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Our MAO inhibitor guide was written by our doctors. The information in this guide incorporates a combination of our collective clinical experiences with prescribing MAO inhibitor treatment and findings supported in the medical literature. Our guide is updated regularly. Check out articles from our guide below.
This article discusses common and rare side effects with MAO inhibitor use and ways to effectively treat them.
This article details the symptoms and management of two major risks: tyramine-induced hypertension and serotonin syndrome.
VERY IMPORTANT: These phenomena have NOT been written up into a case report that has meet the evidentiary standards for publication. We have chosen not to write case reports for our cases below for several reasons, including that although there is value in case reports, they may sometimes do more harm than good. [1] Therefore, any findings reported on this page should not be used to guide patient care nor be cited as evidence to support guidelines for patient care.
Likely mild tyramine-induced hypertension following 60 mg ingestion of levodopa (L-DOPA) in a patient on 60 mg Parnate.
Background: In an attempt to augment MAO inhibitor treatment after failing augmentation from several other medications, a patient was instructed to attempt levodopa (L-DOPA) supplementation. Patient obtained levodopa from a well-known company that produces a wide array of supplements. Patient’s particular supplement was advertised as a mucuna extract, 800 mg per capsule. The bottle noted that the levodopa content was 15% or 120 mg per capsule. Other ingredients include: cellulose, cellulose powder, stearic acid, and magnesium stearate.
Case: On the first day of supplementation with levodopa, the patient was instructed to open the capsule and dump 75-80% of the capsule’s content into the trash. The patient was told to then reseal the capsule and consume it on an empty stomach. In doing so, the patient only obtained 24-30 mg of levodopa.
The provider’s decision to start with this amount of levodopa was based on several principles:
1. Levodopa is converted to tyramine via two separate chemical reactions that occur from two separate types of bacteria in the intestines. [2] This conversion occurs at a 1:1 ratio (i.e., one molecule of levodopa becomes one molecule of tyramine). Given both levodopa and tyramine have similar molecular weight, 100% conversion of 24-30 mg of levodopa would produce roughly 24-30 mg of tyramine.
2. Bioavailability of levodopa is 30%, therefore 7-9 mg of levodopa will likely be absorbed in the patient before being able to be converted to tyramine. [3] Therefore, at most (assuming 100% conversion of the levodopa that is not absorbed and assuming 100% absorption of the tyramine produced), 17-21 mg will be absorbed.
3. Some levodopa (or derivatives of levodopa) may pass through the gut before being absorbed into the systemic circulation as tyramine. In other words, even if levodopa is converted to tyramine, given the uncertain time course for this reaction, some of the production of tyramine may occur in the distal small intestine or colon where absorption may be reduced. [4] But again whether this occurs and to what extent is unknown. (In hindsight, due to the patient’s relatively quickly spike in blood pressure following levodopa consumption, discussed below, it is likely that conversion of levodopa to tyramine occurs rapidly and in large amounts within the gut.)
4. Because of the largely unknown in-vivo conversion rate of levodopa to tyramine by gut microbiota (a two-step process), production of tyramine likely occurs through the superimposition (albeit, shifted in time) of two bell-shaped curves for typical production of substrates by enzymes. [5] In other words, absorption of tyramine likely occurs over a period of time that is greater than if it was consumed directly. This is independent of the already skewed bell shape curve of most drug absorptions that tyramine absorption likely also follows [6]. Whether this increased period of time for absorption is significant enough to lower the peak plasma level of tyramine or not is unknown.
5. Thus 24-30 mg of L-Dopa was reasoned to be a fair starting test dose to assess for potential tyramine-induced hypertension prior to increasing the dose of levodopa.
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