Pharmacology and Coumadin dosing - Research Paper Example

Pharmacology and Coumadin dosing One of the most important and most influential fields in biology is pharmacogenomics, which is a recent revolutionary area that integrates the genomic information generated from DNA analysis and the pathophysiology of preventive medicine (Bhagat and Nhachi 9). Once an individual’s genetic profile in terms of disease risk and drug response is determined, a personalized approach to treatment and therapy may be designed. It is a novel field where the norm “one drug fits all” no longer holds true; and this is true in Coumadin dosing. Pharmacists must be very careful in their knowledge of their patient, and not dose too much or too littl. The concept of pharmacogenomics is based on “therapy with the right drug at the right dose in the right patient” (Mancinelli 84). The approach involves classification of patients according to their phenotypic disease profile into discrete subcategories, which are, in turn, defined by genetic variations associated with the disease, or drug response, or both (Persidis 8). One advantage to this type of approach is that drug therapy in genetically defined populations can be more effective and more importantly—less toxic than broad-range target populations. Therefore, using this focused approach individual dosing for medicine like Coumadin can be more focused, thus making sure there is no terrible side-effect for the patient. One decade ago, the application of genetically-defined drug therapy to different fields of medicine was weak. It was then observed that inter-individual differences in the genetic makeup dramatically alter the ability of inherent enzymes to deactivate pharmacological agents, which then lead to prolonged drug effects (Kalow 97). Other notable observations include differences in clearance time for certain drugs or modification of certain prescription drugs to active metabolites leading to a drug overdose, or a reduced capacity of a patient to reach plasma level of therapeutic range. Hence, the one-to-one relation of genotype to phenotype ratio may not be followed. The employment of pharmacogenetics in medicine involves two aspects. One involves the use of drug-responsiveness as a tool for a better understanding of complex genetic traits, and the other aspect concerns the role of genetic variation to individualized pharmacological therapy. This focus on the individual has created a safer focus on dosing medicine like Coumadin, which requires a very specific level for each individual patient. The conventional way of treating a specific illness involves a trial-and-error approach, which mainly aims to determine the correct drug and the optimal, minimal dose that will illicit a drug response yet avoid drug toxicity, as it was with coumadin dosing. It is a normal scenario that a certain percentage of patients will not completely respond to prescribed treatment. In addition, a certain percentage of those patients that respond to the prescribed drug treatment will experience a relapse or serious side effects that may prevent the patient from continuing the intake of the drug. Such results have triggered the design and creation of newer drugs yet each novel drug also generates its own novel side-effects. The field of pharmacogenomics may provide the capability to determine the most effective drug treatment based on the individual’s genetic profile (Goldstein 27). However, several investigations are needed to confirm and validate any variations in the target genes before a certain DNA sequence motif or pattern can be called a robust and reliable DNA marker for pharmacogenetic applications. This type of research involves screening a large population of patients for single-nucleotide polymorphisms in both target genes and at the same time, taking note of the patient’s response to the drug treatment (Arranz 82). Currently, personalized medicine has been limited to screening small patient populations for only a single nucleotide polymorphism or a small number of SNPs, also including coumadin dosing. Case-control studies are important to pharmacogenomic studies, as well as investigations on unresponsive patients. Researchers should, however, be very cautious during the implementation of pharmacogenomic studies, because there is a large chance of generating false-positive results alongside screening categories. Family-based approaches to pharmacogenomic studies are not that informative because it will only complicate analysis due to the addition of patterns of horizontal inheritance. Coumadin dosing has its own specific focus within the field of phramacogenmic studies. According to RX list: COUMADIN (crystalline warfarin sodium) is an anticoagulant which acts by inhibiting vitamin K-dependent coagulation factors. Chemically, it is 3-(α-acetonylbenzyl)-4-hydroxycoumarin and is a racemic mixture of the R- and S-enantiomers. Crystalline warfarin sodium is an isopropanol clathrate. The crystallization of warfarin sodium virtually eliminates trace impurities present in amorphous warfarin. Its empirical formula is C19H15NaO4 (RX List paragraph 1). Coumadin and warafin dosing is used for patients with mechanical prostatic heart valves. The human heart is a delicate organ and the dosing that the pharmacist must decide on must be exact. Dosing varies widely from individual to individual, and therefore the pharmacist will have to take this into account when working on the dose. The pharmacist must take into account the individual’s needs, backgrounds, and results on heart tests, because too much or too little of the drug can result in almost fatal affects. This is where the pharmacogenomic study of the individual will come into play. By posing pharmacogenomic tests on the individual needing the Coumadin dosing, a prescribed amount of the dose individualized for that patient can be provided. This will help prevent any toxicity or overdoes, or the other problem of too small of a dose, also not helpful to the patient. So, coumadin dosing is something a pharmacist must be careful about, and must educate himself about. Toxicity was already mentioned above, and issues with too heavy a dose could result in terrible toxicity levels. However, the pharmacist can make a specific decision about dosing by paying close attention to the patient’s needs and tests. Of course, there are advantages and disadvantages to this method. As with any drug that is so sensitive, Coumadin dosing measurements can be wrong, even with the most careful testing. Therefore, the individuals assigned to the dosing of the drug should be carefully watched and monitored when first prescribed the medication. While this can be costly and time consuming and is certainly a disadvantage of the drug, it is necessary to the patient’s health. The patient has to come first, no matter what the costs. However, as technology improves, and it constantly does, a clear advantage emerges. More than likely, the genetic tests used to determine these doses will become more and more precise. Because pharmacogenetics relies so much on the concept of technology, and technology always becomes better, the use of the tests themselves will improve. As in many fields, the technology will eventually catch up with the patient’s needs. Eventually, then, the tests themselves related to determining the level of Coumadin dosing will be more precise, and this means that more than likely only one test, and little monitoring of the patient will be required; this is in comparison to the current industry, in which much monitoring is required. As research in pharmacogenetics strengthens, more tests for robustness and reliability of data should be performed, in order to apply the findings in a clinical setting. For Coumadin dosing, the use of tests is critical in determining the factors relating to individual welfare, and whether the dosages are too heavy, or too little The amount of variance in each dose associated with a particular medical condition will be well-characterized and explained in terms of genetic mechanisms and control. Pre-treatment testing of patients for more specific molecular targets will be possible after testing, resulting in a quicker, more effective, and less costly treatment of medical heart conditions. Works Cited Arranz, Mary. Pharmacogenetic prediction of clozapine response. Lancet 355:1615–1616, 2000. Bhagat, Kim. Pharmacogenomics: today, tomorrow and beyond. Cent. Afr. J. Med. 45(12):335-7, 2001. “Coumadin. RX List. 12 March 2010. 18 May 2011. < http://www.rxlist.com/coumadin-drug.htm>. Goldstein Daniel. Potential genetic causes of heterogeneity of treatment effects. Am. J. Med. 120(4 Suppl 1):S21-5, 199. Kalow Walter. Pharmacogenetics in biological perspective. Pharmacol. Rev. 49:369-79, 1994. Mancinelli Lonnie. Pharmacogenomics: The promise of personalized medicine. AAPS PharmSci. 2(1):1-13, 2004. Novello Sam. Toward therapies tailored to patient characteristics. J. Thorac. Oncol. 2(5 Suppl):S38-41, 2007. Persidis Allan. Pharmacogenomics and diagnostics. Nat. Biotechnol. 16(8):791-2, 2001. Read More