A 12-cm Mass with No Symptoms and Unremarkable Laboratory Results

Abstract

A 60-year-old man presented to his general practitioner with complaints of indigestion and flu-like symptoms. The results of a clinical examination were unremarkable. The only abnormality found in routine hematology and biochemistry investigations was an increased serum alkaline phosphatase concentration (131 U/L; reference interval, 35–120 U/L). Given his abdominal discomfort, the patient was referred for an abdominal ultrasound evaluation, which revealed a 12-cm cystic mass in the area of the left kidney. Further imaging with computed tomography scanning suggested that the mass arose from the left adrenal gland (Fig. 1). The patient's medical history was notable for hypertension, which was controlled with 8 mg candesartan once daily. The patient reported no headaches, palpitations, or diaphoresis. Fig. 1. Computed tomography images. Coronal (A) and axial (B) images showing a 12-cm mass in the left adrenal gland. The patient was referred for further investigation. Plasma free metanephrines (PMets)6 were measured. Initial results showed borderline increases in plasma normetanephrine (NMN) and metanephrine (MN) that were not diagnostic of pheochromocytoma (PCC). PMet measurements were repeated with a separate plasma sample, and total fractionated urine MNs (UMets) were measured in a sample of an acidified 24-h urine collection. Urine and plasma analysis results were concordant, with borderline increases in NMN (Table 1). The patient was not on any medications known to cause a physiological increase in PMets. View this table: Table 1. Plasma free MN and urine total fractionated MN results.a On the basis these findings, the size of the mass, and the lack of interfering medications, the patient underwent α-blockade with 10 mg phenoxybenzamine 3 times per day and surgical resection of the adrenal mass. A subsequent histologic analysis revealed a cystic PCC with evidence of intratumoral hemorrhage and degeneration. PMet concentrations returned to normal after tumor resection (Table 1). Subsequent testing identified no germline mutations in PCC-predisposing genes, a result consistent with sporadic disease. During follow-up the patient remained normotensive and …