Search

Medication adjustments in 7 out of 3 patients as a result of pharmacogenetic testing initiated by primary care pharmacists based on specific inclusion protocols (SA-PGx pilot) Background Pharmacogenetic analysis is currently performed at 16 certified laboratories in the Netherlands. For 90 different drugs pharmacogenetic advice is available, of which 23 drugs are frequently prescribed in primary care. Despite these opportunities the use of pharmacogenetic testing in primary care is still limited. Objective Investigate to what extent pharmacogenetic inclusion protocols and expert opinion of a pharmacist will lead to medication adjustments in patients. Design Prospective feasibility cohort study. Methods Eligible patients for pharmacogenetic testing are selected based on predefined inclusion protocols or pharmacist's expert opinion. DNA analysis is performed on buccal swab material collected in the pharmacy. Questionnaires, regarding drug-related complaints and patient satisfaction concerning provided care in the pharmacy, are filled in by the patients at baseline and after 1-2 weeks (no medication adjustments) or after 6 weeks (medication adjustments). Following study completion the application of pharmacogenetic testing is evaluated by the participating pharmacists. Results Over a period of 2 years 86 patients were included within 10 primary care pharmacies. Medication changes based on pharmacogenetic results were registered in 25 patients (29%). Almost 1/3 of these patients were selected based on the inclusion protocols. The most frequently changed drugs were clopidogrel, statins, pantoprazole and metoprolol. Drug complaints were reduced in 19% (n = 3) of the patients (not significant). The lack of imbursement in case of pharmacogenetic test requests from pharmacists was the most frequently mentioned barrier towards broad implementation of pharmacogenetics in primary care pharmacy. Conclusion Pharmacogenetic requests initiated by the pharmacist lead to medicatio

Effective pharmacologic treatments for psychiatric disorders are available, but their effect is limited due to patients’ genetic heterogeneity and low compliance-related to frequent adverse events. Only one third of patients respond to treatment and experience remission. Pharmacogenetics is a relatively young field which focusses on genetic analyses in the context of the metabolism and outcome of drug treatment. These genetic factors can, among other things, lead to differences in the activity of enzymes that metabolize drugs. Recently, a clinical guideline was authorized by the Dutch Clinical Psychiatric Association (NVvP) on the clinical use of pharmacogenetics in psychiatry. The main goal was to provide guidance, based on current evidence, on how to best use genotyping in clinical psychiatric practice. A systematic literature search was performed, and available publications were assessed using the GRADE methodology. General recommendations for psychiatric clinical practice were provided, and specific recommendations per medication were made available. This clinical guideline for caregivers prescribing psychotropic drugs is the product of a broad collaboration of professionals from different disciplines, making use of the information available at the Dutch Pharmacogenetics Working Group (DPWG) and the Clinical Pharmacogenetics Implementation Consortium (CPIC) so far. We summarize the relevant literature and all recommendations in this article. General recommendations are provided and also detailed recommendations per medication. In summary we advise to consider genotyping, when there are side effects or inefficacy for CYP2C19 and CYP2D6. When genotype information is available use this to select the right drug in the right dose for the right patient.

Introduction: The transporter OCT1 is involved in the influx of metformin into the liver and the transporter MATE1 is involved in the efflux of metformin out of the liver. Recently, we identified that the polymorphism rs622342 in the gene coding for OCT1, and the polymorphism rs2289669 in the gene coding for MATE1, are associated with the degree of glucose-lowering effect by metformin. In this study, we analysed the existence of interaction between these two polymorphisms. Design and methods: We identified all incident metformin users in the Rotterdam Study, a population-based cohort study. Interaction between these two polymorphisms and change in HbA1c levels was analyzed. Results: In incident metformin users with the OCT1 rs622342 AA genotype, no association was found between the MATE1 rs2289669 genotype and the HbA1c-lowering effect (p = 0.39). In users with the OCT1 rs622342 AC genotype a non-significant tendency was found between the MATE1 rs2289669 genotype and the HbA1c-lowering effect (p = 0.070), and in users with the OCT1 rs622342 CC genotype a significant association was found between the MATE1 rs2289669 genotype and the glucose-lowering effect of metformin (p = 0.005). Conclusion: The effect of the MATE1 rs2289669 genotype on the glucose-lowering effect of metformin is stronger in incident users with the rs622342 CC genotype than in incident users with the rs622342 AA genotype. In most patients, metformin will lower HbA1c levels sufficiently, except in patients with a reduced function of the OCT1 transporter and a normal function of the MATE1 transporter.