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The Transdermal Delivery System of Monoamine Oxidase Inhibitors

J Clin Psychiatry 2012;73(suppl 1):25-30
10.4088/JCP.11096su1c.04

Monoamine oxidase inhibitors (MAOIs) were once widely used as effective treatments for major depressive disorder, particularly for patients with atypical or treatment-resistant depression. Today, MAOIs have largely been replaced by newer antidepressants because of concerns over potential serious side effects due to their mechanism of action. Monoamine oxidase (MAO) is an enzyme that metabolizes serotonin, norepinephrine, and dopamine, the neurotransmitters that are most associated with depression; inhibiting MAO, therefore, makes more of these neurotransmitters available for synaptic action. However, MAO also metabolizes tyramine, a trace amine found in some foods that acts as a sympathomimetic. Allowing excess tyramine to accumulate via MAO inhibition can result in hypertensive crisis due to the release of norepinephrine; therefore, patients taking an MAOI have had to follow dietary restrictions to avoid tyramine-rich foods. Hypertensive crisis may also be precipitated by using MAOIs in conjunction with other drugs that have vasoconstrictive properties, that act as sympathomimetics, or that inhibit the reuptake of norepinephrine. Serotonin syndrome is another serious adverse effect that can potentially occur when using an MAOI with another drug that inhibits the reuptake of serotonin. In this article, the mechanism of action of MAOIs is reviewed, along with that of a newer MAOI formulation that lessens the need for dietary restrictions and has a greater safety and tolerability profile than the older oral formulations.

(J Clin Psychiatry 2012;73[suppl 1]:25–30)

From the Department of Pharmacy Practice and the Center for Clinical Research, Mercer University College of Pharmacy and Health Sciences, Atlanta, Georgia.

This article is derived from the planning teleconference series “A Fresh Look at Monoamine Oxidase Inhibitors for Depression,” which was held December 2011 through February 2012 and supported by an educational grant from Mylan Specialty L.P. (formerly known as Dey Pharma, L.P.).

Dr VanDenBerg has received grant/research support from Eli Lilly and Cognitive Research Corporation.

Corresponding author: Chad M. VanDenBerg, PharmD, BCPP, 3001 Mercer University Drive, DV-129, Atlanta, GA 30341 (Vandenberg_c@mercer.edu).