Genetic Polymorphism in CYP2D6 and its Association with the Safety and Efficacy of Fluvoxamine in Patients with Major Depressive Disorder

Abstract

The nonresponder phenomenon is often associated with the use of fluvoxamine, a selective serotonin reuptake inhibitor when used for treating major depressive disorder (MDD).  Several patients experience adverse effects such as xerostomia, anxiety, indigestion, vertigo, and headache. The gene that is primarily responsible for the metabolism of fluvoxamine is CYP2D6, which is highly polymorphic. This study was designed to investigate whether the efficacy and adverse effects of fluvoxamine are associated with polymorphism in the CYP2D6 gene. We investigated 70 patients with MDD. CYP2D6 genotyping was done through the allele-specific polymerase chain reaction. Fluvoxamine efficacy was measured through the ‘Hamilton rating scale for depression’ (HDRS) while adverse effects were measured by administering ‘Liverpool University Neuroleptic Side Effects Rating’ (LUNSER) scale. Our results showed that there was no statistically significant association between the efficacy or safety of fluvoxamine and our investigated single nucleotide polymorphism (SNP). This study demonstrates that the efficacy of fluvoxamine in patients with depressive disorder may not be predicted on the basis of CYP2D6 1846G>A (rs3892097) genetic marker.