Endocrine Abstracts

While phaeochromocytomas are rare tumours, their identification is essential to avoid morbidity and mortality; their biochemical identification is crucial. Plasma and 24 urinary metanephrines are used as first line investigations, with plasma metanephrines increasingly used first due to its simplicity and high sensitivity/specificity. False positive results, however, can be as high as 20%, particularly secondary to medications; their exclusion is essential to avoid unnecessary imaging and operation. However, most interfering factors cause elevation of less than fourfold above the normal range. In our case, we show the effect of midodrine- an α1 receptor agonist- in causing grossly elevated plasma, but not urinary, metanephrine. 41-year old lady was referred to our endocrine clinic in Oxford with a possible phaeochromocytoma. She had 6-year history of dizziness and syncope, initially diagnosed with vasovagal syncope, but latterly diagnosed with postural orthostatic tachycardia syndrome (POTS). Her symptoms were episodes of dizziness, shortness of breath, nausea, headaches, with or without loss of consciousness. Her cardiovascular investigations showed sinus tachycardia and hypotension associated with her symptoms. As part of investigations, plasma metanephrines were assessed and were grossly abnormal: plasma metanephrine > 25 000 pmol/l and normetanephrine of 1758 pmol/l. Her medications included midodrine 7.5 mg 3 h, bisoprolol and slow sodium. Doxazosin, an α1-adenoceptor antagonist, had recently been added following the above results. There was no relevant family history, and examination was unremarkable. Investigations included a repeat plasma metanephrines which showed similar results. However, 24-h urinary metanephrines, PTH, thyroid function and pituitary profile were normal, as was adrenal CT scan. Midodrine was then withheld for a week, and plasma metanephrines levels became normal. Doxazosin was subsequently stopped. Most reported drug interference with metanephrine levels cause mild to moderate elevation, due to a variety of mechanisms. We highlight the massive interference in plasma metanephrines assay by the α-adrenoceptor agonist midodrine.