Kashi Health offers testing for pain management biomarkers to help maximize the effectiveness of analgesic drug use. Managing chronic pain is a challenge for healthcare providers because of each patient’s unique tolerance to pain and differing reactions to prescribed medications. Unpleasant opioid side effects, such as nausea, vomiting, constipation and sedation, are common with pain management medication. The side effects can lead to work absences, poor work performance, the risk of job loss, and a diminished quality of life. An individual’s genetic makeup may predispose them to adverse effects of pain and reduced efficacy of medications. Pharmacogenomics may help connect the dots towards mitigating adverse drug reactions among genetically-vulnerable individuals and provide information for improved dosage recommendations for therapeutic effect.

Variant alleles for genes in the CYP pathway are common. However, prevalence differs among ethnic populations. For example, when considering CYP2D6, up to 20 percent of African Americans, and 10 percent of Caucasians have the poor metabolizer phenotype, whereas this phenotype is rarely observed in Asians. Because of this large variation in patient phenotypes it is important to determine each individual’s unique genetic background in order to help predict their response to pain medications.

Genetic Markers Included in the PGx Comprehensive Panel

CYP2D6Key role in the metabolism of opioids including: codeine, tramadol, and oxycodone
CYP2C19Impacts dosages requirements for tricyclic antidepressants
CYP2C9Crucial to the breakdown of NSAIDS including: diclofenac, naproxen, and ibuprofen
COMTEffects morphine dosage requirements and perceptions of pain

Ideal Candidates are Patients with the Following Symptoms or Conditions

  • Patients with decreased adverse drug reactions
  • New patients with mood related symptoms to provide reduced trial and error period for an effective medication

Example Table of CYP Metabolizers by Phenotype

Results from Kashi Health’s Pain Management Panel classify patients by how effectively a patient is likely to metabolize a medication. This classification is based on how many copies of functional or variant alleles inherited. In general, the genetic variability of CYP genes can be grouped into four phenotypes: ultra-rapid metabolizers (UM), normal (extensive) metabolizers (EM), intermediate metabolizers (IM) and poor metabolizers (PM).
Ultra-rapid metabolizer (UM)Increased enzymatic activity due to duplications or multiplications of the functional allele
Extensive metabolizer (EM)Normal enzymatic activity due to the presence of at least one functional allele
Intermediate metabolizer (IM)Moderately-decreased enzymatic activity with either two decreased activity alleles or one decreased activity allele and one null allele
Poor metabolizer (PM)Lack of enzyme activity as a result of two null (non-functional) alleles

Limitations of Pharmacogenomics

Interactions with environmental elements and other medications need to be taken into consideration with the genetic makeup of the patient when determining efficacy of a drug. Rare genetic differences may not be detected because the panel screens for the most common and well documented gene variants. Read Scientific References

For more information about the clinical implications of pharmacogenomics please visit: www.pharmgkb.org.

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