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Query: UMLS:C0409974 (lupus)
22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was undertaken to determine if there is an association between increased titers of five different antiphospholipid antibodies (aPLA) in young patients' sera and the occurrence of acute myocardial infarction (AMI). Antibodies to anticardiolipin (aCL), anti-phosphatidylserine (aPS), antiphosphatidylinositol (aPI), anti-phosphatidylcholine (aPC), and anti-phosphatidylethanol amine (aPEA) were measured in 214 patients (102 patients, 102 healthy controls and 10 patients with antiphospholipid syndrome). These antibodies were measured twice (within 4h of onset of acute myocardial ischemic chest pain and 3 months after the myocardial infarction) by enzyme linked immunosorbent assay (ELISA). Elevated titers of four different aPLA were detected in 6.9% of all patients with AMI on hospitalization. Titers of aPLA in AMI were elevated in the younger age group < 50 years old (P < 0.001) and in men only (not statistically significant). No correlation was found between the presence of aPLA and cardiovascular risk factors (smoking, hypertension, diabetes mellitus and hyper-cholesterolemia). Three of the seven patients with increased titers of aPLA did not have any other cardiovascular risk factors. The titers of aPLA were within normal range 3 months after AMI. Evidence of significantly elevated titers of different aPLA at the early stage of AMI suggests that these autoantibodies are present before the AMI and are not secondary to them. The disappearance of the elevated aPLA 3 months after AMI may be due to an absorption effect or possibly a cyclic phenomenon similarly found in other autoimmune diseases. aPLA may be an additional risk factor for AMI, and should especially be considered in a patient of the younger age group without apparent cardiovascular risk factors.
Lupus 1995 Aug
PMID:The presence of antiphospholipid antibodies in acute myocardial infarction. 852 29

We reviewed the case records of 10 Oriental patients with systemic lupus erythematosus (SLE) who developed pulmonary haemorrhage (PH) between 1987 and 1996 to determine their clinical presentation and outcome. All the patients had clinical evidence of PH including a sudden onset of dyspnoea, tachycardia, fall in haemoglobin (at least 1.5 gm%) and bilateral diffuse alveolar infiltrates on chest radiographs. At the time of PH, nine patients had a disease duration of 2 years or less and all the patients had clinical and/or laboratory evidence of active lupus disease. Fever and lung crepitations were present in 90% of patients while haemoptysis and chest pain occurred in only three and two patients, respectively. All the patients were treated with high dose intravenous corticosteroids and in addition seven had a combination of pulse methylprednisolone and cyclophosphamide, and four had received plasmapheresis. Four patients died as a result of PH. One patient died of pneumonia three years after recovering from PH while the remaining five had no recurrence of PH after a median follow-up of 22 months. Our study suggests that PH in Oriental lupus patients often occurs early in the disease, rarely presents with haemoptysis and has a high mortality despite aggressive immunosuppressive therapy.
Lupus 1997
PMID:Pulmonary haemorrhage in Oriental patients with systemic lupus erythematosus. 941 86

A 70-year-old physician was admitted to our hospital because of bilateral pleural effusion and left-sided chest pain on deep inspiration. On admission, the APTT was prolonged and was not corrected with a 1:1 mixture of normal plasma. Results of serological examinations included a positive lupus-anticoagulant test and a positive ANA test at a titer of 1:1,280 in a homogeneous pattern. The patient's age, sex, symptoms, signs, and laboratory results all argued against the diagnosis of SLE except for ANA and lupus anticoagulant test. Because procainamide had been prescribed (250 mg every 6 h) for premature ventricular contractions for eight years before admission, procainamide-induced lupus was suspected. Procainamide was discontinued. Chest pain persisted and tests for c-reactive protein were positive. Prednisolone was administered. Procainamide induced lupus was diagnosed, because anti-histone H 2 A-H 2 B complex antibodies were high by enzyme-linked immunosorbent assay, and IgM-class anti-histone antibodies were found in response to H1, H 2 B and H 2 A-H 2 B complex (immunoblotting), which suggested the drug induced lupus. There are only a few reports of drug induced lupus in which the lupus-anticoagulant test was positive and prednisolone was indicated. The measurements of anti-histone antibodies and of expression of anti-histone antibodies were useful in distinguishing drug-induced lupus from SLE.
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PMID:[Procainamide-induced lupus in a patient with bilateral pleural effusion]. 975 5

