Endocrine Abstracts

Objective: Despite combination with peripheral decarboxylase inhibitors significant amounts of L-dopa are peripherally metabolised. In patients with Parkinson’s disease (PD) treated with L-dopa and a dopa decarboxylase inhibitor, urinary dopamine concentrations are markedly elevated. We describe here a L-dopa treated PD patient presenting with a clinical and biochemical picture suspicious of phaeochromocytoma.

Case report: A 73-year-old female patient diagnosed with dopamine-secreting phaeochromocytoma was referred to the Department of Internal Medicine for preoperative pharmacological treatment of severe and symptomatic paroxysmal hypertension. Endocrine evaluation of an adrenal mass had revealed markedly increased urinary dopamine levels and urinary epinephrine and norepinephrine levels within the normal range. On admission the patient reported that she had been diagnosed three years ago with PD. Medication comprised L-dopa 100 mg/benserazide 25 mg qid and pramipexole 0.7 mg tid. Endocrine evaluation confirmed markedly elevated urinary dopamine and homovanillic acid levels as well as plasma dopamine levels. Cortisol diurnal rhythm was normal. Plasma aldosterone concentration and plasma renin activity were within the normal range. Iodine-131-meta-iodobenzylguanidine (MIBG) scintigraphy proved negative. L-dopa/benserazide treatment was discontinued for three days and replaced by amantadine 200 mg qd. Twelve hours after discontinuation we observed a normalisation of the elevated urinary and plasma dopamine levels as well as the increased urinary homovanillic acid levels, indicating that increased dopamine levels were not due to phaeochromocytoma but due to PD therapy. Radiological follow-up of the adrenal incidentaloma was advised.

Conclusions: Clinicians should be alerted to increased urinary dopamine levels in patients treated with L-dopa. Unawareness of this association may lead to the misdiagnosis of phaeochromocytoma.