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

The authors report a case of a 19-year-old woman admitted for the investigation of fever and hemolytic anemia for the previous 2 months. As an inpatient, she had convulsions and sudden loss of consciousness, developing hemoptysis, hypoxia, and respiratory insufficiency. Examination showed pericardial effusions on the echocardiogram and bilateral alveolar condensations on the thoracic radiograph. A hypothetical diagnosis of systemic lupus erythematosus was made, and measurement of the antinuclear factor was requested along with daily pulse therapy methylprednisolone, in spite of which the outcome was fatal. Afterwards, the result of the antinuclear factor test was positive, with a titer of 1:5120, showing a fine punctiform pattern, fulfilling the criteria for systemic lupus erythematosus according to the American College of Rheumatology. Secondary pulmonary hemorrhage in this connective tissue disease is an uncommon but serious complication that involves a high level of mortality in spite of intensive treatment, as is also reported in the literature.
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PMID:Pulmonary hemorrhage as a manifestation of systemic lupus erythematosus. 1502 85

Pulmonary hemorrhage and hemoptysis are uncommon in childhood, and the frequency with which they are encountered by the pediatric pulmonologist depends largely on the special interests of the center to which the child is referred. In those centers caring for children with cystic fibrosis or congenital heart disease, these will be by far the most common causes of hemoptysis. Other causes of hemoptysis are far less common, such as bleeding from localized lesions in the upper airway or tracheobronchial tree. Even less common is bleeding into the lungs as part of a systemic disease, usually with renal involvement (pulmonary-renal syndromes), such as systemic lupus erythematosis or Goodpasture's syndrome. Bleeding into the lungs in children with a bleeding diathesis probably only occurs in immunosuppressed children after transplantation. When no other cause is found for pulmonary hemorrhage, the presumed diagnosis is idiopathic pulmonary hemosiderosis. This review discusses the various causes of hemoptysis and pulmonary hemorrhage, and the appropriate investigations to aid in determining the correct diagnosis. The management and prognosis of idiopathic pulmonary hemosiderosis, based on cumulative experience from published reports, are considered in more detail.
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PMID:Pulmonary hemorrhage/hemoptysis in children. 1511 47

The presence of anti-phospholipid antibodies (anticardiolipin antibodies and lupus anticoagulant) associated to venous and/or arterial thrombotic phenomena and fetal losses define the anti-phospholipid syndrome. On rare occasions severe hypoprothrombinemia associated with this disease as a cause of hemorrhagic manifestations has been described. In addition very few cases of alveolar hemorrhage in anti-phospolipid syndrome (APS) have been described, being this complication usually related to microthrombosis and/or capillaritis of pulmonary vessels. We describe two patients without previous clinical manifestations of anti-phospholipid syndrome that showed pulmonary hemorrhage with anticardiolipin antibodies positivity. The first of them, a 33-year-old male, began his disease with low prothrombin time and the presence of antiprothrombin antibodies. In the biopsy by thoracoscopy the presence of pulmonary hemorrhage without capillaritis nor thrombotic phenomena was demonstrated, becoming evident certain clinical improvement and normalization of the prothrombin time after receiving immunosuppressive treatment but with persistence of the pulmonary hemorrhage 5 years later. The second case, a 89-year-old male, began his condition with bilateral lung infiltrates and hemoptysis, anticardiolipin antibodies positivity, and thrombopenia, with recurrence of the condition 1 year later. After other etiological possibilities were ruled out, and despite hemorrhagic trait in both patients, we consider that they should be in the clinical context of the anti-phospholipid syndrome, although at this time they did not meet the criteria recognized in order to diagnose this disease. Within the ampliable clinical spectrum of the anti-phospholipid syndrome we should take into account the pulmonary hemorrhage.
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PMID:[Pulmonary hemorrhage and anti-phospholipid syndrome]. 1676

