<i>CYP2D6</i>Basic Genotyping of Patients with Chronic Pain Receiving Tramadol or Codeine. A Study in a Greek Cohort

Batistaki, Chrysanthi; Chrona, Eleni; Kostroglou, Andreas; Kostopanagiotou, Georgia; Gazouli, Maria

doi:10.1093/pm/pnaa122

Cited by 5 publications

(3 citation statements)

References 19 publications

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“…The intake of prodrugs, for example, codeine, requires satisfactory metabolism by CYP2D6 to be converted into its active substance (morphine). Thus, patients with slow metabolizing phenotypes may fail to achieve adequate analgesia and are predicted to develop more adverse reactions related to the accumulation of codeine ( 38 ). In this case, alternative drugs (non-CYP2D6 substrates), such as paracetamol, non-steroidal anti-inflammatory drugs (NSAIDs), or morphine, are recommended ( 39 ).…”

Section: Discussionmentioning

confidence: 99%

Pharmacogenes that demonstrate high association evidence according to CPIC, DPWG, and PharmGKB

Alshabeeb

Alyabsi²,

Aziz³

et al. 2022

Front. Med.

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BackgroundDifferent levels of evidence related to the variable responses of individuals to drug treatment have been reported in various pharmacogenomic (PGx) databases. Identification of gene-drug pairs with strong association evidence can be helpful in prioritizing the implementation of PGx guidelines and focusing on a gene panel. This study aimed to determine the pharmacogenes with the highest evidence-based association and to indicate their involvement in drug-gene interactions.MethodologyThe publicly available datasets CPIC, DPWG, and PharmGKB were selected to determine the pharmacogenes with the highest drug outcome associations. The upper two levels of evidence rated by the three scoring methods were specified (levels A–B in CPIC, 3–4 in DPWG, or 1–2 levels in PharmGKB). The identified pharmacogenes were further ranked in this study based on the number of medications they interacted with.ResultsFifty pharmacogenes, with high to moderately high evidence of associations with drug response alterations, with potential influence on the therapeutic and/or toxicity outcomes of 152 drugs were identified. CYP2D6, CYP2C9, CYP2C19, G6PD, HLA-B, SLCO1B1, CACNA1S, RYR1, MT-RNR1, and IFNL4 are the top 10 pharmacogenes, where each is predicted to impact patients' responses to ≥5 drugs.ConclusionThis study identified the most important pharmacogenes based on the highest-ranked association evidence and their frequency of involvement in affecting multiple drugs. The obtained data is useful for customizing a gene panel for PGx testing. Identifying the strength of scientific evidence supporting drug-gene interactions aids drug prescribers in making the best clinical decision.

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Section: Discussionmentioning

confidence: 99%

Pharmacogenes that demonstrate high association evidence according to CPIC, DPWG, and PharmGKB

Alshabeeb

Alyabsi²,

Aziz³

et al. 2022

Front. Med.

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“…Moreover, CYP2D6*2N patients exhibited increased risks of side effects. A prospective cohort study with 76 chronic pain patients receiving codeine or tramadol was conducted to assess the prevalence of CYP2D6 genotype among the cohort [104]. The authors analyzed the nine most common variants (CYP2D6 *2-6, *9, *10, *14, and *17), as well as those without polymorphic alleles (CYP2D6*1, wild type (wt)).…”

Section: Pharmacogenomics In Management Of Clbpmentioning

confidence: 99%

Can Implementation of Genetics and Pharmacogenomics Improve Treatment of Chronic Low Back Pain?

et al. 2020

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Etiology of back pain is multifactorial and not completely understood, and for the majority of people who suffer from chronic low back pain (cLBP), the precise cause cannot be determined. We know that back pain is somewhat heritable, chronic pain more so than acute. The aim of this review is to compile the genes identified by numerous genetic association studies of chronic pain conditions, focusing on cLBP specifically. Higher-order neurologic processes involved in pain maintenance and generation may explain genetic contributions and functional predisposition to formation of cLBP that does not involve spine pathology. Several genes have been identified in genetic association studies of cLBP and roughly, these genes could be grouped into several categories, coding for: receptors, enzymes, cytokines and related molecules, and transcription factors. Treatment of cLBP should be multimodal. In this review, we discuss how an individual’s genotype could affect their response to therapy, as well as how genetic polymorphisms in CYP450 and other enzymes are crucial for affecting the metabolic profile of drugs used for the treatment of cLBP. Implementation of gene-focused pharmacotherapy has the potential to deliver select, more efficacious drugs and avoid unnecessary, polypharmacy-related adverse events in many painful conditions, including cLBP.

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“…The supporting information can be downloaded at: . Adapted from Ballester et al, 2022 [ 50 , 51 , 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 , 60 , 61 , 62 , 63 , 64 , 65 , 66 ].…”

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confidence: 99%

Pharmacogenetic Guided Opioid Therapy Improves Chronic Pain Outcomes and Comorbid Mental Health: A Randomized, Double-Blind, Controlled Study

Agulló

Aguado²,

Muriel

et al. 2023

IJMS

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Interindividual variability in analgesic response is at least partly due to well-characterized polymorphisms that are associated with opioid dosing and adverse outcomes. The Clinical Pharmacogenetics Implementation Consortium (CPIC) has put forward recommendations for the CYP2D6 phenotype, but the list of studied drug-gene pairs continues to grow. This clinical trial randomized chronic pain patients (n = 60), referred from primary care to pain unit care into two opioid prescribing arms, one guided by CYP2D6, μ-opioid receptor (OPRM1), and catechol-O-methyl transferase (COMT) genotypes vs. one with clinical routine. The genotype-guided treatment reduced pain intensity (76 vs. 59 mm, p < 0.01) by improving pain relief (28 vs. 48 mm, p < 0.05), increased quality of life (43 vs. 56 mm p < 0.001), and lowered the incidence of clinically relevant adverse events (3 [1–5] vs. 1 [0–2], p < 0.01) and 42% opioid dose (35 [22–61] vs. 60 [40–80] mg/day, p < 0.05) as opposed to usual prescribing arm. The final health utility score was significantly higher (0.71 [0.58–0.82] vs. 0.51 [0.13–0.67] controls, p < 0.05) by improving sleepiness and depression comorbidity, with a significant reduction of 30–34% for headache, dry mouth, nervousness, and constipation. A large-scale implementation analysis could help clinical translation, together with a pharmaco-economic evaluation.

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CYP2D6Basic Genotyping of Patients with Chronic Pain Receiving Tramadol or Codeine. A Study in a Greek Cohort

Abstract: Objective To assess CYP2D6 genotype prevalence in chronic pain patients treated with tramadol or codeine. Design Prospective cohort study. Setting General hospital, pain management unit. Subjects Patients with chronic pain, treated with codeine or tramadol. … Show more

Cited by 5 publications

References 19 publications

Pharmacogenes that demonstrate high association evidence according to CPIC, DPWG, and PharmGKB

Pharmacogenes that demonstrate high association evidence according to CPIC, DPWG, and PharmGKB

Can Implementation of Genetics and Pharmacogenomics Improve Treatment of Chronic Low Back Pain?

Pharmacogenetic Guided Opioid Therapy Improves Chronic Pain Outcomes and Comorbid Mental Health: A Randomized, Double-Blind, Controlled Study

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