. Author manuscript; available in PMC: 2014 Nov 1.

Published in final edited form as: Pharmacotherapy. 2013 Apr 18;33(11):1199–1213. doi: 10.1002/phar.1270

Table 6.

Studies Addressing the Influence of Pharmacogenetics on INR Reversal

	Sconce⁷³	Briz⁷⁴
Number of Patients	35	87 episodes (60 patients)
Racial Composition	100% white	Not given
Patient Summary	Atrial fibrillation patients with unstable warfarin anticoagulation control and previous warfarin use for ≥ 9 months (target INR 2–3)	Asymptomatic/minor bleeding patients presenting with INR≥6 and target INR range of 2–4
Gene(s) examined	VKORC1	VKORC1 and CYP2C9
Polymorphism	VKORC1 1639 G>A	Not given
Intervention	150 mcg/day vitK	Mean dose of 1.7 mg vitK^a
Length of Intervention	7 days	A single dose over a 24 hour period
Initial Mean INR	GG 2.47, GA 2.86, AA 2.58	8.02
Post Intervention INR	GG 1.52, GA 1.98, AA 2.40	2.62
Conclusion	Patients with the GG genotype had a larger INR decrease and required a larger increase in warfarin dose compared to the GA and AA genotypes.	An association was found between the change of INR and the initial INR, vitK dose, and body surface area. There were no associations found with INR decrease and age, sex, warfarin dose, and genotype.

INR = international normalized ratio; vitK = vitamin K.

Patients were assigned a vitamin K dose based on the following dosing algorithm: Vitamin K dose = [(Change in INR + 3.51−0.654 (Initial INR)] / 1.9406.

VKORC1 genotype: GG indicates wild-type, AG indicates heterozygote and AA indicates homozygote for variant allele.