Medication management
oncologists, and nurses, and delayed the patient’s treatment. Both errors, (see if you can spot them), can be prevented using ePMA solutions. While no clinical incident occurred, it is symptomatic of the large volume of ‘below the radar’ resource and time-hungry errors that frequently occur with paper-based medicines systems, in addition to those that do result in patient harm. Certainly, ePMA solutions that form part
of the broader electronic patient record are increasingly being adopted by secondary care organisations and are mitigating many of the adverse errors associated with paper-based systems. However, new and emerging science and technologies suggest that what we have today are just the foundations for what is emerging in relation to personalised medicine.
Pharmacogenomics Genomics, the study of DNA to understand its impact upon health, remains an evolving science with a set of technologies that will continue to evolve for the foreseeable future. However, appreciation for the transformational potential of genomics for the prediction, treatment, and management of disease is well recognised and undisputed. The use of genomics as a routine frontline clinical intervention is increasingly being articulated and strategised by national healthcare services and governmental bodies in the UK, European Union, US, and Australasia - to name but a few. Pharmacogenomics, a sub-specialty of genomics, is focused on understanding the relationship between genes and how well a person may respond to medications. Some people may respond well, others not at all, and others may develop adverse side-effects
Carbamazapine
Patients of Southeast Asian origin have a higher incidence of variances in the HLA-B*15:02 gene leading to toxic responses such as life-threatening Stevens—Johnson syndrome and toxic epidermal necrolysis (SJS-TEN)
5-Fluororacil
10-40% of patients develop serious adverse reactions due to a variation of the DYPD gene. Testing for the variant helps to set the appropriate dose for the patient
Gentamicin Codeine
Patients with a variation of the RNR1 gene can suffer permanent hearing loss (irreversible deafness for neonates) following the administration of gentamicin
Patients with a variation of the CYP2D6 gene can be poor or ultra-metabolisers of codeine resulting in subtherapeutic responses (pain is poorly managed) or toxicity resulting in life-threatening responses
Clopidogrel
Patients with a variation of the CYP2C19 are at an increased risk of major cardiovascular events such as stent thrombosis
Table 1 – Example medication responses based upon genomic profile
It is estimated that at any given time in England alone there are the equivalent of seven 800 bed hospitals filled with patients who have had adverse medication responses (including sub-therapeutic) purely based upon patient genomic profiles.
that include fatal or life changing responses. This can be the result of many factors, but it is increasingly understood that a person’s genes have a significant determination for how they respond to medications. Medicines are currently prescribed as a ‘one-size-fits-all’ approach, with dosing
regimens being categorised by broad groupings that include age, gender, body surface area, blood results, and clinical observations. Yet people with exactly the same profiles in these groupings can respond very differently to the same medication prescribed with the same route, dose, frequency, and duration. Pharmacogenomics has identified three
categorisations of patients based upon their genomic profile. l Poor metabolisers: These individuals have genetic variations that result in reduced enzyme activity responsible for metabolising certain drugs. As a result, they metabolise drugs at a slower rate than average. This can lead to higher drug concentrations in the body, potentially increasing the risk of adverse effects or toxicity. Poor metabolisers may require lower doses or alternative medications that are metabolised differently.
l Intermediate metabolisers: This group has some functional enzyme activity but at a reduced rate compared to normal metabolisers. Their ability to metabolise certain drugs falls between that of poor metabolisers and normal metabolisers. This can result in variability in drug response and may require dose adjustments based on
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www.clinicalservicesjournal.com I June 2024
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