate the incidence of cardiac abnormalities and the possible correlation with the presence of antiphospholipid antibodies. 33 patients (55%) had major cardiac abnormalities as valvular stenosis and/or regurgitation (35%), pericardial effusion or thickening (26%), left ventricular hypertrophy (21%), regional or global left ventricular dysfunction (10%). Some patients presented more than one cardiac dysfunction: five patients had one major and one minor lesion, 11 presented with two major lesions, and in five of them a pancarditis was found. Minor cardiac abnormalities as mitral valve prolapse, valvular thickening without valvular dysfunction, calcification of the mitral annulus were demonstrated in nine patients (15%). Increased levels of antiphospholipid antibodies were found in 25 out of 60 patients (41.6%). No clear correlation was evident between endocardial or pericardial involvement and such autoantibodies. In fact, valvular heart diseases were present in 36% of the patients with antiphospholipid antibodies and in 34% of the patients without antiphospholipid antibodies; pericardial involvement was evident in 24% and in 28% of patients with and without them, respectively. On the contrary the demonstration of antiphospholipid antibodies in five out of six patients with regional or global left ventricular dysfunction could suggest a pathogenetic role of these autoantibodies in myocardial hypokinesis. Therefore, antiphospholipid antibodies could represent only one of the pathogenetic factors of the cardiac lesions in SLE patients, together with immunologic and iatrogenic factors. The involvement of other systems as renal, vascular and pulmonary certainly play an important role in predisposing to the development of secondary cardiac manifestations.
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PMID:[Cardiac abnormalities in systemic lupus erythematosus and their association with antiphospholipid antibodies]. 823 32

The aim of this study was to assess the relationship between the incidence and severity of valvular regurgitation and the presence of high levels of anticardiolipin antibodies in a group of patients with systemic lupus erythematosus. Fifty patients aged 35.5 +/- 13.4 years and 84 healthy age and sex matched controls were studied with two dimensional echocardiography with color flow imaging. IgG and IgM anticardiolipin antibodies were measured in all patients within a week of the echocardiographic study. Patients had a similar incidence of aortic, tricuspid and pulmonic regurgitation than normals. However there was a greater incidence of mitral regurgitation among patients (56 vs 21% p < 0.001). The seven patients with moderate or severe mitral regurgitation had Libman Sacks vegetations of the valve. Twenty five of 28 patients with mitral regurgitation had increased anticardiolipin antibodies; moreover, these levels were significantly higher among patients with mitral regurgitation and thickened mitral valves than those with normal valves. Patients with increased anticardiolipin antibodies had a higher incidence of Libman Sacks vegetations. No association between the presence of these antibodies and the severity of aortic, pulmonic or tricuspid regurgitation was observed. It is concluded that the incidence of mitral valve regurgitation is increased in systemic lupus erythematosus and related to raised anticardiolipin antibodies.
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PMID:[Systemic lupus erythematosus: valvular regurgitation and its relation to anticardiolipin antibodies]. 830 11

A 22-year-old female patient with an 8-year history of mixed connective tissue disease (systemic sclerosis overlapping with systemic lupus erythematosus) presented with marked respiratory distress, sinus tachycardia (135 bpm), and pulsus paradoxus. The chest x-ray showed an enlargement of the cardiac silhouette, which was due to a 3-cm-wide, circular pericardial effusion, as demonstrated by two-dimensional echocardiography. Pericardiocentesis performed to decompress cardiac tamponade did not lead to clinical improvement. The increase in dyspnea was caused by a rise in pulmonary wedge pressure from 21 to 40 mm Hg following an acute increase of mitral valve regurgitation. In the presence of global hypokinesia of the left ventricle, cardiac output decreased from 3.25 to 2.63 l/min. Intensive care including hemodialysis and plasmapheresis as well as high-dose application of cyclophosphamide and steroids led to a stabilization of the hemodynamic situation over a period of days. The case report presented here supports the general recommendation to perform pericardiocentesis in a stepwise manner under hemodynamic monitoring. This holds true primarily for patients with mitral valve regurgitation and/or cardiac involvement in connection with an underlying disease.
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PMID:[Pulmonary edema as a complication during pericardial puncture in "mixed connective tissue disease"]. 835 45


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