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 association of systemic lupus erythematosus (SLE) with amyloidosis is exceptional. We present a 37-year-old patient who was diagnosed five months earlier for SLE. She developed an acute episode of chest pain, cough and dyspnoea. Hypoxemia and obstructive changes in respiratory tests were present. The chest X-ray was repeatedly normal. Open lung biopsy revealed lupus pneumonitis with positive stain for immunoglobulins and complement, bronchiolitis obliterans, and pulmonary amyloidosis.
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PMID:Pulmonary amyloidosis and unusual lung involvement in SLE. 783 23

We describe a 42-year-old anti-Ro/SS-A antibody positive non-lupus patient who developed interstitial pneumonitis in combination with several common clinical features with previously reported lupus pneumonitis patients whose anti-Ro/SS-A antibodies were positive, while whose antinuclear antibodies were negative. We consider that these patients may belong to a same new clinical entity. A variety of characteristic manifestations related to anti-Ro/SS-A antibodies has been reported in patients with systemic lupus erythematosus (SLE) and other connective tissue diseases [1] [2], and an association between these antibodies with pulmonary parenchymal involvement has been reported by Hedgpeth and Boulware in patients with SLE [3] [4]. We report here a 42-year-old non-lupus male patient with pulmonary fibrosis who presented with anti-Ro/SS-A antibodies.
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PMID:Anti-Ro/SS-A antibody-positive interstitial pneumonitis in a non-lupus patient. 786 26

Non-resolved chronic pulmonary thromboembolism is a frequent cause of pulmonary hypertension. In long-standing disease hypertension is progressive due to intimal and medial changes in the perfused vessels. Non-resolution of thromboemboli is often associated with underlying coagulopathies; the presence of a lupus anticoagulant may pose a significant problem in the peri-operative management of these patients. Pulmonary thrombendarterectomy presents an efficient option of treatment which is feasible in the majority of patients. By means of pulmonary angiography and computed tomography operability is verified by the often difficult recognition of thromboembolic changes in the central pulmonary arteries. Patients with solely peripheral thromboembolic changes or primary pulmonary hypertension must be excluded. In presence of significant exertional dyspnea and/or pulmonary pressure elevation surgery is indicated. Mortality is high and mainly related to unrelieved pulmonary hypertension or pulmonary complications; pulmonary reperfusion edema, respiratory failure or pneumonia and sepsis. In all survivors the reduction of pulmonary hypertension is highly significant and persistent. Thromboembolic pulmonary hypertension may be treated curatively in most patients by thrombendarterectomy. Correct selection of surgical candidates is mandatory, and the patients should preferably be diagnosed and undergo surgery in an early stage of their disease.
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PMID:[Surgical treatment of thromboembolism-induced pulmonary hypertension]. 786 94

The case of a patient with systemic lupus erythematosus who developed pneumonia caused by Aspergillus fumigatus is described. She was treated with itraconazole 200 mg twice daily, with a rapid response. After a follow-up period of 5 years no recurrence of the infection has been detected. To our knowledge this is the first report on the use of itraconazole in patients with systemic lupus erythematosus. Considering the poor prognosis associated with Aspergillus pneumonia in patients with systemic lupus erythematosus, we believe that itraconazole constitutes a safe and effective alternative to amphotericin B in these patients.
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PMID:Aspergillus pneumonia successfully treated with itraconazole in a patient with systemic lupus erythematosus. 789 23

A 69-year-old Japanese female was admitted because of general fatigue. Laboratory data showed elevation of serum total bilirubin, transaminase, gamma-glutamyl transpeptidase, and creatinine levels. An immunological study revealed hypergammaglobulinemia, low titer of complement, and high titers of antinuclear antibody, anti-DNA antibody, and circulating immune complexes. Antibodies to parainfluenza virus 3 were positive. Histology of the liver disclosed numerous giant cell hepatocyte transformations with the lobular architecture being slightly distorted by portal inflammation and fibrosis. These findings led us to make a diagnosis of giant cell hepatitis associated with systemic lupus erythematosus. Prednisolone was effective in improving the anemia and the serum immunoglobulin, immune complex, and antinuclear antibody levels. The addition of cyclosporine to the initial corticosteroid therapy was also beneficial in decreasing the transaminase level and in improving liver histology. The patient died of acute pneumonitis and renal failure on the 166th day after admission. Parainfluenza virus 3 and autoimmune mechanisms were thus considered to be the causes of the giant cell hepatitis.
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PMID:Post-infantile giant cell hepatitis in an elderly female patient with systemic lupus erythematosus. 806 7

