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

Our laboratory has concentrated on the possible regulation the benzamides and nicotinamides may have on the processes of DNA repair and apoptosis. Recent reports have suggested that both apoptosis and inflammation are regulated by the transcription factor NF-kappaB. We have initiated studies regarding the hypothesis that the benzamides and nicotinamides could inhibit the production of tumor necrosis factor alpha (TNFalpha) and the inflammatory response as well as induce apoptosis via inhibition of NF-kappaB. Our data have shown that nicotinamide and two N-substituted benzamides, metoclopramide (MCA) and 3-chloroprocainamide (3-CPA), gave dose dependent inhibition of lipopolysacharide induced TNFalpha in the mouse within the dose range of 10-500 mg/kg. Moreover, lung edema was prevented in the rat by 3 x 50 mg/kg doses of 3-CPA or MCA, and 100-200 microM doses of MCA could also inhibit NF-kappaB in Hela cells. Taken together these data strongly support the notion that benzamides and nicotinamides have potent anti-inflammatory and antitumor properties, because their primary mechanism of action is regulated by inhibition at the gene transcription level of NF-kappaB, which in turn inhibits TNFalpha and induces apoptosis.
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PMID:Newly discovered anti-inflammatory properties of the benzamides and nicotinamides. 1033 48