Rhodococcus equi, is a grampositive intracellular bacillus, that causes infection mainly in immunocompromised hosts. We report the case of a 52 years old woman, with a systemic lupus erythematosus and a progressive 10 months evolution with cough, dyspnea, mucous-purulent sputum, occasionally hemoptysis, intermittent fever, and weight loss of 10%. With partial response to antibiotic treatment, radiological evolution of thoracic scanners evidenced the development of multiple bilateral areas of consolidation, some of them nodular. Percutaneous thoracic biopsy showed characteristic histology and microbiological analysis yielded the identification of Rhodococcus equi in both bronchoalveolar lavage and pulmonary biopsy. She received prolonged bi-associated antibiotic treatment with good clinical and radiological response. This agent must be considered in the study of immunocompromised patients that present with a prolonged evolution of pneumonia.
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PMID:[Necrotizing pneumonia due to Rhodococcus equi in non HIV immunocompromised host. Case report and review]. 1589 96

A 36-year-old woman was admitted for recurring chest pain and hemoptysis. Blood pressure in the right and left arms was equal, and no murmurs or bruits were heard. Body temperature was normal on admission and remained within the normal range during the hospital stay. C-reactive protein was slightly elevated (2.3 mg/dL) and lupus anticoagulant was positive. Angiography showed no abnormality of the aorta or its branches, but the left pulmonary artery showed occlusion at the proximal portion. Computed tomography (CT) revealed segmental wall thickening of the thoracic aorta. Fluorine-18-fluorodeoxyglucose positron emission tomography (18FDG PET) showed high uptake in the proximal portion of the left pulmonary artery and in the thoracic aorta with wall thickening on CT. Based on these findings, a diagnosis of Takayasu's arteritis associated with antiphospholipid syndrome was made and high-dose steroid therapy (prednisolone 30 mg/day) was started. Two months later, the C-reactive protein level had decreased from 2.3 mg/dL to 1.1 mg/dL, and both the focal wall thickening and (18)FDG uptake of the thoracic aorta were decreased. 18FDG PET was useful for evaluating the efficacy of the steroid therapy in addition to making a diagnosis of Takayasu's arteritis associated with antiphospholipid syndrome.
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PMID:Usefulness of fluorine-18-fluorodeoxyglucose positron emission tomography in a patient with Takayasu's arteritis associated with antiphospholipid syndrome. 1660 57

Defined as an expectoration of blood from the subglottic airways, the hemoptysis is a symptom that suggests a variety of pathologies that can be more or less benign and even fatal, a life threatening for the person who suffers it. Between the most common causes we have bronchitis, bronchiectasis and bronchopulmonary neoplasia. Less frequent causes are: Goodpasture's syndrome, Wegener's granulomatosis, systemic lupus erythematosus, between others. The authors present a case of hemoptysis in a patient who suffered sudden aggravation of his general state with the need for intensive care.
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PMID:[Hemoptysis: an uncommun case]. 1828 44

Antiphospholipid syndrome is an autoimmune disease characterized pathophysiologically by the presence of antiphospholipid antibodies and > or =1 clinical manifestation, the most common being venous or arterial thrombosis. We describe the case of a 40-year-old male with unexplained severe pulmonary arterial hypertension with a seven-day history of progressive shortness of breath, hemoptysis, chest discomfort and bilateral pedal edema. Electrocardiographic, echocardiographic and imaging studies showed changes consistent with chronic thromboembolic pulmonary hypertension. Further work-up showed positive anticardiolipin antibodies and lupus anticoagulant with negative features for lupus with negative primary thrombophilic studies as well. The patient was managed adequately with oral anticoagulation with improvement of his clinical status and referred to a tertiary care center to be screened for pulmonary thromboendarterectomy. For patients meeting surgical selection criteria, pulmonary thromboendarterectomy has demonstrated positive outcomes with respect to survival, functionality and quality of life. We discuss the pathophysiology and treatment as well as novel therapies in nonsurgical candidates with chronic thromboembolic pulmonary hypertension in the setting of primary antiphospholipid syndrome.
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PMID:Chronic thromboembolic pulmonary hypertension as an uncommon presentation of primary antiphospholipid syndrome. 1859 78

