Potential interaction between @entity11271 and @entity3522 , @entity1623 and XXXX and role of @entity5060 genotype.

@entity1 @entity11271 @entity548 @entity1423 @entity1524 @entity3522 @entity5018 @entity1623 @entity5060 @entity715 @entity1229
NSAIDs are reported to increase the risk of @entity548 in @entity1524 users. The mechanism underlying this risk is inhibition of @entity1423 , however a pharmacokinetic mechanism resulting in an increased International Normalised Ratio (INR) was proposed in some case reports in @entity1229 treated @entity1 . In this retrospective cohort study the influence of @entity3522 , @entity1623 and @entity5018 on the INR of outpatients stabilised on @entity11271 therapy was investigated. We also determined the role of @entity5060 ( @entity5060 ) polymorphism on @entity1524 dosage and INR in NSAID users. The study was carried out at the Groningen Outpatient @entity715 Service. A retrospective cohort study among @entity1 who received both @entity11271 and one of the NSAIDs under study was performed. @entity1 whose INR rose above the upper level of the therapeutic range (INR above 3.5 or 4.0) after an NSAID under study was added to the @entity11271 therapy, were compared with @entity1 who did not show such an elevation. A two-sample t-test (average @entity11271 dosage, age), and chi-square tests (sex, therapeutic range, type of NSAID) were used to test for differences. Genotyping was carried out by analysing blood samples for the relevant @entity5060 alleles. The study population consisted of 112 @entity1 on stable @entity11271 therapy, of which 52 (46%) showed an elevation of the INR above the desired therapeutic level (INR 3.5 and 4.0 respectively) after the start of an NSAID under study. In 12 @entity1 , the INR increased above 6. The INR of the other 60 @entity1 (54%) remained constant after the start of one of the NSAIDs under study. There were no statistically significant differences between @entity1 with increased INR and @entity1 without increased INR with regard to age, sex, therapeutic range and average @entity11271 dosage. Eighty @entity1 , of whom 36 showed an increased INR as a result of a potential @entity11271 -NSAID drug interaction, were included in the genotyping study. No association between @entity5060 genotype and an increased INR as a result of the drug-drug interaction was found. In nearly half of a cohort of elderly @entity1 , the INR increased beyond the therapeutic range (INR 3.5 or 4.0) as a result of a potential pharmacokinetic drug-drug interaction between @entity11271 and @entity3522 , @entity1623 and @entity5018 . The average increase in INR was between 1 and 4. Polymorphism of @entity5060 does not seem to be a relevant risk factor for the NSAID- @entity11271 interaction.
