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)

Lung tissue obtained from eight consecutive patients with systemic lupus erythematosus complicated by severe, acute pulmonary disease was studied by both light and immunofluorescence microscopy. Light microscopic examination disclosed interstitial pneumonia in four cases, cytomegalovirus pneumonitis in one case, bronchiolitis and peribronchiolitis in one case, pulmonary infarction in one case and focal atelectasis in the remaining case. Direct immunofluorescence examination revealed focally bound immunoglobulins or complement (C3) within pleural and/or pneumocyte nuclei in each specimen. Immunohistologic studies in these cases may thus suggest a diagnosis of systemic lupus erythematosus with acute pulmonary complications, despite the lack of specificity of the pathologic changes seen by light microscopy.
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PMID:Acute pulmonary complications in systemic lupus erythematosus. Immunofluorescence and light microscopic study. 33 72

Twenty-seven patients with perplexing pleural effusion were studied to determine clinical outcome. The value of performing pleuroscopic examination or open pleural biopsy (or both) in search of a diagnosis was assessed. After a mean follow-up period of six months, a diagnosis was reached in 16 patients, while 11 patients had no diagnosis after a mean follow-up period of 24 months. The causes for the effusions were neoplasm (eight patients), tuberculosis (one patient), blastomycosis (one patient), systemic lupus erythematosus (one patient), pulmonary infarction (two patients), and fractures of the ribs (three patients). The diagnosis was made by pleuroscopic examination or open biopsy in five patients, by autopsy in four, and by long-term follow-up studies in seven patients. When neoplasm or granulomatous disease was not suspected before surgery, pleuroscopic examination or open biopsy or both were nondiagnostic. These data support a policy of selecting patients for these procedures when a presumptive diagnosis of neoplasm or granulomatous disease is made but cannot be confirmed by less invasive methods. When the clinical data are too nonspecific to formulate a meaningful clinical impression, a more conservative approach is recommended.
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PMID:Perplexing pleural effusion. 69 49

We experienced a case of idiopathic hypereosinophilic syndrome (HES) associated with pulmonary infarction. The case was a 22-year-old woman with marked eosinophilia (16835/microliters) and peripheral edema and cyanosis. During hospitalization, she suddenly developed lower right chest pain, and infiltrative lesions with pleural effusions in the right lung were prominent. A diagnosis of pulmonary infarction was made after perfusion scan and angiography of the lung. Lupus anticoagulant was found to be positive and a transient increase of anti-cardiolipin antibody slightly in her serum was also observed. Recurrent thrombosis is known to be complicated by HES but its mechanism remains to be clarified. There has also been no study reported in the literature on the role of lupus anticoagulant in this process; its possible role in this patient is discussed.
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PMID:[A case of idiopathic hypereosinophilic syndrome (HES) complicated by pulmonary infarction]. 195 37

A 22-year-old man was admitted because of hemosputum and progressive dyspnea with 3 attacks of chest pain and dyspnea over the previous 4 months. Chest roentgenography showed pulmonary infarction of the left lower lobe, and the diagnosis was confirmed by pulmonary perfusion and inhalation scintigraphy and pulmonary arteriography. Thrombolytic therapy was performed, but no significant effect could be obtained and anticoagulant therapy was performed continuously. No deep-vein thrombosis could be seen. He was considered to have autoimmune hemolytic anemia with lupus anticoagulant on the basis of auto-antibody data. Lupus anticoagulant is an antibody to phospholipid, and it is suggested that a decrease in the production of prostanoid in the endothelium causes thrombosis. In this case, as the patient showed a low level of 6-keto-PGF1 alpha in the blood, it is suggested that one of the etiological factors of pulmonary thromboembolism is a disorder of prostacyclin production in the endothelium, causing thrombosis by lupus anticoagulant.
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PMID:[A case of pulmonary thromboembolism due to circulating lupus anticoagulant]. 212 Apr 98

A patient with systemic lupus erythematosus developed pulmonary haemorrhage and pulmonary infarction as rare initial manifestations of her disease. The latter was associated with the presence of the circulating lupus anticoagulant. She recovered with pulse doses of methylprednisolone and plasmapheresis. Anticoagulants were not administered.
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PMID:Pulmonary haemorrhage, pulmonary infarction, and the lupus anticoagulant. 314 19

This case involves a 41-year-old woman with SLE. The patient began having symptoms of arthralgia in 1978 and developed fever, pleuritis and lupus psychosis in 1986. Laboratory exams showed positive antinuclear-antibody, LE-cell phenomenon, hypocomplementemia and lupus anticoagulant. Echo cardiography demonstrated mitral regurgitation and stenosis. She was treated with 50 mg of prednisolone and these manifestations subsided. In 1989, she developed dyspnea on exertion and echo cardiography revealed severe mitral stenosis. Pulmonary infarction was detected by MAA lung scintigraphy. At this time, she was diagnosed as SLE associated with antiphospholipid syndrome (APS). A mitral valvular replacement operation was performed in 1991. Pathological studies of mitral valve demonstrated Libman Sacks endocarditis. APS is known occasionally to complicate with left-sided valvular diseases, mitral stenosis is quite rare in both SLE and APS. This patient reveals a rare case of SLE associated with APS and mitral stenosis. It is suggested that this patient developed mitral stenosis with Libman Sacks endocarditis, associated with the presence of antibody against phospholipids.
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PMID:[A case of SLE associated with antiphospholipid syndrome and mitral stenosis]. 755 44

