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Abstract
Adverse drug reactions still pose an important clinical problem. Dihydropyrimidine dehydrogenase (DPD) is an enzyme that regulates 5-FU quantities available for anabolic processes and hence affects its pharmacokinetics, toxicity and efficacy. There are several studies describing a hereditary (pharmacogenetic) disorder in which individuals with absent or significantly reduced DPD activity may even develop a life-threatening toxicity following exposure to 5-FU. The most common mutation is known as the DPYD*2A or as the splice-site mutation (IVS14 + 1G A) leading to creation of a dysfunctional protein. An objective behind the study was to ascertain existence of the IVS14 + 1G A mutation among the population of Bosnia and Herzegovina. Our research has undeniably attested to existence of one heterozygote for the DPYD gene mutation, i.e. one heterozygote for IVS14 + 1 G > A, DPYD*2A mutation.
Highlights
Adverse drug reactions still pose an important clinical problem. erein, it was estimated that in the last decade alone they caused over, deaths annually in the United States
fluoro ’deoxyuridine- ’-monophosphate (FdUMP) acts as an inhibitor of the thymidylate synthetase (TS), causing an intracellular accumulation of the deoxyuridine monophosphate and a reduction in a level of deoxythymidine monophosphate
This induces an arrest of a DNA synthesis. e initial and rate-limiting enzyme in the catabolism of the -FU is dihydropyrimidine dehydrogenase (DPD) that catalyses a -FU reduction into, -dihydrofluorouracil (DHFU). en on, DHFU is degraded down to fluoro-β-ureido propionic acid (FUPA) and flouro-β-alanine (FBAL) ( )
Summary
Adverse drug reactions still pose an important clinical problem. erein, it was estimated that in the last decade alone they caused over , deaths annually in the United States. Ere is a direct link between therapeutical effects and toxicity of -FU and the drug’s anabolic process related to nucleotides. This may inhibit activities of thymidylate synthetase or incorporate -FU into RNA and/or DNA. FdUMP acts as an inhibitor of the thymidylate synthetase (TS), causing an intracellular accumulation of the deoxyuridine monophosphate (dUMP) and a reduction in a level of deoxythymidine monophosphate (dTMP). This induces an arrest of a DNA synthesis. This induces an arrest of a DNA synthesis. e initial and rate-limiting enzyme in the catabolism of the -FU is dihydropyrimidine dehydrogenase (DPD) that catalyses a -FU reduction into , -dihydrofluorouracil (DHFU). en on, DHFU is degraded down to fluoro-β-ureido propionic acid (FUPA) and flouro-β-alanine (FBAL) ( )
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