Objective: to present a poor metabolizer patient carrying CYP2D6*4/*4 genotype manifesting dystonia associate to fluoxetine therapy

Background: Major side effect of antipsychotics is acute dystonic reaction (ADR). It may depends on the plasma concentration of the drug and CYP2D6 genotypes. Fluoxetine is primarily metabolized by CYP2D6 to compounds with little pharmacological activity, and is also a strong inhibitor of the CYP2D6. Olanzapine and aripiprazole are substantially, but not extensively metabolized by CYP2D6

Method: A 19-years-old female Caucasian patient was addmited to Neurology Clinic beacause of cervical dystonia. She developed involuntary movements 7 days after additing fluoxetine to her standard therapy of olanzapine 5 mg twice daily and aripiprazole 5 mg daily for psychosis for the last year. A year eralier, after a few days of haloperidol 5 mg twice daily and fluvoxamine 100 mg daily, she exhibited myoclonic head yerks, which stopped after the therapy was discontinued.

Results: Pharmacogenetic testing showed two nonfunctional CYP2D6 alleles (*4/*4) indicating no enzymatic activity.

Conclusion: Genetics variations in CYP2D6 enzymes determine enzymatic activity, which can have a large effect on drug levels and toxicity. In the presence of strong CYP2D6 inhibitor, individuals with a poor metabolizer genotype have a greater risk of manifesting poor metabolizer phenotype and adverse reaction. Genotyping may reflect the CYP2D6 poor metabolizer phenotype when using multiple drugs that are substrates and/or inhibitors of CYP2D6.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/dystonia-associated-with-fluoxetine-in-a-patient-cyp2d64-4-poor-metabolizer-role-of-drug-drug-interactions/