Response of a Nonmalignant Pleural Effusion to Bevacizumab
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《新英格兰医药杂志》
To the Editor: The potential role of vascular endothelial growth factor in malignant as well as nonmalignant pleural effusion1,2 prompted us to use bevacizumab, a monoclonal antibody against vascular endothelial growth factor, in a 68-year-old man with primary cardiac amyloidosis who had severe dyspnea and underwent repeated thoracenteses for pleural effusions. Cytologic assessments of the pleural fluid did not detect malignant cells. Primary amyloidosis had been diagnosed by myocardial biopsy four weeks previously, but there were no other manifestations of amyloidosis. At the time of the patient's admission, left ventricular function was moderately reduced (ejection fraction, 40 percent). A radiograph of the chest showed massive pleural effusion in the right hemithorax. The C-reactive protein level was markedly increased (27.2 mg per deciliter), but no inflammatory infiltrate was seen in the radiograph of the lung. Thoracentesis was unsuccessful because of the segmented nature of the effusion. Because of the elevated C-reactive protein level, we began broad-spectrum antibiotic treatment and gave the patient an intravenous diuretic. After five days, the C-reactive protein level was reduced, but the clinical condition, with severe dyspnea, and the chest radiograph remained unchanged. The patient was judged unable to undergo anesthesia for surgical intervention and pleurodesis.
Because the severe dyspnea continued despite intensive conventional treatment for another seven days, we decided to treat the patient with bevacizumab (Avastin, Roche).3 After obtaining the patient's consent, we administered the dose used for the treatment of colorectal cancer (5 mg per kilogram of body weight given intravenously over a period of 90 minutes).4 On the first day after the administration of bevacizumab, the patient reported increased urine production and markedly reduced dyspnea. One week after bevacizumab treatment, the chest radiograph showed a dramatic reduction in the pleural effusion. This finding was confirmed in a second radiograph two weeks after the administration of bevacizumab.
To our knowledge, this is the first report of the treatment of a nonmalignant pleural effusion with bevacizumab. Considering the prompt clinical improvement and the reduction in the effusion after administration of the antibody, there is good reason to believe that clinical improvement and diminished effusion were associated with bevacizumab therapy.
Oskar Pichelmayer, M.D.
Christoph Zielinski, M.D.
Markus Raderer, M.D.
Medical University of Vienna
1090 Vienna, Austria
markus.raderer@meduniwien.ac.at
References
Senger DR, Galli SJ, Dvorak AM, Perruzzi CA, Harvey VS, Dvorak HF. Tumor cells secrete a vascular permeability factor that promotes accumulation of ascites fluid. Science 1983;219:983-985.
Sack U, Hoffmann M, Zhao XJ, et al. Vascular endothelial growth factor in pleural effusions of different origin. Eur Respir J 2005;25:600-604.
Ferrara N, Hillan KJ, Gerber HP, Novotny W. Discovery and development of bevacizumab, an anti-VEGF antibody for treating cancer. Nat Rev Drug Discov 2004;3:391-400.
Hurwitz H, Fehrenbacher L, Novotny W, et al. Bevacizumab plus irinotecan, fluorouracil, and leucovorin for metastatic colorectal cancer. N Engl J Med 2004;350:2335-2342.
Because the severe dyspnea continued despite intensive conventional treatment for another seven days, we decided to treat the patient with bevacizumab (Avastin, Roche).3 After obtaining the patient's consent, we administered the dose used for the treatment of colorectal cancer (5 mg per kilogram of body weight given intravenously over a period of 90 minutes).4 On the first day after the administration of bevacizumab, the patient reported increased urine production and markedly reduced dyspnea. One week after bevacizumab treatment, the chest radiograph showed a dramatic reduction in the pleural effusion. This finding was confirmed in a second radiograph two weeks after the administration of bevacizumab.
To our knowledge, this is the first report of the treatment of a nonmalignant pleural effusion with bevacizumab. Considering the prompt clinical improvement and the reduction in the effusion after administration of the antibody, there is good reason to believe that clinical improvement and diminished effusion were associated with bevacizumab therapy.
Oskar Pichelmayer, M.D.
Christoph Zielinski, M.D.
Markus Raderer, M.D.
Medical University of Vienna
1090 Vienna, Austria
markus.raderer@meduniwien.ac.at
References
Senger DR, Galli SJ, Dvorak AM, Perruzzi CA, Harvey VS, Dvorak HF. Tumor cells secrete a vascular permeability factor that promotes accumulation of ascites fluid. Science 1983;219:983-985.
Sack U, Hoffmann M, Zhao XJ, et al. Vascular endothelial growth factor in pleural effusions of different origin. Eur Respir J 2005;25:600-604.
Ferrara N, Hillan KJ, Gerber HP, Novotny W. Discovery and development of bevacizumab, an anti-VEGF antibody for treating cancer. Nat Rev Drug Discov 2004;3:391-400.
Hurwitz H, Fehrenbacher L, Novotny W, et al. Bevacizumab plus irinotecan, fluorouracil, and leucovorin for metastatic colorectal cancer. N Engl J Med 2004;350:2335-2342.