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Query: UMLS:C0019079 (hemoptysis)
 6,129 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The clinicopathological features of four patients with systemic lupus erythematosus and pulmonary hemorrhage are described. Our study confirms that pulmonary hemorrhage may be a dominant clinical expression of lung involvement in this disease. Its clinical manifestations are usually quite characteristic. However, hemoptysis may be absent. Radiographically, bilateral alveolar infiltrates resembling pulmonary edema or infection may be seen. Pulmonary hemorrhage was a major contributing factor to the death of three of our patients. The possible pathogenetic mechanisms responsible for pulmonary hemorrhage in our patients and other patients previously recorded in the literature are reviewed. Evidence supporting an immune complex pathogenesis is presented. Our immunopathological and ultrastructural studies demonstrate deposition of immune aggregates in the lungs in the alveolar septa, large blood vessels, and bronchioles in a manner similar to that which has been observed in the experimental serum sickness model of immune complex mediated pulmonary injury. The histological abnormalities, although nonspecific, are consistent with this interpretation, and collectively show diffuse alveolar lining cell and endothelial cell injury. However, an immune complex pathogenesis may not completely explain the occurrence of pulmonary hemorrhage in SLE. Other factors, including bleeding disorders, pulmonary infection, oxygen toxicity, and the "shock lung" syndrome, may also have contributed to lung hemorrhage in some of these patients.
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PMID:Pulmonary hemorrhage in systemic lupus erythematosus. 36 23

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

We studied 18 patients, 9 women and 9 men, ranging in age from 18 to 76 years. The main symptom was hemoptysis and the underlying pathology was tuberculosis, actinomycosis, lung cancer, metastatic carcinoma and systemic lupus. Nonsurgical patients, with recurrent hemoptysis or massive bleeding were selected. The embolization substances were spongostan, avitene (R) and PVA; they all produce temporary as well as persistent hemostasis. The procedure was successful in 16 patients. In two patients the embolization was not performed, one for technical reasons and the other because the vessel to be treated was the source of an anterior spinal artery. It is considered that the endovascular treatment constitutes an alternative for hemoptysis, even during the acute period, mainly in the management of nonsurgical patients.
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PMID:[The endovascular treatment of hemoptysis]. 134 Sep 2

Five patients with pulmonary hemorrhage associated with SLE were studied. Chest radiographs showed extensive alveolar opacity immediately after hemoptysis or dyspnea in four patients. In one patient an interstitial pattern seen initially progressed rapidly to an alveolar pattern. Three patients were successfully treated with corticosteroids and are doing well at present. The diagnosis and treatment of pulmonary hemorrhage is vital to patients with SLE. In the appropriate clinical setting chest radiographic findings of acute alveolar disease should suggest pulmonary hemorrhage, and empiric treatment with corticosteroids should be considered.
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PMID:Pulmonary hemorrhage in patients with systemic lupus erythematosus. 185 2

Diffuse lung hemorrhage (DLH) is a rare complication of systemic lupus erythematosus (SLE). We observed lung abnormalities in 72 cases (39.5%) out of 182 SLE patients. DLH was confirmed in 3 male patients with steroids and cyclophosphamide was favorable in all cases but there was a recurrence in one case. None of the patients died due to this condition, although artificial live maintaining measures were necessary in one patient. DLH is more difficult to suspect of in the absence of hemoptysis and when there is not a previous diagnosis of SLE. However, the decrease in hematocrit and serum complement levels in a patient with bilateral lung infiltrate can be orientative. DLH must be included in the differential diagnosis of bilateral alveolar infiltrates in SLE inspite its low frequency, since it is a condition with e high mortality rate but with possible cure if it is promptly diagnosed.
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PMID:[Diffuse pulmonary hemorrhage in systemic lupus erythematosus]. 194 84

Hemoptysis in systemic lupus erythematosus (SLE) may occur in up to 17% of cases. The vast majority of the cases are secondary to bacterial, tuberculosis or opportunistic infections. Also uremia, pulmonary embolism and lung hemorrhage must be considered. The majority of the above referred entities are usually alarming events in any patient with SLE. In contrast, we describe a patient with inactive SLE, who developed hemoptysis secondary to Paragonimus sp., which was treated "easily" with praziquantel. Fluke infection must be considered in the differential diagnosis of hemoptysis in SLE.
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PMID:Paragonimiasis: an infrequent but treatable cause of hemoptysis in systemic lupus erythematosus. 231 24

We describe 12 patients with systemic lupus erythematosus (SLE) who developed massive pulmonary hemorrhage with very active disease. Other causes of pulmonary bleeding were excluded. Eleven of the 12 patients died, but only 4 had hemoptysis. Massive pulmonary hemorrhage should be suspected, even in the absence of hemoptysis, in severely ill patients with lupus who develop acute respiratory distress with bilateral pulmonary infiltrates and a drop in hemoglobin of 3 or more g/dl. Because of the deadly nature of this complication of SLE, when it is suspected, intensive corticosteroid and immunosuppressive treatment should be instituted.
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PMID:Fatal pulmonary hemorrhage in systemic lupus erythematosus. Occurrence without hemoptysis. 404 53

We have reviewed the alveolar hemorrhage (AH) syndromes, defined as immune or idiopathic disorders associated with diffuse microvascular hemorrhage into the acinar portion of the lung. The disorders that are most often associated with AH include antibasement membrane antibodies (ABMA) disease, idiopathic pulmonary hemosiderosis, systemic lupus erythematosus, systemic vasculitides, and idiopathic rapidly progressive glomerulonephritis. An approach to the recognition, diagnosis, and treatment of the AH syndromes has been outlined and several illustrative case studies have been presented. Recognition of AH is not usually difficult, but does require a high index of suspicion, since many disease processes may give rise to hemoptysis with infiltrates on chest roentgenogram. Recognition of AH is aided by careful clinical and laboratory assessment for evidence of extrapulmonary disease; simple hematologic studies such as sequential hemoglobins and iron studies; and measurement of carbon monoxide uptake by the lungs. Early recognition of AH may decrease the likelihood of respiratory failure and end-stage renal disease. The specific etiology of AH is usually determined by clinical examination, serologic assay for ABMA, and percutaneous renal biopsy by immunofluorescence. Open-lung biopsy is required in a minority of cases. High-dose pulse methylprednisolone appears to effectively control AH of diverse etiology. Combined plasma exchange and immunosuppression controls AH in ABMA disease and is the treatment of choice in this disorder. Cyclophosphamide is used for Wegener's granulomatosis, and sometimes in systemic necrotizing vasculitis, in an attempt to prevent irreversible damage to the kidneys.
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PMID:Alveolar hemorrhage syndromes: diffuse microvascular lung hemorrhage in immune and idiopathic disorders. 639 80

Large-volume plasma exchange can now be rapidly and safely done using cell separator technology. Significant depletion of immunoglobulins and immune complexes can be achieved by repeated intensive plasmapheresis, but sustained depletion of these constituents requires concomitant immunosuppressive therapy. Plasmapheresis appears to work in some disorders by removing pathogenic antibodies, but other mechanisms of action have been postulated. It is the treatment of choice for thrombotic thrombocytopenic purpura and for the hyperviscosity syndrome due to macroglobulinemia. Apheresis can be useful in the treatment of many other disorders, most notably myasthenia gravis, glomerulonephritis associated with hemoptysis (Goodpasture's syndrome), refractory systemic lupus erythematosus, cryoglobulinemia and immune cytopenic disorders.
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PMID:Plasmapheresis in clinical medicine. 660 32


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