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)

Acute lupus pneumonitis was the presenting manifestation of systemic lupus erythematosus in six of 12 cases in this series. The clinical picture was characterized by severe dyspnea, tachypnea, fever and arterial hypoxemia. Radiographic findings included an acinar filling pattern which was invariably found in the lower lobes and was bilateral in 10 of the cases. Studies failed to reveal evidence of infection as a cause of the acute pulmonary infiltrates. All patients were treated with oxygen and corticosteroids; seven received azathioprine. Six patients survived and are clinically well 14 months to four years following their acute illness. Three of these patients have residual interstitial infiltrates with persistent pulmonary function test abnormalities indicating progression to chronic interstitial pneumonitis. Histologic sections of the lungs available from four patients revealed hyaline membranes and interstitial edema (four cases), acute alveolitis (two cases), arteriolar thrombosis (one case) and a prominent lymphocytic interstitial pneumonitis with organizing bronchiolitis (one case).
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PMID:Pulmonary manifestations of systemic lupus erythematosus: review of twelve cases of acute lupus pneumonitis. 12 38

Acute massive pulmonary hemorrhage is described as part of the clinical picture of SLE. Seven patients had sudden onset of high fever, dyspnea, tachycardia, and cough with blood-tinged sputum that within hours progressed to massive hemoptysis and death. There were no vasculitis or other inflammatory lung changes found at autopsy. Only one of the seven reported cases survived when treated with 2 g of intravenous hydrocortisone daily. The mechanism of this pulmonary bleeding is unknown but seems to be an immune complex mediated phenomenon.
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PMID:Acute massive pulmonary hemorrhage in systemic lupus erythematosus. 14 42

Serum FDPs were investigated in 30 healthy and 95 patients with pulmonary thrombembolia, not-stabilized angina pectoris, myocardial infarction, rheumatism, rheumatoid arthritis, lupus erythematodes and dermatomyositis. FDPs are determined by hemagglutination inhibition according to Merskey. They are found in the sera of the healthy in average values of 3.73 mkgr/ml. The highest average values in the first 24 h were found in case of pulmonary thrombembolia up to 106.64 mkgr/ml, followed by rheumatoid arthritis 26.3 mkgr/ml, myocardial infarction with complication 22.4 mkgr/ml, rheumatism +5.58 mkgr/ml, not-stabilized angina pectoris 5.5 mkgr/ml; and noncomplicated myocardial infarction 4.3 mkgr/ml. By the third day of the disease FDP in pulmonary thrombembolia decreased, whereas a negligible elevation was observed in case of non-complicated myocardial infarction. The results were interpreted as well as the cause for the presence of the mentioned products in those groups of diseases. FDP determination is recommended as a routine method in case of: diagnosis of pulmonary thrombembolia, differentiation of myocardial infarction with or without complications, differentiation of pulmonary thrombembolia from myocardial infarction in emergency states, progressing with chest pain, collapse phenomena, dyspnea and establishment of the activity of the process of rheumatoid arthritis. FDP determination in stenocardia and rheumatism is not expedient.
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PMID:[Level of fibrinogen/fibrin degradation products (F/FDP) in certain internal diseases]. 49 29

A 29-year-old woman with systemic lupus erythematosus (SLE) developed dyspnea, hemoptysis, pleuropericarditis, and azotemia shortly after an episode of arthritis and progressive hair loss. She had a high titer of radioimmune anti-DNA Antibodies, positive fluorescent anti-smooth muscle antibodies, and depressed C3 levels in her serum. Antiglomerular basement membrane antibodies were negative, and the titer of antibodies against extractable nuclear antigen was within normal limits. Cryoglobulins and lupus erythematosus cell preparations were negative. Despite steroid therapy and other supportive measures, including dialysis, she died ten days after admission. Percutaneous renal and pulmonary biopsies were performed postmortem at bedside and were processed for immunohistology. Identical granular deposits of C3 and IgG were found in both the lungs and the kidneys. This finding suggests that a common pathogenetic mechanism is operating in the development of pneumonitis and nephritis in SLE, and is in agreement with the currently held views on immune-complex diseases.
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PMID:Immunohistologic findings in the lung in systemic lupus erythematosus. 57 88

A 35-year-old woman had a 13-year history of systemic lupus erythematosus (SLE) with recurrent flares since 1972 responding to corticosteroid therapy. In August, 1990 she presented with a 2-month history of dyspnea at rest, 4-pillow orthopnea and paroxysmal nocturnal dyspnea. Respiratory rate was 32-36/min, chest expansion 2 cm and crackles were present at the lung bases. On chest radiograph diaphragms were elevated. Pulmonary function tests (PFT) showed further reduction in lung volumes, maximum inspiratory pressures, maximum expiratory pressures and arterial blood gases. Ventilation/perfusion and gallium lung scans were normal. A diagnosis of "shrinking lungs syndrome" was made. Treatment with 40 mg of prednisone resulted in resolution of the patient's shortness of breath. PFT showed improvement in all variables. Corticosteroid therapy for acute "shrinking lungs syndrome" in active SLE can improve symptoms and pulmonary function.
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PMID:The "shrinking lungs syndrome" in systemic lupus erythematosus--improvement with corticosteroid therapy. 129 50

