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Case Reports
. 2011 Jun 9;364(23):2268-70.
doi: 10.1056/NEJMc1101502#SA1.

Drugs and pheochromocytoma--don't be fooled by every elevated metanephrine

Nicola M Neary, Kathryn S King, Karel Pacak
Case Reports

Drugs and pheochromocytoma--don't be fooled by every elevated metanephrine

Nicola M Neary et al. N Engl J Med. .
No abstract available

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Figures

Figure 1
Figure 1. Mechanisms of Pharmacologic Interference with Catecholamines and Metanephrines
Sympathomimetic agents such as ephedrine, amphetamine, caffeine, and nicotine increase the release of norepinephrine and epinephrine. Monoamine oxidase (MAO) inhibitors block the conversion of norepinephrine and epinephrine to dihydroxyphenylglycol (DHPG), leading to increased concentrations and availability of these two catecholamines. Drugs that inhibit norepinephrine and epinephrine reuptake, such as serotonin–norepinephrine reuptake inhibitors (e.g., venlafaxine), “selective” serotonin-reuptake inhibitors, and tricyclic antidepressants, lead to increased concentrations of norepinephrine and epinephrine in the synaptic clefts. The α-adrenergic-receptor blockers and β-adrenergic-receptor blockers reduce the effects of catecholamines on end organs such as the brain, heart, gastrointestinal tract, and others. DOPA denotes dihydroxyphenylalanine.
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