Alveolar hemorrhage (AH) is a rare, dramatic, and life-threatening manifestation of systemic lupus erythematosus (SLE), which may occur early or late in disease evolution. Presentation is highly variable, and hemoptysis may be absent. The most reliable clinical signs include a drop in hemoglobin accompanied by new pulmonary infiltrates. Extrapulmonary disease, especially nephritis, is common; however, milder SLE symptoms may be minimal and "masked" in patients receiving immunosuppression for other symptoms of SLE. Predictors of patients at risk for this complication are unclear at this time. An aggressive diagnostic approach to exclude infection is indicated. Use of broad-spectrum antibiotics, coincident with immunosuppressive treatment of the AH, while awaiting initial culture results, is prudent. Treatment regimens lack standardization because of the absence of controlled clinical trials and the rarity of this complication. Timely intensification of immunosuppression is required and effective. The capacity of AH to occur and recur, despite ongoing immunosuppressive therapy, is noted, but long-term AH-free episodes among survivors are attainable.
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PMID:Systemic lupus erythematosus-associated alveolar hemorrhage: presentation, treatment, and outcome. 1907 98

We report a case of hydralazine-induced alveolar hemorrhage and anti-neutrophil cytoplasmic antibody (ANCA)-positive pauci-immune glomerulonephritis, with serum anti-histone antibodies present, features not previously described in the literature with this drug. A 50-year-old Caucasian female had hypertension treated with hydralazine 75mg TID for three years, and a lung nodule followed up periodically with chest-computed tomographies. She was admitted to the hospital for hemoptysis and newly discovered diffuse pulmonary ground-glass opacities. Transbronchial lung biopsy showed alveolar hemorrhage. Serum creatinine was 3.5 mg/dL and urinalysis showed 2+blood, 30-50RBC/hpf and red blood cell casts. ANCA against myeloperoxidase were present. Anti-double-stranded DNA, ANA, and anti-histone antibodies were positive. Serum complements were normal. Renal biopsy revealed focal crescentic necrotizing glomerulonephritis with negative immunofluorescence, consistent with pauci-immune ANCA-positive vasculitis. Serum creatinine returned to baseline three days after hydralazine was discontinued, and the hemoptysis resolved after treatment with cyclophosphamide and prednisone was started. We concluded that this case represents a hydralazine-induced small vessel vasculitis rather than an idiopathic one. The possibility of hydralazine-induced vasculitis should be considered when patients treated with hydralazine develop a pulmonary-renal syndrome. Anti-histone antibodies may be present in the absence of full classification criteria of drug-induced lupus.
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PMID:Hydralazine-induced ANCA-positive pauci-immune glomerulonephritis: a case report and literature review. 1981 44

Pneumothorax is a rare pleuropulmonary manifestation of systemic lupus erythematosus. We encountered a 37-year-old Japanese woman who had systemic lupus erythematosus complicated by recurrent pneumothorax during treatment for recurrent serositis with glucocorticoid therapy. She was admitted for the third episode of lupus peritonitis in December 2005. Intravenous cyclophoshamide and increased dose of oral prednisolone were administered. In early January 2006, hemoptysis was observed and bronchofiberscopy revealed hemorrhage from the left lower lobe. After intravenous methylprednisolone pulse therapy and oral cyclosporine therapy were added, pleurisy and pulmonary hemorrhage improved. On February 22nd, she suddenly developed pneumothorax on the right side, followed by pneumothorax on the left side after 2 days. This pneumothorax on the left side did not improve despite chest tube drainage for over one month. She underwent thoracoscopic partial lobectomy of lower lobe of the left lung, and her symptoms improved. Review of the literature identified 10 case reports of systemic lupus erythematosus complicated by pneumothorax. All of the patients including our case had underlying pulmonary lesions, and 9/11 patients had pleurisy. Besides 10/11 patients received glucocorticoid therapy before the occurrence of pneumothorax. Tissue fragility caused by these factors might contribute to the complication of pneumothorax in patients with systemic lupus erythematosus.
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PMID:Systemic lupus erythematosus complicated by recurrent pneumothorax: Case report and literature review. 2060 38


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