The authors present the cases of two young patients, a man and a woman, who presented with myocardial infarction, in the absence of ischemic heart disease or stenosis of the coronary arteries. The woman was known to have systemic lupus erythematosus (SLE) for the past 3 years (the immunoglobulin M [IgM] anticardiolipins antibodies were positive), without a history of coronary risk factors. Suddenly she presented with acute chest pain on rest that lasted 4 hours and culminated in anterior wall myocardial infarction. She was admitted to the coronary care unit, where no thrombolysis was given. She did not have echocardiographic evidence of Libman-Sacks endocarditis, but myocardial infarction was evident at the electrocardiogram (ECG). The young man had SLE (the IgM anticardiolipins were absent, but he was positive for lupus anticoagulant antibodies), he was hyperlipidemic, was a moderate smoker and moderately obese, and had no history of ischemic heart disease. He suddenly presented with an acute myocardial infarction documented by ECG, enzymes, and gammagraphy. In both patients, coronary angiography findings were normal and myocardial biopsy did not show evidence of arteritis. The relevance of these cases is the rare association of ischemic heart disease in SLE, with normal coronary arteries and without evidence of arteritis or verrucous endocarditis.
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PMID:Myocardial infarction in patients with systemic lupus erythematosus with normal findings from coronary arteriography and without coronary vasculitis--case reports. 1008 5

Infliximab is a chimeric anti-tumour necrosis factor-alpha monoclonal antibody that has been studied for the treatment of Crohn's disease and rheumatoid arthritis. In several placebo controlled, randomized clinical trials and open trials, 771 patients have been given infliximab (a further 192 received placebo). Follow-up for safety has included the time of study (12 weeks after the last infusion), plus three additional years. Acute infusion reactions (headache, fever, chills, urticaria, chest pain) were seen in 17% of patients receiving infliximab compared with 7% of those receiving placebo. While infections were reported more frequently overall in the patients given infliximab (26% over 27 weeks of follow-up versus 16% of placebo-treated patients over 20 weeks of follow-up), there was no increased risk of serious infections. There was no difference in the overall mortality rate between the groups. While low titres of autoantibodies developed in less than 10% of patients, drug-induced lupus was seen in less than 1%, with these cases resolving upon discontinuation of the drug. Overall, infliximab showed an acceptable safety profile.
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PMID:Long term safety of infliximab. 1102 58

INFLIXIMAB: Is a chimeric antitumour necrosis factor-alpha monoclonal antibody that has been studied for the treatment of Crohn's disease and rheumatoid arthritis. A LONG TERM SAFETY: In several placebo controlled, randomized clinical trials and open trials, 771 patients have been given infliximab (a further 192 received placebo). Follow-up for safety has included the time of study (12 weeks after the last infusion), plus 3 additional years. GENERAL TOLERANCE: Acute infusion reactions (headache, fever, chills, urticaria, chest pain) were seen in 17% of patients receiving infliximab compared with 7% of those receiving placebo. While infections were reported more frequently overall in the patients given infliximab (26% over 27 weeks of follow-up versus 16% of placebo-treated patients over 20 weeks of follow-up), there was no increased risk of serious infections. There was no difference in the overall mortality rate between the groups. AT THE POINT OF VIEW IMMUNOLOGIC: While low titres of autoantibodies developed in less than 10% of patients, drug-induced lupus was seen in less than 1%, with these cases resolving upon discontinuation of the drug. Overall, infliximab showed an acceptable safety profile.
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PMID:[Treatment of inflammatory diseases: safety of long-term use of infliximab]. 1131 23

