Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019079 (hemoptysis)
 6,129 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Report on an 18-year-old patient who developed a respiratory distress syndrome after trauma without bone fractures and with only minimal soft tissue contusion. Twelve hours after the accident fever and dyspnea appeared, accompanied later by hemoptysis, microhematuria, a fall in hemoglobin and in platelet count, petechiae on the skin and in the conjunctiva, cotton-wool lesions in the retina and micronodular shadows in the lungs. Various pathogenetic mechanisms other than bone marrow fat embolism are discussed in the light of this case.
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PMID:[Fat embolism syndrome without fractures]. 63 9

Evidence for severe intrapulmonary bleeding was obtained in 3 anticoagulated patients who presented with pulmonary infiltrates. The diagnosis of pulmonary hemorrhage was based on findings of markedly elevated quantities of stainable hemosiderin and hemoglobin in alveolar macrophages retrieved by bronchopulmonary lavage. In 2 of the patients, roentgenographic abnormalities regressed after anticoagulation was reversed. The third patient died and massive bilateral pulmonary hemorrhage was found at autopsy. The syndrome of occult pulmonary hemorrhage was characterized clinically by dyspnea, unexplained acute anemia, and infiltrates with an alveolar pattern on chest roentgenogram. Hemoptysis was conspicuously absent. Bronchopulmonary lavage and quantification of alveolar macrophage hemosiderin content may be useful in identifying intrapulmonary bleeding occurring in an otherwise occult manner. Recognition of pulmonary hemorrage in anticoagulated patients is important because reversal of anticoagulation can be life saving.
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PMID:Occult pulmonary hemorrhage in anticoagulated patients. 114 81

A 38-year-old man was hospitalized for proteinuria, and pitting edema. He had noticed Raynaud's phenomenon at about age fifteen. One month prior to admission, his urine contained protein and the serum creatinine was 3.0 mg/dl. On admission, sclerodactylia, digital pitting scar of fingertips, digital bone absorption and pulmonary fibrosis were observed and a diagnosis of progressive systemic sclerosis (PSS) was made. Laboratory investigations revealed: 24-hour urine protein excretion 3 g; serum creatinine 5.6 mg/dl; creatinine clearance 13.5 ml/min; antinuclear factor strongly positive in a speckled pattern; antibodies to nRNP positive with a titer of 1: 20, 480; antibodies to DNA, Sm, SS-A, SS-B, Scl-70, centromere and Jo-1 negative; serum complement normal. A renal biopsy revealed focal and segmental necrotizing glomerulonephritis with 70% crescents but no vascular changes. Circulating antiglomerular basement membrane antibodies were negative. Immunofluorescence disclosed granular deposits of IgM and C3 in the mesangium and along the capillary walls. Treatment was begun with methylprednisolone pulse therapy. After 5 month, serum creatine and creatinine clearance were 1.9 mg/dl and 35 ml/min, respectively. A year after the discharge, he was readmitted for hemoptysis and worsening of proteinuria and microhematuria. A chest radiograph demonstrated bilateral alveolar consolidation. Serum creatinine was elevated to 3.5 mg/dl. The continuous hemoptysis resulted in a severe dyspnea associated with a rapid fall in the hemoglobin. On the fourth hospital day, the PaO2 was 41 Torr on oxygen by mask that necessitated mechanical ventilation and pulse therapy was started. However, the patient died on the ninth hospital day of respiratory failure due to pulmonary hemorrhage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of progressive systemic sclerosis complicated by crescentic glomerulonephritis and diffuse pulmonary hemorrhage]. 147 23

A sixty-years-old man was admitted to the hospital because of acute myocardial infarction of anterior location. He had four episodes of ventricular fibrillation each requiring defibrillation and short-term cardiopulmonary resuscitation (less than 10 minutes). He was then managed with thrombolytic therapy, therapeutic doses of heparin and aspirin. He had persistent haemoptysis, chest X-ray revealing a diffuse bilateral alveolar infiltration. There was a continuous decrease in hemoglobin and hematocrit levels, with an evident clinical-radiographic dissociation. Right cardiac catheterisation showed a normal left ventricular function. The single breath carbon monoxide diffusing capacity (DLCOsb) was high, indicative of a diffuse intrapulmonary haemorrhage causing the alveolar infiltration.
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PMID:[A diffuse pulmonary hemorrhage following thrombolytic therapy in an acute myocardial infarct]. 163 92

A 64-year-old woman with a monoclonal gammopathy was admitted to Nagoya National Hospital with the complaint of occasional hemoptysis. On examination, there was no hepatosplenomegaly or no lymphadenopathy. The hemoglobin was 10.1 g/dl; platelets 22.5 X 10(4)/microliters; white blood cells 4.9 X 10(3)/microliters, with 4% of atypical lymphocytes. Immunoglobulin analysis of the serum by immunodiffusion revealed an IgG of 1,459 mg/dl, an IgA of 219 mg/dl, and an IgM of 5,091 mg/dl. Serum viscosity was 4.9. Serum immunoelectrophoresis demonstrated atypical precipitant arcs reacting with mu and kappa antisera. Urine immunoelectrophoresis showed a positive reaction against kappa antiserum. Radiologic studies of the bones revealed generalized osteoporosis with multiple punched out lesions of the skull. Thirty percent of bone marrow nucleated cells was atypical plasma cells, the presence of which was verified by electron microscopy. Although they were positive mainly for cytoplasmic mu and kappa chains by immunoperoxidase studies, cells positive for gamma, alpha, or lambda chains were occasionally found, indicating that normal immunoglobulin synthesis was not suppressed in this case of IgM myeloma.
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PMID:[IgM myeloma without depression in serum IgG and IgA--a case report]. 250 75

