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VOLUME 9 NUMBER 1 • MARCH 2012
PATIENT INFORMATION LEAFLET
SA JOURNAL OF DIABETES & VASCULAR DISEASE
signed to augment, not eliminate, testing and therapy management that
is overseen by a doctor. Patients who self-test must notify their doctors
of clotting time results so they can make the proper adjustments to their
medication.
Patients interested in finding out more about self-testing their PT/INR
should talk to their doctors.
For more information on the CoaguChek XS system for patient self-
testing, visit www. ASmartWayToTest.com.
INTERACTION WITH OTHER MEDICATIONS: AN EASY FORMAT
FOR PATIENT EDUCATION
Using broad classes of drugs and including common entities that either
enhance or reduce warfarin’s anti-coagulant efficacy, clinicians can sim-
plify patient education. The A–S list below could be useful.
Enhancers of warfarin efficacy
Alcohol: occasional large intake of alcohol is likely to enhance briefly
•
the effects of warfarin, but more importantly, regular immoderate
intake potentiates warfarin activity, especially if liver functions are
compromised.
Anabolic steroids potentiate warfarin effects.
•
Analgesics
•
− Non-steroidal anti-inflammatory type (NSAIDs): the anti-aggregatory
effects of the NSAIDs on platelets are likely to play a major role in adding
to the anticoagulant activity of warfarin. Their effects are largely dose
dependent, and aspirin is a prominent offender. It seems that meloxi-
cam, nabumetone and naproxen are much less inclined to interact in
this manner. It should be noted that extensive use of topical NSAIDs may
also enhance warfarin efficacy.
− Paracetamol, once thought to be unlikely to interact with warfarin, is
now known to be a major potentiator of the anticoagulant effect. How-
ever, low, single or infrequent therapeutic doses of paracetamol are
documented as unlikely to have any anticoagulant-potentiating activity.
− Opioids: propoxyphene and tramadol may well enhance the ef-
ficacy of warfarin, but careful observation for such effects is needed
with all high-dose prolonged use of opioids.
Anaesthetics of the inhalational type: broadly speaking, great caution
•
is recommended when these agents are utilised in persons receiving
warfarin. Note that propofol may reduce the efficacy of warfarin.
Anti-arrhythmics: notable in this category are amiodarone, disopyra-
•
mide, propafenone and quinidine.
Anti-infective agents: in this very large category (including quinine),
•
most potentiate warfarin. However, cloxacillins, rifampins, griseofulvin,
ribavirin and terbinafine reduce the activity of warfarin.
Anticonvulsants: while most enhance warfarin efficacy, the barbiturate
•
type, cabamazepine and phenytoin may reduce the activity of warfarin.
Antidepressants: those that are selective serotonin re-uptake inhibitors
•
are the most likely culprits from among the antidepressant category.
Antithyroid agents have been implicated in enhancing, but also in di-
•
minishing warfarin efficacy.
Antidiabetic agents (oral): especially the sulphonylurea types.
•
Antiplatelet agents: all chemical entities with antiplatelet activity, in-
•
cluding fish oil concentrates and many herbal substances, such as
ginseng, ginkgo biloba, aloe, dandelion, cranberry and garlic should
be avoided.
Beta-blockers: atenolol and propranolol are the most frequent offend-
•
ers in this category, but others may not be exempt.
Botanicals: a vast variety of botanical/herbal preparations potentiate
•
the activity of warfarin by their coumarin-type activity and/or via their
antiplatelet effects. Significant effects usually are associated with regu-
lar use.
Corticosteroids: prolonged high doses.
•
Fibrates: such as fenofibrate.
•
Gastric acid suppressants: cimetidine and the azole-type proton-pump
•
inhibitors are the major offenders.
Statins: simvastatin, lovastatin and possibly fluvastatin enhance war-
•
farin activity, while the effects of pravastatin are likely to be unpredict-
able.
Reducing warfarin’s efficacy
These include antacids (non-absorbable), antihistamines (many), an-
•
tipsychotics (many), barbiturates, carbamazepine, chlordiazepoxide,
cloxacillins, griseofulvin, meprobamate, oral contraceptives, phenytoin,
rifampins, selective oestrogen receptor modulators, spironolactone, St
John’s wort, thiouracils, trazodone, ubiquinone (co-enzyme Q
10
), vita-
min C (high dosage), vitamin K, and food items rich in vitamin K.
References
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1.
et al
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Genetic determinants of response to warfarin during initial anticoagulation.
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VKORC1- Rational and perspectives.
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et al
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Corporation, 2006.
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