Dabigatran is an anticoagulant, it is a reversible direct thrombin inhibitor.


Indications for measuring +

  • Guide dose-adjustment towards optimal drug exposure in relation to drug efficacy and toxicity
  • Diagnosis
    • Disease resistant to drug vs inadequate drug exposure
    • Adverse drug reaction vs underlying disease
  • Assessing safety for upcoming intervention associated with increased risk of adverse drug reaction
  • Consider alternative gauges of drug effect depending on turnaround time of drug assay

How to measure

Assay details

See Canterbury Health Labs dabigatran etexilate assay information.

Timing of concentration sample collection

  • Sample should be taken as a trough concentration – i.e. sample taken just prior to next dose being due.
  • Consider the half-life in that person, steady state is reached between 3-7 days after commencing, or changing dose.

Alternatives to monitoring concentration

  • Dabigatran concentrations are measured in the toxicology laboratory routinely once a week. 
  • Coagulation testing is available for urgent clinical scenarios.
  • Thrombin time is sensitive to the presence of dabigatran and can be used clinically to exclude the presence of dabigatran e.g. in presence of clinically significant bleeding or perioperatively/preprocedural monitoring.
  • Other coagulation results (aPTT, INR) are less useful for estimating dabigatran concentration.  APTT or INR levels subtantially above the reference range should raise concerns of ‘over treatment’

How to interpret

Reference Range 

The trough concentration reference range is 30-130 ug/L in the CDHB assay.

This was determined by analysin gdata from RE-LY trial, in patients with AF randomised to fixed dose dabigatran (110 mg BD or 150 mg BD) not guided by routine coagulation monitoring.

  • 10th-90th centile trough monitoring after 1 month of treatment was 28-155 ug/L in 110 mg BD group, and 40-215 ug/L in 150 mg BD group.
  • Higher concentrations associated with lower embolic event rate (treatment failure) and higher major bleeding rate.
  • Optimal range of 30-130 ug/L derived from this data.

Higher or lower target concentrations can be used depending on indication and individual patient factors.

  • Drug exposure and concentrations in trials for different indications (VTE treatment and VTE prophylaxis) varied.
  • Individual patients may have higher or lower than average embolic risk or bleeding risk (consider factors in CHA2DS2-VASc/HAS-BLED scores) 

Factors that may give a false assay result

Idarucizumab, a humanised monoclonal antibody fragment, is used to reverse anticoagulant effects (dabigatran antagonist). It binds to free and thrombin-bound dabigatran with high affinity, neutralising the anticoagulant effects of dabigatran. The dabigatran assay does not  differentiate between free and idarucizumab-bound dabigatran. Hence, dabigatran concentrations should not be measured after use of idarucizumab.

For monitoring patients after treatment with idarucizumab , thrombin time should be used.

Dose individualisation and adjustment

The dabigatran concentrations increases in proportion to dose.

The Initial dose is selected based on clinical factors including age, renal function, concurrent medications, embolic risk, and bleeding risk. See drug information section below, and Hospital Health Pathways.

In an individual patient, dosing is directed by specific thromboembolic and bleeding risks to determine whether an overall benefit is likely.

Pharmacokinetics +

F: 0.07Vd (L/kg): 0.9Cl (L/h/kg): 1t½: 14 hours
Protein binding: 0.35Fe: ~0.8Metabolism glucuronidation

Drug interactions +

Pharmacokinetic interactions

  • Drugs inhibiting P-gp will increase the concentrations of dabigatran
    • e.g. itraconazole, clarithromycin, erythromycin, protease inhibitors, amiodarone, verapamil, diltiazem, cyclosporin, tacrolimus.
  • Drugs inducing P-gp will reduce the concentrations of dabigatran
    • e.g. intestinal P-glycoprotein induction – rifampicin, St John’s wort, carbamazepine, phenytoin, phenobarbital.
  • Drugs that increase intestinal pH will decrease dabigatran concentration
    • e.g. proton pump inhibitors.

Pharmacodynamic interactions

  • Anticoagulants – increased bleeding risk
  • Antiplatelets – increased bleeding risk
  • NSAIDs – increased bleeding risk
  • SSRIs – increased bleeding risk

Key References

Foerster KI, Hermann S, Mikus G & Haefeli WE (2020). Drug-drug interactions with direct oral anticoagulants. Clinical pharmacokinetics 59: 967-980.  https://link.springer.com/content/pdf/10.1007/s40262-020-00879-x.pdf


https://www.pinkbook.org.nz/index.htm?toc.htm?93361.htm#o93362 – p-glycoprotein inhibitors and inducers.

Chin PKL, Wright DFB, Patterson DM, Doogue MP & Beff EJ (2014). A proposal for dose-adjustment of dabigatran etexilate in atrial fibrillation guided by thrombin time. British Journal of Clinical Pharmacology 78(3): 599-609.

Chin PKL (2015). Which patients may benefit from dose adjustment of non-vitamin K antagonist oral anticoagulants? Seminars in Thrombosis and Hemostasis 41(2): 195-207.

Reilly PA, Lehr T, Haertter S, Connolly SJ, Yusef S, Eikelboom JW, Ezekowitz MD, Nehmiz G, Wang S, Wallentin L. The effects of dabigatran plasma concentrations and patient characteristics on the frequency of ischaemic stroke and major bleeding in atrial fibrillation patients in the RE-LY trial. Journal of the American College of Cardiology. 63: 321-328. https://www.medsafe.govt.nz/profs/datasheet/p/Pradaxacap.pdf


JK/PC 2020