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

Four patients with cardiorespiratory failure caused by secondary kyphoscoliosis were studied. Polycythemia, cor pulmonale, restrictive lung pattern (functional residual capacity (FRC), 17 to 27% predicted; vital capacity (VC), 11 to 23% predicted), and abnormal arterial blood gases, primarily hypoventilation (PaO2, 31 to 44 mm Hg; PaCO2, 52 to 73 mm Hg), were seen in all. Supplementary oxygen, digoxin, diuretics, 15 min of intermittent positive-pressure breathing with inspired pressure (PI) 25 cm H2O 4 times daily, and tracheostomy failed to produce improvement. However, 12 h of nighttime ventilation (NTV) with PI 28 to 35 cm H2O through a permanent tracheostomy proved effective. Within 72 h, dyspnea at rest, restless sleep, and frequent waking resolved. Within 8 to 22 days, the PaO2 was approximately 58 mmHg and the PaCO2 was approximately 41 mm Hg while breathing 21% oxygen spontaneously during the day. The right heart failure resolved within 2 to 7 wk, and the hemoglobin count decreased to approximately 165 g/L within 2 to 6 months. There was a mean increase of 700 ml (72%) in functional residual capacity and 430 ml (49%) in vital capacity. The patients were discharged 2 days to 5 wk after NTV commenced. Daytime activity increased, approaching a normal life style. The improvement was sustained over a mean follow-up period of 3.4 yr. Problems included recurrent episodes of tracheobronchitis, mild self-limiting hemoptysis, and speech modification. Nighttime ventilation may be an effective alternative for long-term treatment of cardiorespiratory failure caused by secondary kyphoscoliosis.
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PMID:Nighttime ventilation improves respiratory failure in secondary kyphoscoliosis. 669 24

We report a case of 63-year-old man who developed massive pulmonary hemorrhage following intravenous streptokinase for acute myocardial infarction. Pulmonary hemorrhage was diagnosed by the triad of hemoptysis, a drop in hematocrit, and a new unilateral infiltrate on chest radiograph. This diagnosis was confirmed by autopsy findings. Pulmonary hemorrhage has rarely been reported following thrombolytic therapy. We believe that pulmonary hemorrhage is a rare but a potentially life-threatening complication of thrombolytic therapy and should be considered in the differential diagnosis of pulmonary infiltrates or falling hemoglobin after thrombolytic therapy for acute myocardial infarction with no obvious site of bleeding.
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PMID:Spontaneous pulmonary hemorrhage after thrombolytic therapy for acute myocardial infarction. 795 38

Pulmonary hemosiderosis (PH) has been described in association with a variety of immunological and non-immunological diseases. It is characterised by iron-deficiency anaemia, hemoptysis and diffuse pulmonary infiltrates based on recurrent intraalveolar hemorrhages. We present the case of a child with pulmonary hemosiderosis and a pathological gastroesophageal reflux activity. The child suffered from recurrent anaemic episodes the age of three months (hemoglobin level up to 5.4 g/dl). The symptoms decreased after removal of the gastroesophageal reflux and accompanying steroid therapy. There has been one relapse of pulmonary hemorrhage seven months later (hemoglobin level 6.1 g/dl). Since then the patient has been in good general condition and the steroid was slowly reduced. No more anaemic episodes occurred. We discuss a possible association of pathological gastroesophageal reflux activity in pulmonary hemosiderosis.
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PMID:[Pulmonary hemosiderosis and gastroesophageal reflux in an infant]. 973 94

A 17-year-old man was admitted to our hospital because of exertional dyspnea, fever, and hemoptysis. Chest X-ray films disclosed diffuse alveolar infiltrates and patchy shadows in both lungs. Laboratory data included a hemoglobin level of 6.7 g/dl and white blood cell count of 8,100/microliter. Urinalysis revealed microscopic hematuria with RBC cast. Bronchoalveolar lavage fluid from the right middle lobe bronchus was bloody. Anti-GBM antibodies were detected at low levels in serum (10 EU/ml) by ELISA procedures. Renal and lung biopsies were performed. Immunofluorescent studies revealed linear deposits of IgG along glomerular basement membrane of the kidney, but not in alveolar walls of the lung. This case fulfilled the criteria for Goodpasture's syndrome. The patient was treated with methylprednisolone (1,000 mg/day, for 3 days) and plasma exchange (for 2 days), and demonstrated a dramatic improvement in his clinical condition and chest X-ray findings. We were unable to identify autoantibodies to the NC domain of the alpha 3 chain of type IV collagen. Another conformational epitope may play a role in the disease.
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PMID:[Goodpasture's syndrome initially presenting with alveolar hemorrhage]. 1049 7


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