A case history is presented of a woman with systemic lupus erythematosus, sepsis and pneumonia caused by Streptococcus pneumoniae. Conventional treatment was supplemented with intravenous human immunoglobulin with remarkable effect. The treatment is discussed.
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PMID:[Intravenous immunoglobulin administration to a patient with systemic lupus erythematosus and pneumococcal septicemia]. 806 1

Systemic lupus erythematosus (SLE) frequently involves the pleura with resultant pleural effusion. Previous studies have reported that detection of antinuclear antibodies (ANA) in pleural fluid using animal tissue as substrate was a sensitive and specific method for distinguishing SLE pleural effusions from other etiologies. The HEp-2 ANA, which uses a human cell line as substrate, is now the preferred ANA test; however, to our knowledge, no studies on pleural fluid using this assay have been reported. To determine its sensitivity and specificity, when measured in pleural fluid, HEp-2 ANA levels were determined in pleural effusion samples associated with a variety of different etiologies, including SLE, malignancy, congestive heart failure, pneumonia, tuberculosis, and a miscellaneous group of diseases. Pleural fluid ANA results were positive in 14 of 82 samples. Six of the eight (75 percent) pleural fluid samples collected from patients with SLE were ANA positive, and all but one had high titers (> 1:160) with a homogenous staining pattern. The remaining two patients with SLE with negative pleural fluid ANA had recurrent pulmonary emboli and congestive heart failure, rather than lupus pleuritis. Eight of 74 patients (10.8 percent) without clinical evidence of SLE had a positive pleural fluid ANA, with the majority having a speckled pattern. High titers were noted in three. These results indicate that a negative or low titer ANA and a speckled staining pattern in pleural fluid from a patient suspected of lupus pleuritis suggest an alternative diagnosis. High pleural fluid titers (up to 1:640) were seen occasionally in patients with inflammatory pleural effusions in the absence of SLE.
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PMID:Antinuclear antibodies in pleural fluid. 808 70

We report a 49 years old woman with systemic lupus erythematosus and a WHO type IV nephropathy, treated with prednisone 1 mg/kg/day po and cyclophosphamide 1 g/month iv. After two months in this treatment schedule, she presented with an acute pneumonia; broncoalveolar lavage and lung biopsy disclosed the presence of Pneumocystis carinii. She was treated with trimethoprim-sulfamethoxazole 960 mg tid with a favorable response. Opportunistic infections are frequent in lupus erythematosus and Pneumocystis carinii pneumonia has been recently reported in this disease. The changes in immune response and the adverse effects of drugs used in its treatment may explain the increased susceptibility of these patients to infections by Pneumocystis carinii.
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PMID:[Lupus erythematosus disseminatus and Pneumocystis carinii pneumonia]. 808 67

The pleuropulmonary manifestation of systemic lupus erythematous (SLE) are pleuritis, acute lupus pneumonitis, chronic interstitial lung disease with fibrosis, alveolar hemorrhage, respiratory muscle and diaphragmatic dysfunction, atelectasis, bronchiolitis obliterans, pulmonary vascular disease with pulmonary hypertension, and pulmonary embolism. This article reviews these specific pleuropulmonary consequences of SLE while focusing on clinical, pathologic, and therapeutic considerations.
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PMID:Pleuropulmonary manifestations of systemic lupus erythematosus. 815 98

We characterized urinary excretion of C3 fragments among patients with systemic lupus erythematosus (SLE) as a possible indicator of renal involvement. 28 patients, representing a broad range of disease activity were admitted to our study. Urinary proteins were separated on 4-20% gradient SDS-PAGE gels, under reducing conditions, and transblotted to nitrocellulose. Western blots were developed with a polyvalent goat-anti-human C3d antiserum, and an alkaline phosphatase-conjugated rabbit anti-goat IgG. Three patterns were obtained: 1) no bands detected; 2) bands suggesting the presence of intact C3; and 3) samples with additional low molecular (< 4 x 10(4)) bands. The 12 patients with no C3 bands had minimal disease activity (e.g. fatigue, arthralgia, arthritis, rash, oral ulcers). The seven patients with intact C3 patterns also had minimally active disease. Their primary clinical findings included fatigue, pleurisy, renal disease which had been treated, hemolytic anemia, and arthritis. Patients with low molecular weight C3 fragments in their urine formed two sub-sets, based upon their presenting features. The first group had severe disease and contained all patients with active lupus nephritis (n = 4), while the second consisted of non-renal patients with primary clinical findings of moderate disease activity (e.g. thrombocytopenia, pneumonitis, arthritis). Our results suggest urinary excretion of low molecular weight C3 fragments correlates with active renal disease, but is a variable finding among SLE patients with non-renal manifestations of disease activity.
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PMID:Complement C3 fragments in urine: detection in systemic lupus erythematosus patients by western blotting. 819 18


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