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)

A 59-year-old female was admitted to our hospital because of chest pain. Coronary angiography revealed severe obstruction of the left coronary artery. The findings of hematology and renal biopsy were interpreted as showing active systemic lupus erythematosus (SLE). Coronary artery bypass grafting was performed before steroid therapy because of worsening cardiac function due to myocardial ischemia. Postoperative course had been satisfactory immediately after operation, but the patient showed pulmonary infection about two months after operation and died three months after surgery. In open heart surgery for a patient with active SLE, special care must be taken to the prevention and treatment for infection.
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PMID:[A case of coronary artery bypass grafting in a patient with active systemic lupus erythematosus]. 823 Sep 32

This population study includes the majority of all systemic lupus erythematosus (SLE) patients in Iceland (n = 65). The study lists various self-rated pain descriptions both from a 54-item pain questionnaire and from the somatisation section of the Diagnostic Interview Schedule (DIS). Results show SLE patients to have significantly more joint and chest pain than does another patient group; to use analgesics more frequently; to have been in hospital more often during the past 10 years and to believe they know the reason for their pain. Also listed are factors that patients have found to increase and decrease SLE pain.
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PMID:Pain and pain problems among subjects with systemic lupus erythematosus in Iceland. 843 40

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

A 19 year old female was admitted to our hospital with complaints of fever, dyspnea and chest pain. Chest x-ray film showed a massive right pleural effusion. She was diagnosed to have systemic lupus erythematosus (SLE) because of malar rash, serositis (pleuritis), positive antinuclear antibody and positive anti-DNA antibody. Then she was successfully treated with 50 mg/d prednisolone. This case was unusual and of interest in that she had eosinophilia in the peripheral blood and exudative pleural effusion and a marked elevation of serum IgE level despite no history of allergic diseases and no evidence of parasite infections.
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PMID:[A case of SLE with the onset of pleuritis showing eosinophilia and elevation of serum IgE]. 868 35

A 46-year-old man was admitted to the hospital because of chest pain and left pleural effusion. Fever and dyspnea developed on the third hospital day. Interstitial shadows and pleural effusions in both lower lung fields appeared on chest roentgenograms. Microscopic examination of transbronchial lung biopsy specimens taken on hospital day 5 showed thickening of the alveolar walls and desquamation of macrophages into the alveolar spaces. Analysis of bronchoalveolar lavage fluid revealed many cells and macrophages. Tests for anti-nuclear antibody and anti-DNA antibody were positive, which, in addition to serositis and proteinuria, established the diagnosis of systemic lupus erythematosus. The interstitial shadow on chest roentgenograms was believed to have reflected an acute pulmonary manifestation of systemic lupus erythematosus. The symptoms and the abnormality on chest roentgenograms were relieved within 1 month of the start of pulse therapy with prednisolone.
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PMID:[Acute pulmonary disease in systemic lupus erythematosus successfully treated with prednisolone pulse therapy]. 871 2

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

A 40-year-old female was admitted with right chest pain. SLE was absent from her past history, although she complained of polyarthralgia in winter. Atypical pneumonia/pleuritis was suspected by chest X-ray film, showing a nodular shadow in the right lower field and moderate pleural effusion. Chlamydia pneumonia was diagnosed by elevated anti-C. psittsci antibody, while characteristics of pleural fluid revealed serositis accompanied by SLE because of the high titered anti-DNA antibody and the low titered complement. She was cured by clarithromycin and subsequent administration of prednisolone and cyclophosphamide.
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PMID:[A case of Chlamydia pneumonia and systemic lupus erythematosus (SLE) pleurisy]. 1021 98

We report a patient with systemic lupus erythematosus (SLE) complicated with nocardiosis. This case is very important that the complication of nocardiosis in SLE is very rare and the treatment to both SLE and nocardiosis is very difficult. A twenty-one-year old female was admitted to our hospital because of thoracic empyema and active lupus nephritis. Her medical history revealed that the diagnose of SLE was made when she was 18 with lymphocytopenia, proteinuria, positive antinuclear antibodies, and high titer of antibodies to native DNA. She was treated with prednisolne 60 mg daily and became better. Proteinuria appeared again in September 1995 and she was admitted to the former hospital. Renal biopsy proved diffuse proliferative glomeluronephritis (WHO IVb). She was treated with 1 g per day of methylprednisolone for 3 days and succeeded with 60 mg day of prednisolone. In early November she developed left chest pain and fever and chest X-ray demonstrated left pleural effusion. Antibiotics, antituberculosis, and antifungal therapy failed to subside her pleuritis and it turned to empyema. Then she was transferred to our hospital for further treatment. Nocardia farcinica was detected from the aspirated pleural fluid obtained at the former hospital. Drainage and intrathoracic impenem injection were effective. While long usage of minocycline was continued for the nocardiosis, 500 mg of cyclophosphamide pulse therapy to lupus nephritis was administrated. Two weeks later a new pulmonary lesion with left chest pain and liver abscess developed. Administration of trimethoprim-sulfamethoxazole subsided the nocardiosis. She was discharged with 1 g per day of proteinuria the prescribed 13 mg per day of prednisolone and continuous TMP-SMZ intake for nocardial infection. When immunosuppressive therapy must be given to the immunocompromised host, a more potent therapy must be added to avoid infection.
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PMID:[A case of systemic lupus erythematosus complicated by Nocardia farcinica]. 1038 29


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