Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We retrospectively evaluated the computed tomography (CT) findings in 20 patients with pulmonary drug toxicity that followed high-dose chemotherapy and autologous bone marrow transplantation (ABMT). Eighty-five patients with Stage II or III breast cancer that involved > or = 10 axillary lymph nodes were enrolled in a treatment protocol that included four cycles of standard-dose therapy (CAF) followed by one cycle of high-dose treatment (CPA/cDDP/BCNU). After chemotherapy, ABMT was performed. Twenty-six patients (31%) developed pulmonary drug toxicity. Serial thoracic CT studies were available in 20 of these 26 patients. All 20 patients exhibited clinical symptoms (i.e., dyspnea, nonproductive cough, and fever) and abnormal pulmonary function following transplantation. Thirteen patients had pathologically proven drug toxicity, and seven patients had clinical features and treatment responses highly suggestive of this diagnosis. Multiple sputum and blood cultures were negative in all patients. CT scans of 13 patients (65%) demonstrated scattered, predominantly peripheral ground-glass or consolidated opacities that occasionally looked nodular or masslike. Two patients (10%) had CT scans suggestive of pulmonary edema and in five patients (25%), the CT examinations revealed no significant abnormalities. Pleural effusions and adenopathy were uncommon. Pulmonary drug toxicity after high-dose chemotherapy and ABMT should be suspected in the appropriate clinical and radiographic setting, and therapy may be initiated on the basis of these observations.
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PMID:Pulmonary drug toxicity following high-dose chemotherapy with autologous bone marrow transplantation: CT findings in 20 cases. 820 80

This study was performed to demonstrate an experimental procedure of pulmonary edema induced by angiotensin I (AT I) in rats and to elucidate the mechanism of hemodynamic pulmonary edema. In the previous pilot study, 20 microg/kg of AT I was found to be an adequate dose for inducing pulmonary edema. To elucidate the mechanism of AT I pulmonary edema and protective measures against it, we observed the effects of captopril (CAP, 5 and 10 mg/kg), an angiotensin converting enzyme inhibitor; losartan (LOS, 10 mg/kg), an angiotensin II (AT II)-receptor antagonist; and phentolamine (PHE, 10 mg/kg), an alpha-adrenergic receptor blocker, on AT I-induced pulmonary edema in rats. Similarly, we also observed the effects of CAP (10 and 20 mg/kg) on pulmonary edema induced by 25 microg/kg of adrenaline (ADR) in rats. The development of AT I-induced pulmonary edema was significantly suppressed by CAP and LOS, but was unaffected by PHE. In contrast, the development of ADR-induced pulmonary edema was not suppressed by CAP. These results suggest that AT I-induced pulmonary edema is developed via the AT II and a specific AT II-receptor, without the indirect action of adrenaline.
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PMID:Pulmonary edema induced by angiotensin I in rats. 951 4