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)

Pneumothorax caused by the rupture of a mycetoma into the pleural space is rarely reported in patients undergoing intensive cytotoxic therapy for hematologic malignancies. We reviewed 46 episodes of mycetoma that developed in 43 patients undergoing antineoplastic therapy; six (13%) of these episodes were further complicated by the occurrence of pneumothorax that developed after bone marrow recovery with return to normal granulocyte count. Etiologic agents included Aspergillus fumigatus, Aspergillus fumigatus plus Blastoschizomyces capitatus, and Mucor (one case each). No pathogen was detected in the remaining three cases of pneumothorax. Four of the six patients died (7, 10, 27, and 50 days after the onset of pneumothorax). Two of the six patients with pneumothorax died of massive hemoptysis, whereas only one of the 40 patients who did not develop pneumothorax died of hemoptysis. This suggests that both pneumothorax and hemoptysis may represent the clinical expression of a more destructive course of invasive fungal diseases.
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PMID:Spontaneous pneumothorax complicating pulmonary mycetoma in patients with acute leukemia. 238 67

The influence of bone marrow recovery on the clinical and radiographic course of invasive pulmonary aspergillosis in patients with acute leukemia has not been well characterized. We studied 26 patients with acute leukemia and invasive pulmonary aspergillosis, comparing those who recovered from chemotherapy-induced granulocytopenia (Group 1, 15 patients) with those who did not (Group 2, 11 patients). Radiographic evidence of pulmonary cavitation was not seen in any Group 2 patient, but developed in 11 of 15 (73%) Group 1 patients (p less than 0.005). In these patients, cavitation always occurred after marrow recovery, an average of 2.0 days (range: 0 to 6 days) after the granulocyte count exceeded 500/mm3. Eight patients in Group 1 and 2 in Group 2 experienced a total of 38 episodes of hemoptysis. Four of the 26 patients, all in Group 1, developed massive hemoptysis (greater than 150 ml of blood per episode), leading to 1 death. In 3 of these 4 patients, cavitation preceded the episode of massive hemoptysis. At the time of massive bleeding, the granulocyte count was greater than 500/mm3, the platelet count greater than 38,000/mm3, and the other coagulation parameters were normal in all 4 patients. Our findings demonstrate that in patients with acute leukemia undergoing chemotherapy, bone marrow recovery markedly influences the clinical and radiographic course of invasive pulmonary aspergillosis. Development of a granulocyte count greater than 500/mm3 is associated with pulmonary cavitation, and on occasion with massive hemoptysis.
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PMID:Pulmonary cavitation and massive hemoptysis in invasive pulmonary aspergillosis. Influence of bone marrow recovery in patients with acute leukemia. 396 97

The air crescent sign is regarded as an important diagnostic finding in invasive pulmonary aspergillosis (IPA). This study examined the incidence, clinical importance, and natural history of air crescents in 25 patients with acute leukemia and IPA. Twelve (50%) of the patients had cavities (ten with an air crescent) that appeared an average of 15 days after the initial infiltrate. The diagnostic utility of the air crescent sign was relatively minor; cavities developed after the diagnosis was established in 50% of cases and after therapy was started in 75% of cases. In each case, the pneumonia improved at the time of cavitation. In six patients (50%), the cavities resolved over 2-8 months. Three patients (25%), however, experienced massive hemoptysis. Air crescent formation, previously shown to be dependent on granulocyte recovery, was associated with improved survival (67%) compared with the group without cavitation (8%). In the latter group, the pneumonia in ten (77%) of 13 patients progressed to diffuse disease. In patients with leukemia, the diagnostic value of the air crescent sign is limited by cavities that develop relatively late, as the infection improves after white blood cell recovery; cavities that do not occur in patients who remain neutropenic; and associated hemorrhage, at times life-threatening, that obscures the air crescent. The diagnosis of IPA should not await observation of air crescents in these patients.
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PMID:Invasive pulmonary aspergillosis and acute leukemia. Limitations in the diagnostic utility of the air crescent sign. 405 47

A 58-year-old woman with Goodpasture syndrome and active ulcerative colitis is described. On admission, the patient had exertional dyspnea, hemoptysis, severe hypertension, and peripheral edema. Her serum levels of urea nitrogen and creatinine were increased, and her hemoglobin concentration was reduced. The patient had a rapidly progressive glomerulonephritis with acute renal failure. She was treated with methylprednisolone, cyclophosphamide, and plasmapheresis but failed to regain renal function. Circulating anti-glomerular basement membrane (anti-GBM) antibody was positive; however, serum antinuclear antibody, proteinase-3-antineutrophil cytoplasm antibody and myeloperoxidase-antineutrophil cytoplasm antibody were negative. Nineteen months after initial presentation, she developed abdominal pain and severe diarrhea. These symptoms did not improve with conventional treatment. Colonoscopy performed after 3 months showed multiple ulcers in the colon. She was diagnosed with ulcerative colitis. She underwent granulocyte and monocyte adsorption apheresis once per week for 5 weeks. At 8 weeks, her symptoms had improved; her stool number was markedly decreased, and the bloody stools and abdominal pain disappeared. These results suggest that granulocyte and monocyte apheresis may be of benefit in the therapy of a patient with ulcerative colitis who previously had Goodpasture syndrome
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PMID:Granulocyte and monocyte adsorption apheresis in a patient with antiglomerular basement membrane glomerulonephritis and active ulcerative colitis. 1279 51

It is a disease of obscure cause that is characterized by the accumulation of a granular material that contains abundant lipid within the alveoli of lung. Pulmonary alveolar proteinosis (PAP) has been divided into a congenital and an adult form. The acquired form has been subdivided into a idiopathic form and a secondary form associated with a know disorder or exposure as silica, aluminium, titanium. Dyspnea and cough are the most common presenting symptoms. Chest pain, hemoptysis, fever and weight loss are variably reported. Pathogenesis remains unknown, but evidence points to a dysfunction of alveolar macrophages. Mice genetically deficient in granulocyte macrophagecolony stimulating factor (GM-CSF) show an alveolar proteinosis. A neutralizing antibody against GM-CSF was found in bronchoalveolar lavage fluid and serum of patients with idiopathic PAP. Currently, no specific therapy exists for pulmonary alveolar proteinosis, and sequential whole lung lavage is standard treatment.
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PMID:[Pulmonary alveolar proteinosis]. 1475 54