The convergence of translational genomics and biomedical informatics has changed healthcare delivery. Institutional consortia have begun implementing lab testing and decision support for drug–gene ...

There is growing interest in utilizing pharmacogenetic (PGx) testing to guide antidepressant use, but there is lack of clarity on how to implement testing into clinical practice. We administered two surveys at 17 sites that had implemented or were in the process of implementing PGx testing for antidepressants. Survey 1 collected data on the process and logistics of testing. Survey 2 asked sites to rank the importance of Consolidated Framework for Implementation Research (CFIR) constructs using best‐worst scaling choice experiments. Of the 17 sites, 13 had implemented testing and four were in the planning stage. Thirteen offered testing in the outpatient setting, and nine in both outpatient/inpatient settings. PGx tests were mainly ordered by psychiatry (92%) and primary care (69%) providers. CYP2C19 and CYP2D6 were the most commonly tested genes. The justification for antidepressants selected for PGx guidance was based on Clinical Pharmacogenetics Implementation Consortium guidelines (94%) and US Food and Drug Administration (FDA; 75.6%) guidance. Both institutional (53%) and commercial laboratories (53%) were used for testing. Sites varied on the methods for returning results to providers and patients. Sites were consistent in ranking CFIR constructs and identified patient needs/resources, leadership engagement, intervention knowledge/beliefs, evidence strength and quality, and the identification of champions as most important for implementation. Sites deployed similar implementation strategies and measured similar outcomes. The process of implementing PGx testing to guide antidepressant therapy varied across sites, but key drivers for successful implementation were similar and may help guide other institutions interested in providing PGx‐guided pharmacotherapy for antidepressant management.

Metoprolol is a medication commonly utilized in select patients to achieve a reduction in heart rate, systolic blood pressure, or other indications. A majority of metoprolol metabolism occurs via CYP2D6. Decreased expression of the CYP2D6 enzyme increases the concentration of metoprolol. Current pharmacogenomics guidelines by the Dutch Pharmacogenomics Working Group recommend slower titrations and dose decreases to minimize adverse effects from poor metabolizers or normal metabolizers taking concomitant medications that are strong inhibitors of CYP2D6 (phenoconverters). This study aimed to evaluate adverse effects such as bradycardia, hypotension, and syncope in patients who are expected to have absent CYP2D6 enzyme activity due to drug–drug or drug–gene interactions. The secondary aims of this study were to evaluate heart rate measurements for the included participants. Retrospective data were collected for individuals with CYP2D6 genotyping results obtained for clinical purposes. Three categories (CYP2D6 normal metabolizers, poor metabolizers, and phenoconverters) were assigned. A total of 325 participants were included. There was no statistically significant difference found in the primary composite outcome between the three metabolizer groups (p = 0.054). However, a statistically significant difference was identified in the incidences of bradycardia between the poor metabolizers and the normal metabolizers or phenoconverters (p < 0.0001). The average heart rates were 2.8 beats per minute (bpm) and 2.6 bpm lower for the poor metabolizer and phenoconverter groups, respectively, compared to the normal metabolizers (p < 0.0001 for both comparisons). This study further supports the role of genetic testing in precision medicine to help individualize patient care as CYP2D6 poor metabolizers taking metoprolol were found to have an increase in bradycardia. Additional research is needed to clarify the dose relationship in this drug–gene interaction.

Purpose: Evidence-based guidelines recommend regular depression screening among individuals with type 2 diabetes mellitus (T2DM). The purpose of this study is to examine depression screening patterns among a primary care population with T2DM, through use of the Patient Health Questionnaire-9 (PHQ-9). Methods: In total, 1817 patients with T2DM were analyzed through a retrospective observational study at 2 sites, a regional health center and a federally qualified health center (FQHC). The T2DM sample was divided into those with and without a major depressive disorder (MDD) diagnosis. Depression screening rates and depression severity were assessed through the PHQ-9. Results: Both sites had higher rates of PHQ-9 screening among individuals with a history of MDD (64.82%) vs those without MDD (11.39%). Individuals from the FQHC without a history of depression had a higher mean PHQ-9 score (10.11) than those with a previous MDD diagnosis at both RHS and FQHC (7.16 and 9.85, respectively). Conclusions: Depression screening rates among individuals with diabetes and no history of MDD were remarkably low. Patients with diabetes but no MDD diagnosis who sought health care at a FQHC clinic had more depressive symptoms than those with a history of MDD at both sites. Individuals with diabetes and who have a MDD diagnosis are much more likely to receive regular depression screening than those without MDD, which leaves a substantial proportion of patients with undetected depression. Depression screening must be enhanced for all individuals with diabetes, particularly for low-income individuals and those without a previous diagnosis of MDD.

Several healthcare organizations across Minnesota have developed formal pharmacogenomic (PGx) clinical programs to increase drug safety and effectiveness. Healthcare professional and student educat...