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Background: Few new psychiatric drugs have entered the market in recent decades; in contrast, the number of drugs carrying pharmacogenomic labels continues to increase. For the foreseeable future, the advancement of psychiatry and drug therapy may hinge on personalized treatment. Currently, antipsychotic or antidepressant choices rely heavily on the clinical experience of psychiatrists and potentially lengthy iterative trials. During these trials, the clinical response to treatment in acutely depressed patients can be assessed only after several weeks of exposure to the drug. Although pharmacogenomic testing has been used in clinical care for several years, most Chinese clinicians struggle to utilize the information accurately, resulting in expensive tests that provide little real benefit to patients. Here, we demonstrate how to combine the results of pharmacogenomic testing to develop an individualized treatment plan. Our goal is to find the optimal medication regimen and dosage for the patient in the shortest possible time, control symptoms as soon as possible, and predict adverse drug reactions. This approach aims to offer a practical therapeutic idea for clinical practice.
Case Presentation: We present the case of a 27-year-old female patient experiencing a relapse of depression. Despite previous attempts with empiric medication, her symptoms remained uncontrolled, leading to exacerbation and drug withdrawal reactions. Utilizing the results of pharmacogenetic testing, we crafted an individualized treatment plan, resulting in rapid remission without any adverse drug reactions.
Conclusion: Recognizing the complexity of antidepressant response, our patients aim to improve their understanding, as well as that of other healthcare providers, by undergoing pharmacogenomics testing. This enhances the credibility of their medication choices. While pharmacogenomics is just one aspect considered in selecting a treatment regimen for depression, it remains a valuable tool for increasing credibility and mitigating potential adverse events.
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http://dx.doi.org/10.1186/s12888-025-06481-4 | DOI Listing |
CNS Drugs
September 2025
Global Health Neurology Lab, Sydney, NSW, 2150, Australia.
Acute ischemic stroke (AIS) remains a leading cause of mortality and long-term disability globally, with survivors at high risk of recurrent stroke, cardiovascular events, and post-stroke dementia. Statins, while widely used for their lipid-lowering effects, also possess pleiotropic properties, including anti-inflammatory, endothelial-stabilizing, and neuroprotective actions, which may offer added benefit in AIS management. This article synthesizes emerging evidence on statins' dual mechanisms of action and evaluates their role in reducing recurrence, improving survival, and mitigating cognitive decline.
View Article and Find Full Text PDFToxicol Mech Methods
September 2025
Cellular and Molecular Biology Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran.
Fluoropyrimidines are a class of chemotherapy drugs used to treat various solid tumors. 5-Fluorouracil (5-FU) an antimetabolite in the fluoropyrimidine family, which has shown remarkable efficacy against a variety of solid tumors, is a crucial medication in the treatment of cancer. However, severe organ toxicities frequently restrict its therapeutic potential.
View Article and Find Full Text PDFFront Biosci (Landmark Ed)
August 2025
Animal Genetics, University of Tuebingen, 72076 Tuebingen, Germany.
Background: Membrane transport proteins are critical determinants of systemic and intracellular drug levels, thereby contributing substantially to drug response and/or adverse drug reactions. Therefore, the U.S.
View Article and Find Full Text PDFClin Biochem
September 2025
Department of Pathology and Laboratory Medicine, University of Saskatchewan, Saskatoon, SK S7N 5E6, Canada; Department of Pathology and Laboratory Medicine, Saskatchewan Health Authority, Saskatoon, SK S7M 0Z9, Canada. Electronic address:
Background: 5-Fluorouracil (5-FU) and its pro-drug, capecitabine, are widely used to treat solid tumors. Patients with dihydropyrimidine dehydrogenase (DPYD) deficiency are at increased risk for severe treatment-related toxicity. This study reported the implementation of DPYD genotyping in clinical practice and assessed the impact of genotype-guided dosing on clinical outcomes.
View Article and Find Full Text PDFClin Pharmacol Ther
September 2025
Molecular Brain Science Department, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Tanenbaum Centre for Pharmacogenetics, Toronto, Ontario, Canada.
Pharmacogenomics enables the personalization of drug therapy by linking genetic variations to differences in drug metabolism, efficacy, and risk of adverse reactions. Genetic polymorphisms within cytochrome P450 (CYP) genes significantly affect enzyme activity, influencing drug plasma levels, responses, and safety. Central to this process is accurate genotype-to-phenotype translation, especially for the CYP enzyme family, which metabolizes 70-80% of clinically used drugs.
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