PMID- 21073556
OWN - NLM
STAT- MEDLINE
DCOM- 20110114
LR  - 20220129
IS  - 1365-2796 (Electronic)
IS  - 0954-6820 (Linking)
VI  - 268
IP  - 6
DP  - 2010 Dec
TI  - Antiplatelet drug interactions.
PG  - 516-29
LID - 10.1111/j.1365-2796.2010.02299.x [doi]
AB  - Both laboratory studies in healthy volunteers and clinical studies have suggested 
      adverse interactions between antiplatelet drugs and other commonly used 
      medications. Interactions described include those between aspirin and ibuprofen, 
      aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), and the 
      thienopyridine, clopidogrel, and drugs inhibiting CYP2C19, notably the proton 
      pump inhibitors (PPI) omeprazole and esomeprazole. Other interactions between 
      thienopyridines and CYP3A4/5 have also been reported for statins and calcium 
      channel blockers. The ibuprofen/aspirin interaction is thought to be caused by 
      ibuprofen blocking the access of aspirin to platelet cyclo-oxygenase. The 
      thienopyridine interactions are caused by inhibition of microsomal enzymes that 
      metabolize these pro-drugs to their active metabolites. We review the evidence 
      for these interactions, assess their clinical importance and suggest strategies 
      of how to deal with them in clinical practice. We conclude that ibuprofen is 
      likely to interact with aspirin and reduce its anti-platelet action particularly 
      in those patients who take ibuprofen chronically. This interaction is of greater 
      relevance to those patients at high cardiovascular risk. A sensible strategy is 
      to advise users of aspirin to avoid chronic ibuprofen or to ingest aspirin at 
      least 2 h prior to ibuprofen. Clearly the use of NSAIDs that do not interact in 
      this way is preferred. For the clopidogrel CYP2C19 and CYP3A4/5 interactions, 
      there is good evidence that these interactions occur. However, there is less good 
      evidence to support the clinical importance of these interactions. Again, a 
      reasonable strategy is to avoid the chronic use of drugs that inhibit CYP2C19, 
      notably PPIs, in subjects taking clopidogrel and use high dose H2 antagonists 
      instead. Finally, anti-platelet agents probably interact with other drugs that 
      affect platelet function such as selective serotonin reuptake inhibitors, and 
      clinicians should probably judge patients taking such combination therapies as at 
      high risk for bleeding.
CI  - (c) 2010 The Association for the Publication of the Journal of Internal Medicine.
FAU - Mackenzie, I S
AU  - Mackenzie IS
AD  - Medicines Monitoring Unit (MEMO), Division of Medical Sciences, University of 
      Dundee, Ninewells Hospital & Medical School, Dundee, UK.
FAU - Coughtrie, M W H
AU  - Coughtrie MW
FAU - MacDonald, T M
AU  - MacDonald TM
FAU - Wei, L
AU  - Wei L
LA  - eng
GR  - G106/1249/MRC_/Medical Research Council/United Kingdom
PT  - Journal Article
PT  - Review
DEP - 20101114
PL  - England
TA  - J Intern Med
JT  - Journal of internal medicine
JID - 8904841
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Platelet Aggregation Inhibitors)
RN  - R16CO5Y76E (Aspirin)
SB  - IM
MH  - Anti-Inflammatory Agents, Non-Steroidal/adverse effects
MH  - Aspirin/adverse effects
MH  - Drug Interactions
MH  - Evidence-Based Medicine/methods
MH  - Humans
MH  - Pharmacoepidemiology
MH  - Platelet Aggregation Inhibitors/*adverse effects
MH  - Randomized Controlled Trials as Topic/methods
EDAT- 2010/11/16 06:00
MHDA- 2011/01/15 06:00
CRDT- 2010/11/16 06:00
PHST- 2010/11/16 06:00 [entrez]
PHST- 2010/11/16 06:00 [pubmed]
PHST- 2011/01/15 06:00 [medline]
AID - 10.1111/j.1365-2796.2010.02299.x [doi]
PST - ppublish
SO  - J Intern Med. 2010 Dec;268(6):516-29. doi: 10.1111/j.1365-2796.2010.02299.x. Epub 
      2010 Nov 14.