Endocrine Abstracts

A 21-year-old man presented with tonic–clonic seizures and two-week history of nocturnal headaches, sweatiness, hot flushes and abdominal pain. Blood pressure was 220/110 mmHg and pulse 120–160 bpm. A GTN infusion was commenced and the blood pressure improved to 150/90 mmHg. Examination revealed a large, hard mass in the left hypochondrium. There was no palpable lymphadenopathy and no papilloedema. A 2 cm hard, irregular mass was present on the left testis. CT showed a 20×13×13 cm heterogenous mass compressing the left kidney, extending past the midline and encasing the aorta and IVC. MR brain was consistent with posterior reversible encephalopathy syndrome (PRES).

Phenoxybenzamine did not control the hypertension. The GTN was weaned and lisinopril and propranolol started. However, the blood pressure only improved once nifedipine has been commenced. Urinary catecholamines: noradrenaline 795 nmol/24 h (<560), adrenaline 188 nmol/24 h (<144). Tumour markers: LDH 5530 iu/l (240–480), AFP <3 iu/ml (<10), hCG 29 iu/l (<3). Aldosterone was raised at 2518 pmol/l (135–400).

Ultrasound-guided biopsy demonstrated non-seminomatous germ cell tumour (GCT). Proximity to the great vessels precluded resection but it responded well to to four cycles of BEP chemotherapy (bleomycin, etoposide, cisplatin). The reduction in mass size correlated with an improvement in hypertension: initially on four anti-hypertensives (nifedipine MR 20 mg, doxazosin MR 8 mg, lisinopril 2.5 mg, propranolol MR 80 mg) blood pressure was 153/79 mmHg; three months after presentation, off all agents, blood pressure was 113/62 mmHg. He has now been referred for retroperitoneal lymph node dissection, left orchidectomy and left nephrectomy.

This case presented with many of the classical features of phaeochromocytoma. However, resistant hypertension and the testicular mass suggested an alternative pathology, highlighting the importance of testicular examination. Renovascular hypertension may occur after chemotherapy or surgery for GCT but is rarely a presenting feature. Here hypertension may have arisen from direct renal artery compression by tumour or as a result of GCT hormone production.