A 44-year old woman hospitalized because of chest pain, pleuropneumonic lesions and high temperature is described. Disease of connective tissue was suspected because of symptoms (fever, chest pain) aggravated despite antibioticotherapy. During diagnostic procedures hypoxemia was observed and thrombotic lesions were discovered in the right popliteal vein and in numerous pulmonary arteries. Pulmonary thrombosis was recognised and patient was admitted to the Intensive Care Unit. Anti-ds.-DNA antibodies were not found but anticardiolipin (aCL) antibodies and lupus anticoagulant (LA) were present in high concentrations in serum. We didn't find all symptoms required for SLE diagnosis. Anticoagulant treatment was effective and we recognised primary antiphospholipid syndrome (APS). It is a less frequent syndrome than "secondary APS" connected with systemic lupus erythematosus. Patient should be treated with anticoagulant drugs and observed whether symptoms of SLE would appear.
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PMID:[Antiphospholipid syndrome--primary or secondary? Therapeutic problem]. 1214 82

Primary Pulmonary Artery Sarcoma is a rare entity, which shares some clinical features with Thromboembolic Pulmonary Disease (TEPD), complicating differential diagnosis. The authors report a Clinical Case of a Primary Pulmonary Artery Sarcoma in a 59 years old man, admitted with a history of dyspnoea on exertion, chest pain and general symptoms. Chest X-ray, Computed Tomography Scan, Angiographies and Magnetic Resonance Imaging suggested TEPD. Blood Analysis performed before anticoagulation therapy: Lupus Anticoagulant-and Ig M Anticardiolipin +. Our presumptive initial diagnosis was TEPD in a patient with a hypercoagulable state. Intravenous heparin was started, with some clinical improvement but 2 months later he was readmitted, due to clinical and radiological deterioration. Pulmonary Thromboendarterectomy was considered but a right pneumonectomy was necessary because of bleeding. He died of ARDS in a single lung in the 7th day after surgery. Pathology revealed pulmonary artery sarcoma with pulmonary and pleural metastases.
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PMID:[Pulmonary Artery Sarcoma - diagnostic and treatment difficulties]. 1295 67

Spontaneous coronary artery dissection (SCAD) is an uncommon condition that may lead to sudden coronary artery occlusion resulting in a fatal acute myocardial infarction. It usually affects young to middle age women. A Medline search from 1966 to 2001 (using keywords: coronary artery dissection and systemic lupus erythematosis) revealed no prior reports of coronary dissection in a patient with systemic lupus erythematosis (SLE). We describe a 48-year old woman with SLE who sustained a fatal spontaneous left main coronary artery dissection. Coronary angiogram was notable for marked variability in the size of coronary lumen from systole to diastole. This case demonstrates the need to consider SCAD in the evaluation of chest pain and myocardial infarction in patients with SLE. Furthermore, in the absence of classical angiographic findings of coronary dissection, a detailed review of phasic changes in coronary lumen during a cardiac cycle could help reach this diagnosis.
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PMID:Spontaneous coronary artery dissection in a patient with systemic lupus erythematosis. 1470 66

Regional or localized pericarditis has been infrequently reported. We report a patient with systemic lupus erythematosus (SLE), who presented with retrosternal pleuritic-type chest pain without audible friction rub, electrocardiographic changes or detectable pericardial effusion on echocardiography. Computed tomography, however, revealed a circumscribed area of pericardial inflammation, suggesting a diagnosis of localized lupus-associated pericarditis. This case demonstrates that localized pericarditis may occur in SLE and that chest CT may be required as part of the work-up in the diagnosis of lupus pericarditis.
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PMID:Localized pericardial inflammation in systemic lupus erythematosus. 1530 Dec 50


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