The objective of this study was to determine the incidence of pulmonary involvement in patients with systemic lupus erythematosus (SLE) and to clarify the clinical and laboratory characteristics in SLE patients with various pulmonary involvements. A retrospective study (n = 137) revealed that the types of pulmonary involvement found in SLE patients were: pleuritis (9%), interstitial pneumonia (8%), pulmonary infarction (7%), pulmonary infection (4%), pulmonary hypertension (2%), restrictive dysfunction (28%) and decreased diffusion capacity (43%). The incidences of pericarditis (P < 0.01), arthralgia (P < 0.05) and hypoalbuminemia (P < 0.05) were significantly greater in patients with pleuritis than in those without, while in patients with interstitial pneumonia, the incidence of anti-SS-A antibody (P < 0.05) and sicca syndrome (P < 0.05) were significantly greater than in those without. A longitudinal follow-up study of patient groups with various pulmonary involvements revealed: 1. significant changes of erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), lactate dehydrogenase (LDH) and thrombomodulin (TM) in patients with pleuritis, and 2. significant changes of WBC and LDH in patients with interstitial pneumonia. The increased ESR, CRP and TM levels during disease episodes suggest that the involvement of inflammatory processes is related to vasculitic events in the pathogenesis of lupus pleuritis. A higher incidence of anti-SS-A antibody in lupus patients with interstitial pneumonia suggests a potential role for this autoantibody in the pathogenesis of this complication.
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PMID:Clinical and laboratory features of lupus patients with complicating pulmonary disease. 1046 59

We reported an autopsy case of cerebral infarction with primary lung cancer. The patient was a 50-year-old man. Despite having been treated with warfarin potassium and ticlopidine hydrochloride, he relapsed cerebral infarction. His laboratory data on admission showed that lupus anticoagulant was positive, together with a high value of beta-thromboglobulin, thrombin-antithrombin III complex, markers of platelet and coagulation activation, CEA and CA 19-9. The autopsy finding revealed a primary papillary adenocarcinoma in the right lower lung, multiple cerebral infarction, renal infarction, pulmonary infarction and splenic infarction. The atherosclerotic changes were mild in the whole tissues and findings of vasculitis were not observed. Recurrence of cerebral infarction was effectively suppressed with the addition of steroid therapy to antithrombotic therapy. This case was considered as catastrophic antiphospholipid syndrome. It is necessary to differentiate antiphospholipid syndrome in case of the abnormal coagulation and fibrinolytic factors with recurrent cerebral infarction. Moreover, systemic examinations are important, because malignant tumor may exist on the background of the case.
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PMID:[An autopsy case of catastrophic antiphospholipid syndrome presenting with recurrent multiple cerebral infarction associated with lung cancer]. 1068 94

Pulmonary hypertension (PH) sometimes occurs in patients with systemic lupus erythematosus (SLE). We report a case of 51-year-old-woman with PH associated with SLE. She had been diagnosed as SLE on the basis of pericardial effusion, hematological disorder, positive antinuclear antibody, and hypocomplementemia. Despite minimal lupus activity, she had marked elevation of pulmonary arterial pressure (101/53 mmHg) and decreased cardiac index (1.5 l/min/m2). Symptoms related to PH were progressive under treatment with oral corticosteroids, oxygen, calcium antagonists, and warfarin. After 17 months of epoprostenol treatment, she died of pulmonary infarction. SLE-associated PH is often severe and progressive even in association with minimal activity.
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PMID:Severe pulmonary hypertension in a patient with systemic lupus erythematosus and minimal lupus activity. 1186 96

We have experienced a case of chronic active Epstein-Barr virus infection (CAEBV) complicated in systemic lupus erythematosus (SLE) and antiphospholipid antibody syndrome (APS). A 35-year-old woman was admitted to our hospital with complaints of fever and dyspnea on exertion. She was diagnosed as having SLE on the basis of arthritis, oropharyngeal ulcer, lymphopenia, and positive autoantibodies against DNA, RNP and SSA. The diagnosis of APS was also made because of positive anti-cardiolipin IgG antibodies and the existence of multiple pulmonary infarction with pulmonary hypertension. The administration of 30 mg/day of prednisolone and anti-coagulation significantly improved clinical symptoms. However, she was again admitted to the hospital four months later because of progressive liver damage and pancytopenia. Increment of prednisolone did not improve the clinical situation and she expired because of pulmonary hemorrhage. At autopsy, there were a significant increase of histiocytes with hemophagocytosis and a dense infiltration of atypical lymphocytes in the liver, spleen, lymph nodes and bone marrow. Infiltrated lymphocytes were positive for CD 3 and EBER 1 in immunohistochemical staining and EBVmRNA was detected by in situ hybridization. Final pathological diagnosis was CAEBV with hemophagocytic syndrome in association with lupus nephritis, pulmonary hemorrhage and pulmonary infarction.
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PMID:[An autopsied case of chronic active Epstein-Barr virus infection complicated in systemic lupus erythematosus and antiphospholipid antibody syndrome]. 1259 14


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