Initiation of glucose-lowering treatment decreases international normalized ratio levels among users of vitamin K antagonists: a self-controlled register studyVisa övriga samt affilieringar
2016 (Engelska)Ingår i: Journal of Thrombosis and Haemostasis, ISSN 1538-7933, E-ISSN 1538-7836, Vol. 14, nr 1, s. 129-133Artikel i tidskrift (Refereegranskat) Published
Resurstyp
Text
Abstract [en]
Background: It is not known whether initiation of antidiabetic treatment affects the effect of vitamin K antagonists (VKAs). It was previously shown that metformin affects the effect of one VKA, phenprocoumon. Objectives: The aim of this study was to determine if initiation of glucose-lowering treatment affects the international normalized ratio (INR) and dose requirements of the anticoagulant VKAs warfarin and phenprocoumon. Patients/methods: We performed a self-controlled retrospective register-based study. A total of 118 patients commencing glucose-lowering treatment while being treated with warfarin or phenprocoumon were included in the study. We compared INR, dose/INR and proportion of patients with at least one sub-therapeutic INR measurement before and after initiation of glucose-lowering treatment. Results: Initiation of glucose-lowering treatment caused mean INR to decrease from 2.5 to 2.2 (decrease of -0.3 [95% CI: -0.1; -0.5]) and led to more than half of the patients having at least one sub-therapeutic INR measurement. Six to 12 weeks later, the VKA dose/INR was increased by 11%, indicating a weakened effect of the VKA. Conclusion: Initiation of glucose-lowering treatment reduces the anticoagulant effect of VKAs to an extent that is likely to be clinically relevant. This finding needs confirmation and mechanistic explanation.
Ort, förlag, år, upplaga, sidor
2016. Vol. 14, nr 1, s. 129-133
Nyckelord [en]
antidiabetic drugs, drug interactions, pharmacoepidemiology, phenprocoumon, warfarin
Nationell ämneskategori
Hematologi Kardiologi
Identifikatorer
URN: urn:nbn:se:uu:diva-282396DOI: 10.1111/jth.13187ISI: 000370661100015PubMedID: 26559049OAI: oai:DiVA.org:uu-282396DiVA, id: diva2:917018
Forskningsfinansiär
AstraZeneca2016-04-052016-04-052017-11-30Bibliografiskt granskad