Phenoconversion is a mismatch between an individual’s genotype-based prediction of a drug metabolism and its true capacity. In other words, there is a mismatch between the clinically observed phenotype and the phenotype you expect to see from a patient’s genotype. This is a great example of why we don’t want to interpret PGX results in isolation. We want to look at both drug-drug and drug-gene interaction. One can be a normal metabolizer but because an external factor was added, such as smoking or taking another medication, one can phenoconvert to a poor metabolizer. Strong inhibitors such as Prozac can phenoconvert an individual to a PM and the opposite is also true. A strong inducer can turn an individual into an ultra-rapid metabolizer. Therefore, we call this the blind spot of pharmacogenomics (PGx) or what is better know the Achilles' heel of PGx. So, it’s not enough to look at just one medication and see how a person is metabolizing it but rather to look at drug-gene interaction as well. A great example is with the enzyme CYP2D6. Prozac is a strong inhibitor of 2D6 and if we add on Tramadol for pain, as an example, which uses CYP2D6 to activate, we can say we have phenoconverted that individual. The person was a normal metabolizer of CYP2D6 enzyme but adding Tramadol made them a poor metabolizer. This presentation will provide an overview of the concept of phenoconversion and its impact on clinical outcomes.

Learning Objectives:

1. Define the concept of phenoconversion

2. What is the utility of pharmacogenomics in a mental health setting?