Late-life depression (LLD) is a major depressive disorder which affects individuals over the age of 60. It is frequently associated with an ineffective response to antidepressants and polypharmacy. Pharmacogenomics provides a tool for HCPs to determine the genetic cause of response rates and side effects to antidepressants ^3,4.

Polypharmacy is a common issue faced by, but not limited to, the elderly. Pharmacogenomics testing would provide a more logical and empirical approach to polypharmacy by helping alleviate adverse effects from both drug-gene and drug-drug interactions⁵.

Positive pharmacogenomic findings have been found for the majority of cardiovascular drugs, which suggests that testing prior to treatment can improve efficacy and minimise the risk of toxicity⁶ and/ or treatment resistance.

In roughly 80% of cases, the cause of Steven Johnson Syndrome (SJS), a rare and serious disorder of the skin and mucous membranes, is based on a reaction to carbamazepine (CBZ) and CBZ-related drugs (i.e. phenytoin and lamotrigine). The majority of these reactions has been linked to a genetic variant on the HLA-B gene (which provides instructions for making a protein that plays a critical role in the immune system). Carriers of the HLA-B*15:02 allele have a strong association with SJS related to the use of the above-mentioned drugs. The presence of the HLA-B*15:02 allele puts an individual at a 25% increased risk of having a SJS when administered with CBZ. SJS can result in death or ICU for protracted periods of time. Knowing the risk upfront means preventing these severe reactions and hospitalisation. The FDA recommends that prior to initiating carbamazepine therapy, testing for HLA-B*15:02 should be performed in patients with ancestry in populations in which it may be present and that CBZ should not be used in patients positive for HLA-B*15:02 unless the benefits clearly outweigh the risks⁷.

5-Fluorouracil (5-FU) is a medicine used to treat symptoms of breast cancer, as well as cancers of the colon, stomach, and pancreas. Due to the severity of reactions for some individuals to these medications, the international recommendation is to test before administering. There are four known allelelic variants in the DPYD gene with a strong association for severe adverse reactions to 5-FU, capecitabine, and other analogues.

The prevalence of DPD deficiency, based on activity levels measured in blood cells and the uracil breath test, has been reported as 3%-5% in patients of European origin and 8% in patients of African origin. In addition, the US National Library of Medicine reports a prevalence of partial deficiency of 2%-8%, based on the aforementioned study and others^8,9.