PHARMACOGENETICS

    This refers to the influence of genes on the determination of the response to drug therapy. The responses may take the form of an exaggerated physiological response to a drug, resistance to the effect of drugs or an increased frequency of side effects. In some instances pharmacological agents may trigger and precipitate the effects of certain genetic disorders. Other factors which influence the effects of drugs are the ethnic background and specific HLA groups.

    Genes affecting drug metabolism
    Polymorphism of certain genes can significantly affect the activities of certain enzymes that are crucial in the metabolism of certain drugs. Acetylation is critical for the metabolism of many drugs. Polymorphisms in the rate of acetylation in different patients lead to different effects for the same drug. If a patient with tuberculosis is treated with isoniazid and the patient has a phenotype for slow acetylation, the increased levels of the drug in circulation due to the defect will lead to a peripheral neuropathy even with conventional doses. On the other hand, a patient on such treatment, with a phenotype for rapid acetylation will be inadequately treated due to the rapid breakdown of the drug and reduced blood levels and may become more prone to a recurrence of tuberculosis.

    The gene for malignant hyperthermia is dominant and on chromosome 19. Patients carrying this mutated gene when exposed to the anaesthetic agent halothane, produces muscle spasms and hyperthermia with subsequent acidosis. Tests are available for individuals at risk to verify their state.

    Adverse reactions to drugs may be controlled or influenced by genes in the HLA region which in turn influence the immune response. For example patients receiving gold therapy who have the haplotype DRW3 are more likely to have side effects than those who do not have this HLA haplotype.

    Another example seen during anaesthesia is succinylcholine sensitivity. In normal individuals the enzyme cholinesterase hydrolyses choline esters which include acetylcholine, and succinylcholine which is a widely used muscle relaxant. Affected individuals are homozygous for a defective cholinesterase gene (atypical cholinesterase allele), which result in an inability to break down succinylcholine. Such people develop prolonged muscle relaxation and apnoea after anaesthesia with succinylcholine. The abnormal cholinesterase can be detected by laboratory tests.


Copyright Prof. Rohan W Jayasekara. (1st Published 1996, 2nd Edition 1998)
The Internet Edition was designed by Dr. Vajira H. W. Dissanayake. (1st Internet Edition 1998)
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