Laryngeal involvement in systemic lupus erythematosus (SLE) can range from mild ulcerations, vocal cord paralysis, and edema to necrotizing vasculitis with airway obstruction. In this report, four cases showing the range of severity of this disease manifestation are presented, accompanied by a comprehensive review of the literature. The clinical course of 97 patients with laryngeal involvement with SLE are reviewed, of whom 28% had laryngeal edema and 11% had vocal cord paralysis. In the majority of cases, symptoms such as hoarseness, dyspnea, and vocal cord paralysis resolved with corticosteroid therapy. Other, less common causes of this entity included subglottic stenosis, rheumatoid nodules, inflammatory mass lesions, necrotizing vasculitis, and epiglottitis. The clinical presentation of laryngeal involvement in patients with SLE follows a highly variable course, ranging from an asymptomatic state to severe, life-threatening upper airway compromise. With its unpredictable course and multiple causations, this complication remains a diagnostic and therapeutic challenge to physicians involved in the care of patients with SLE.
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PMID:Laryngeal involvement in systemic lupus erythematosus. 129 93

A 39-year-old woman was admitted with abdominal pain and dyspnea, and a diagnosis of systemic lupus erythematosus with renal involvement was established. Laboratory tests revealed highly elevated anticardiolipin antibody, thrombocytopenia and false positive VDRL. Generalized thrombus formation and Libman-Sacks endocarditis were found at postmortem examination. The pancreas showed chronic inflammation with thrombi in pancreatic arteries, but no vasculitic change was observed. Lowering of pancreatic blood flow because of arterial thrombi was a possible cause of pancreatitis in this patient. The spectrum of antiphospholipid antibody associated diseases may be extended to include pancreatitis as a thrombotic complication.
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PMID:Pancreatitis related to antiphospholipid antibody syndrome in a patient with systemic lupus erythematosus. 151 70

A 38-year-old female was admitted to our hospital because she was suffered from severe dyspnea on effort. She had a history of nasal bleeding, endocarditis, fever, proteinuria, and alopecia at the age of 16, and was diagnosed as SLE. She was suffered from recurrent cerebral infarctions at the age of 35 and 38, and then mitral regurgitation was pointed out. Preoperative examination revealed non-active phase of SLE and UCG showed massive mitral regurgitation. Operative findings showed thrombosed verrucca circumferentially on the mitral valve. Mitral valve replacement (B-S #27) was done with using a felt strip in order to reinforce the mitral annular tissues. Histological findings of the verrucca showed Libman-Sacks endocarditis. Postoperative course was uneventful. Surgical treatment for Libman-Sacks endocarditis is extremely rare.
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PMID:[A case of mitral valve replacement for Libman-Sacks endocarditis]. 156 50

Two patients with systemic lupus erythematosus and unexplained dyspnea are described. Both had severe dyspnea and a restrictive lung function pattern without any apparent specific pathology. Both patients initially responded to corticosteroids and/or immunosuppression; one patient, however, relapsed and eventually died. Many factors may contribute to this syndrome, including diaphragmatic dysfunction, splinting of the diaphragm, pleuritis, atelectasis and respiratory muscle dysfunction. This syndrome, which may respond to steroids or immunosuppressive treatment, must be considered in SLE patients with dyspnea lacking a concrete underlying cause.
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PMID:Restrictive lung disease due to diaphragmatic dysfunction in systemic lupus erythematosus. Two case reports. 158 72

A previously healthy 16-year-old girl complaining of fever, hemosputum, chest pain and dyspnea was hospitalized. On admission, physical examination revealed mental confusion, holosystolic heart murmur, and swelling of the left foot. Laboratory investigations showed anemia, leukocytosis, thrombocytopenia, activation of inflammatory reactions, prolongation of PT and APTT, and hypoxia. Antinuclear antibody test was negative. There were no other findings suggestive of collagen diseases such as SLE. Chest X-ray showed consolidation in the left lower lung field and pleural effusion. Echocardiography disclosed a mass lesion in the left atrium in contact with the mitral valve, and mitral regurgitation. No findings indicative of an infectious etiology were present. The patient rapidly improved with high dose corticosteroid and anticoagulant therapy. A venogram of the lower extremity disclosed deep venous thrombosis. A lung ventilation-perfusion scan revealed multiple pulmonary thromboemboli. Elevation of anticardiolipin antibody was noted. Based on these findings, the diagnosis of primary antiphospholipid syndrome was made. Further administration of steroid and anticoagulant resulted in decrease of the titer of anticardiolipin antibody. This is the second report of primary antiphospholipid syndrome in Japan. The clinical significance of this disease is also discussed.
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PMID:[A case of primary antiphospholipid syndrome with fever, pulmonary thromboembolism and endocardial lesion]. 162 84


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