What is the Gage warfarin algorithm?

The Gage algorithm (Gage et al, Clinical Pharmacology & Therapeutics, 2008) is a validated pharmacogenetic model that predicts a patient's warfarin maintenance dose. It combines body surface area, age, CYP2C9 and VKORC1 genotype, and interacting factors such as amiodarone, smoking status and indication to estimate the weekly dose.

Do I need genetic testing to use it?

No. Genotype fields are optional. If CYP2C9 or VKORC1 results are unavailable, leave them as wild type or unknown and the estimate uses clinical factors alone. Genetic data, when present, refines the prediction because both genes strongly influence warfarin sensitivity.

Why is body surface area used instead of weight alone?

The Gage model uses Mosteller body surface area, calculated as the square root of (height in cm times weight in kg, divided by 3600). Surface area correlates better with warfarin volume of distribution than weight alone, so the algorithm uses it as the size term.

Is this a loading dose?

No. The output is an estimated maintenance dose, not an initial loading regimen. Loading typically follows a separate protocol with frequent INR checks. Always titrate the final dose to the patient's measured INR rather than relying on any prediction.

Can I use this for a patient already on warfarin?

It is intended for dose initiation. For a patient already stabilised, the best predictor of future dose is their current dose plus INR trend. Use this estimator mainly when starting therapy or as a sanity check against a markedly different prescribed dose.

What is the Warfarin Dose Estimator (Gage Algorithm)?

Estimate a starting warfarin maintenance dose with the Gage 2008 pharmacogenetic algorithm. Enter age, height, weight, indication, amiodarone use and optional CYP2C9/VKORC1 genotype to get a weekly and daily dose. Runs entirely in your browser. It runs free in your browser on Gera Tools, with nothing uploaded.

Warfarin Dose Estimator (Gage Algorithm)

Name: Warfarin Dose Estimator (Gage Algorithm)
Creator: Gera Tools
License: https://creativecommons.org/licenses/by/4.0/

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Warfarin starting-dose estimator

Warfarin has a narrow therapeutic window and huge between-patient variability — the required maintenance dose can differ more than tenfold. This tool estimates a sensible starting dose using the Gage 2008 pharmacogenetic algorithm, which combines patient size, age, two key genotypes and common interacting factors. It is designed for anticoagulation-clinic pharmacists and prescribers who want a defensible initial estimate before INR titration.

How it works

The algorithm predicts the natural log of the weekly dose, then exponentiates it. The size term uses Mosteller body surface area:

BSA (m²) = sqrt( height_cm × weight_kg / 3600 )

Each factor shifts the predicted log-dose up or down. Two genes dominate:

CYP2C9 metabolises warfarin. The *2 and especially *3 variants slow clearance, so carriers need lower doses — each *3 allele subtracts from the estimate.
VKORC1 (the −1639 G>A promoter variant) sets the drug target’s expression. The A allele lowers the dose requirement, so AG and AA genotypes pull the dose down.

Clinical terms then adjust further: amiodarone and a DVT/PE indication reduce the dose, while smoking and a high target INR raise it. The result is divided by seven to give an equivalent daily dose.

Clinical factors and how they affect the estimate

The model accounts for each factor by adding or subtracting from the log-dose prediction, so the effects compound rather than stack linearly. In broad terms:

Factor	Direction	Clinical reason
Older age	Reduces dose	Slower CYP2C9 activity with age; lower plasma binding
Larger BSA	Increases dose	Greater volume of distribution
CYP2C9 `*2` allele	Reduces dose	Intermediate metaboliser — slower warfarin clearance
CYP2C9 `*3` allele	Reduces dose substantially	Poor metaboliser — much slower clearance
VKORC1 `AA` genotype	Reduces dose	Reduced VKORC1 expression, highly sensitive to the drug
Amiodarone use	Reduces dose	CYP2C9 inhibition — well-established drug interaction
DVT/PE indication	Reduces dose	Lower INR targets are sometimes appropriate; algorithm-specific adjustment
Smoking	Increases dose	CYP1A2 induction increases warfarin clearance slightly
High target INR (3.0)	Increases dose	More anticoagulation needed for mechanical valves, some AF cases

Worked example

For a 65-year-old, 170 cm, 75 kg patient with wild-type CYP2C9 (*1/*1) and wild-type VKORC1 (GG), no amiodarone, non-smoker, AF indication with standard INR target of 2.5, the model estimates roughly 35 mg/week (about 5 mg/day). Adding VKORC1 AA would pull the estimate down noticeably, and adding CYP2C9 *3/*3 on top of that would cut the estimate sharply — reflecting a slow metaboliser facing a highly sensitive drug target. Those two variants together are the most common explanation for patients who achieve therapeutic INR on only 1–2 mg/day.

Important limitations

This is an initiation estimate, not a titration tool. The output is a starting point for INR monitoring, not a final dose.
Genotyping is not required and often not available in practice. Without genotype data, leave fields as wild-type; the clinical estimate is still useful, just less precise.
Round to available tablet strengths (typically 1, 2, 2.5, 3, 4, 5, 6, 7.5, 10 mg in the UK and US) before prescribing.
Local anticoagulation policy and INR monitoring always govern the final dose. This tool does not replace clinical judgement.