Oxycodone is an opioid analgesic commonly prescribed for managing moderate to severe acute or chronic pain. It binds to opioid receptors in the central nervous system, subsequently reducing pain perception and producing euphoria and relaxation.

According to the 2019 National Survey on Drug Use and Health (NSDUH), approximately 3.7 million people aged 12 or older in the United States reported misusing prescription pain relievers, including oxycodone, in the past year. This represented 1.4% of the population in this age group.

While exact statistics on oxycodone addiction rates can be challenging to find, a study published in the journal "Addiction" in 2017 estimated that about 1.7 million people in the United States had a prescription opioid use disorder in 2015. This number includes individuals addicted to various prescription opioids, including oxycodone.

Given the potential consequences, there is a growing interest in integrating pharmacogenetic testing into clinical practice to improve patient care. By determining an individual's metabolizer status before prescribing opioids like oxycodone, healthcare providers can optimize dosing and medication selection, reducing the risk of adverse effects and improving overall pain management.

CYP2D6, or Cytochrome P450 2D6, is an enzyme responsible for the metabolism of up to 25% of pharmaceutical drugs including Oxycodone. Based on their CYP2D6 gene variations, individuals can be categorized into four main phenotypes:

1. Poor metabolizers (PMs): These individuals have little or no CYP2D6 enzyme activity due to two non-functional alleles. They may not effectively metabolize oxycodone, leading to increased drug levels in the bloodstream and a higher risk of side effects. Poor metabolizers may require lower doses of oxycodone or alternative pain management strategies. The standard dosage may result in higher-than-expected drug levels in the bloodstream, increasing the risk of side effects such as respiratory depression, sedation, and even overdose.
2. Intermediate metabolizers (IMs): These individuals have reduced CYP2D6 enzyme activity due to the presence of one functional and one non-functional allele or two reduced-function alleles. They may metabolize oxycodone more slowly than extensive metabolizers, potentially increasing the risk of side effects. Intermediate metabolizers may require lower doses of oxycodone or alternative pain management strategies
3. Extensive metabolizers (EMs): These individuals have normal CYP2D6 enzyme activity due to the presence of two functional alleles. They are considered the "normal" metabolizers and typically metabolize oxycodone effectively, experiencing standard drug efficacy and side effects.
4. Ultra-rapid metabolizers (UMs): These individuals have increased CYP2D6 enzyme activity due to multiple copies of functional alleles. They may metabolize oxycodone more rapidly than extensive metabolizers, potentially reducing the drug's effectiveness and increasing the risk of withdrawal symptoms. Ultra-rapid metabolizers may require higher doses or alternative medications to achieve adequate pain relief.

Ultra-rapid metabolizers, may experience a reduced duration of pain relief and a higher rate of drug clearance, which could potentially lead to the need for more frequent dosing or higher doses to achieve adequate analgesia. This increased dosing pattern may raise the risk of developing dependence or addiction.

On the other hand, poor and intermediate metabolizers may be more sensitive to the side effects of oxycodone, including its euphoric and rewarding properties. This heightened sensitivity might increase the risk of misuse, as individuals may be more susceptible to the positive reinforcing effects of the drug.