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)

Infection, hemorrhage and adult respiratory distress syndrome (ARDS) are pulmonary complications occurring after remission induction therapy for acute leukemia. The aim of this study was to analyze the incidence of these causes by serial roentgenogram, clinical, microbiological and laboratory tests in 21 patients (pts) with relapsed acute leukemia (18 X myeloid, 3 X lymphoblastic), an AML-pt (acute myeloid leukemia) suffering from secondary leukemia, and three pts with primary refractory leukemia following treatment with intermediate (IM) and high-dose cytosine arabinoside (HD-Ara C), in combination with amsacrine (AMSA)(n = 19), etoposide (VP 16) (n = 5) or Mitoxantrone (n = 1). Eleven out of 25 pts developed pulmonary complications, one of them with massive hemoptysis and roentgenographic signs of pulmonary bleeding, one suffering from protracted shock after a tumor lysis syndrome, two pts showing symptoms of a cardiogenic pulmonary edema complicating severe Candida pneumonia in one case and legionnaires' disease in the other. Seven of the eleven pts had a non-cardiogenic pulmonary edema with respiratory failure 1-14 days after cessation of induction or consolidation therapy. In six of the seven, there were no signs of cardiogenic, infectious or metabolic reasons, including fluid overload, for the pulmonary edema, one had as a contributing factor a Candida infection of the lung. Three of the seven patients recovered, four died (two following IM and two after HD-Ara C). Other adverse side effects, clearly attributable to HD-Ara C, included delirious state (n = 3), generalized erythema (n = 3), acute pancreatitis (n = 2), acute abdomen (n = 1) and conjunctivitis in almost all patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Non-cardiogenic pulmonary edema complicating intermediate and high-dose Ara C treatment for relapsed acute leukemia. 336 72

Although hematologic dysplasia is common in HIV disease, evolution to AML is unusual. We report a case of AML in a patient with stage-C3 AIDS who had been previously treated with granulocyte colony-stimulating factor (G-CSF). This 41-year-old black man presented with pancytopenia (Hg 8.6 g/dl, Hct 24.3%, platelets 16,000/mm3, WBC 0.6 x 10(3)/mm3) and hemoptysis. His peripheral smear manifested 19% blasts. His bone marrow biopsy was hypocellular (20%) with greater than 90% blasts, which were positive for myeloperoxidase and Sudan black B. The blasts were negative for nonspecific esterase. Immunophenotypic analysis by flow cytometry showed the majority of cells to be of myeloid lineage, expressing CD13, and CD45 at low intensity. In addition, there was aberrant expression of CD2 and no expression of CD14 or CD4. The diagnosis of AML-FAB-M1 was made. The patient refused chemotherapy. Of the rare cases of AML in HIV patients previously reported in the literature, the majority were of the monocytic or myelomonocytic subtype. This case is of special interest because of prior G-CSF therapy. In this setting, the relationship between HIV, G-CSF, and subsequent AML is controversial.
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PMID:Acute myelogenous leukemia (FAB AML-M1) in the setting of HIV infection and G-CSF therapy: a case report and review of the literature. 976 Jan 57

This report describes the rapid development of multiple meniscal signs complicating invasive pulmonary aspergillosis in a 53-year-old man receiving chemotherapy for acute leukemia. While undergoing first induction therapy for AML, he developed chest pain, and multiple bilateral infiltrations were seen in chest roentgenograms. Administration of antibiotics, antifungal agents, steroid pulse therapy and G-CSF was begun. Pulmonary cavities with meniscal signs developed. The next day, pneumothorax and hemothorax were noted. Although drainage and mechanical ventilation were performed, the patient died after massive hemoptysis. Invasive pulmonary aspergillosis was diagnosed at autopsy.
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PMID:[Rapid development of multiple meniscal signs complicating invasive pulmonary aspergillosis in a patient receiving chemotherapy for acute leukemia]. 1110 7

A 16-year-old girl was hospitalized because of anemia and thrombocytopenia in April 1998, and was diagnosed as having AML (FAB:M2). After failure of initial remission induction therapy, she was successfully treated with the MEC regimen as a second-line chemotherapy. On June 22, the first consolidation therapy was started. One week later, the patient developed a high fever with backache. Chest computed tomography (CT) on July 8 showed a 3cm mass lesion adjacent to the thoracic descending aorta in the left upper lobe. She was given fluconazole and antibiotics, and remained in remission. On July 24, the mass lesion changed to a cavitary lesion on chest CT, suggesting a fungal infection, probably aspergillosis. With recovery from neutropenia, the patient became asymptomatic, and fluconazole was changed to itraconazole. On July 27, she suffered sudden, massive hemoptysis and died. Autopsy revealed a localized adhesion between the cavitary lesion and the thoracic descending aorta, and the aortic wall was ruptured at this site. Microscopic examination revealed invasion of mucormycotic hyphae into the wall of the aorta with infiltration of inflammatory cells. The vasa vasorum were occluded by thrombi, in which mucormycotic hyphae were detected.
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PMID:[An autopsy case of pulmonary mucormycosis with fatal hemoptysis from a rupture of the thoracic descending aorta during remission from acute myelocytic leukemia]. 1119 40