INTRODUCTION: Pulmonary metastases of prostate adenocarcinoma have been well described, but endobronchial lesions are rare. Although neuroendocrine differentiation of prostate cancer is common, it is rarely seen in the context of pulmonary metastases. We present a case of metastatic prostate cancer initially presenting as bronchial carcinoid.
CASE PRESENTATION: A 73 year old East Indian man was referred for assessment of an abnormal chest x-ray. Past medical history was significant for type II diabetes and stage T3c prostate cancer 10 years earlier, treated with radiation and hormone therapy. Recurrences 4 years and 2 years after the initial diagnosis were treated with orchidectomy and flutamide therapy, respectively. There was no smoking history or known asbestos exposure. He had recently traveled to India at which time he developed an illness consisting of dyspnea, fevers, positional chest pain, fatigue, anorexia associated with a 35 lbs weight loss over 3–6 months and a right-sided pleural effusion. There was no history of cough or wheeze, but he did have 2 episodes of hemoptysis. While in India, thoracentesis demonstrated a sterile exudate and he received 6 months of therapy for presumed pleural tuberculosis. Other results from India were unavailable. After returning to Canada, chest x-ray showed a persistent pleural effusion and thickening with associated volume loss. Pulmonary function testing revealed a restrictive process. A repeat attempt at thoracentesis was unsuccessful. Sputum for acid fast bacilli was negative. Computed tomography of the chest demonstrated a right hilar mass (4.4 × 4.3 cm), pleural thickening contiguous with the mass, subcarinal lymph nodes and a small right pleural effusion. Bronchoscopy revealed a smooth, shiny right middle lobe endobronchial mass. Brushings and biopsies of the mass suggested typical carcinoid based on histologic morphology and positive chromogranin and synaptophysin staining. Because the clinical picture was inconsistent with primary pulmonary carcinoid, a pleural biopsy was subsequently performed. The biopsy was weakly positive for prostate specific antigen (PSA) and strongly positive for alpha-methylacyl-CoA racemase (AMACR), consistent with metastatic prostate adenocarcinoma. The carcinoid samples were negative for prostate specific markers. Serum PSA was elevated at 133.6 and bone scan revealed bony metastases.
DISCUSSIONS: Approximately 5% of patients with prostate cancer have radiologic evidence of pulmonary metastases at diagnosis, but clinical detection of lung metastases is infrequent, as the majority of patients remain asymptomatic from pulmonary lesions. Focal or extensive histologic neuroendocrine differentiation of prostate cancer can be seen in up to 50% of prostate tumors by immunohistochemistry, and generally portends a poor prognosis and response to therapy. There are at least three reported cases in the literature of metastatic prostate cancer mimicking pulmonary carcinoid tumors (1). It has been suggested that long-term exposure to hormonal therapy can select for neuroendocrine differentiation in both primary and metastatic tumor deposits. The carcinoid mass in this case did not stain for prostate specific markers, consistent with the possibility of a synchronous primary of lung origin. Indeed, epidemiologic studies have also suggested an almost three-fold higher than expected incidence of prostate cancer in patients diagnosed with primary pulmonary carcinoid tumors (2). The reason for this association is unclear, but may relate to an underlying genetic tendency toward the development of endocrinologic tumors or to unidentified environmental or hormonal factors.
CONCLUSION: This case highlights the importance of being aware of the potential for prostate cancer to undergo neuroendocrine differentiation and the association of pulmonary carcinoid tumors with prostate cancer.
DISCLOSURE: Mitesh Thakrar, No Financial Disclosure Information; No Product/Research Disclosure Information