Malignant pericardial tamponade in a patient with hormone-refractory prostate cancer
Department of Urology, Azumino Red Cross Hospital, Azumino, Nagano, Japan.International Journal of Clinical Oncology (Impact Factor: 2.13). 02/2010; 15(1):101-3. DOI: 10.1007/s10147-009-0002-8
An 82-year-old man who was receiving treatment for prostate cancer and cholangiocellular carcinoma was admitted to our hospital because of chest discomfort and dyspnea. At the time of admission, 16 months after the start of hormone therapy, the prostate-specific antigen level was 454.08 ng/ml. Chest radiography revealed cardiomegaly, and ultrasonography demonstrated significant pericardial effusion. Pericardiocentesis yielded a hemorrhagic exudate, and a routine cytological study revealed malignant cells. It was difficult to determine whether these cells had originated from the prostate cancer or the cholangiocellular carcinoma. However, immunohistochemical analysis of a cell-block section of the pericardial effusion allowed a diagnosis of pericardial metastasis from the prostate cancer. After drainage and intrapericardial injection of cisplatin, the amount of effusion was decreased. After removal of the pericardial drain, the patient was discharged, but the pericardial effusion was found to have accumulated again 1 month later.
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ABSTRACT: Pericardial malignancies are uncommon, usually metastatic, linked to terminal oncology patients, and rarely diagnosed premortem. A very small number of patients will develop signs and symptoms of malignant pericardial effusion as initial clinical manifestation of neoplastic disease. Among these patients, a minority will progress to a life-threatening cardiac tamponade. It is exceedingly rare for a cardiac tamponade to be the unveiling clinical manifestation of an unknown malignancy, either primary or metastatic to pericardium. We present the case of a 50-year-old male who was admitted to the emergency department with an acute myocardial infarction diagnosis that turned out to be a cardiac tamponade of unknown etiology. Further studies revealed a metastatic pericardial adenocarcinoma with secondary cardiac tamponade. We encourage considering malignancies metastatic to pericardium as probable etiology for large pericardial effusions and cardiac tamponade of unknown etiology.
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ABSTRACT: The testosterone surge and disease flare is a feared complication from initiation of gonadotropin-releasing hormone (GnRH) agonist treatment in advanced prostate adenocarcinoma. It is a common practice to start an average 7-day pretreatment regimen with an antiandrogen agent before initiating GnRH agonist therapy, to circumvent disease flare from testosterone surge. However, this might not be the best strategy and can be harmful, especially in patients at high risk of imminent organ damage from minimal testosterone surge. Surgical castration is a simple and cost-effective method that should be considered in these scenarios. But most patients refuse this procedure because of the permanent and psychologic impact of surgery. Novel GnRH antagonists, such as degarelix, and cytochrome P450 17 (CYP17) enzyme inhibitors, such as ketoconazole, achieve castrate-equivalent serum testosterone levels much faster than traditional GnRH agonists without the need for coadministration of antiandrogens. This article reports on 3 cases of impending oncologic emergencies in advanced prostate adenocarcinoma treated promptly with degarelix and ketoconazole without any disease flare related to testosterone surge. In the setting of symptomatic hormone-naïve metastatic prostate cancer, the authors suggest clinical trials using abiraterone, orteronel, and other newer agents that target the CYP17 axis (eg, ketoconazole) for fine-tuning the emergent medical castration methods and avoiding the dangers from the flare phenomenon. Copyright © 2015 by the National Comprehensive Cancer Network.
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