While the study has several limitations, the results are consistent with a growing body of literature that suggests that the pharmacogenetics of depression (an inherently complex disorder) may turn out to be multifactorial, and may include the HTR1A gene in concert with other serotonin-related genes.
Current clinical practice guidelines for the treatment of posttraumatic stress disorder offer varying recommendations regarding the use of pharmacotherapy. Many direct head-to-head comparisons of pharmacotherapy are lacking, and recommendations are based on meta-analyses and small trials. While selective serotonin reuptake inhibitors and serotonin norepinephrine reuptake inhibitors are considered first-line pharmacotherapy, clear distinctions do not exist when considering other classes of psychotropic medications. Ultimately, when selecting an appropriate medication for a patient diagnosed with posttraumatic stress disorder, the clinician needs to consider the current symptomatology being experienced, comorbid conditions, and evidence for efficacy of specific treatments prior to initiating medications.
PGY1 contributes to renal and biliary elimination of drugs by transporting the drug out of the cell and back into the intestinal lumen, where drugs may be further metabolized by intestinal enzymes such as Cytochrome P (CYP)-450 3A4. Its function is to limit the bioavailability of orally administered compounds. Due to the increase in MDR and MRP gene expression seen after the acute treatment with venlafaxine, there could be a potential drug-drug interaction with other medications that are metabolized via CYP450-3A4 when coadministered with venlafaxine.
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