Citation

Chong YK, Mak TW. Clin. Biochem. Rev. 2019; 40(4): 175-185.

Affiliation

Hospital Authority Toxicology Reference Laboratory, Princess Margaret Hospital, Kowloon, Hong Kong, Peoples' Republic of China.

Copyright

(Copyright © 2019, http://www.aacb.asn.au/clinical-biochemist-reviews, Publisher Australasian Association of Clinical Biochemists)

DOI

10.33176/AACB-19-00029

PMID

31857739

PMCID

PMC6892705

Abstract

Superwarfarins are long-acting anticoagulant rodenticides developed from warfarin. The mechanism of action is by inhibition of vitamin K epoxide reductase, resulting in the inability of the body to recycle vitamin K. Deficiency of vitamin K thereafter leads to inability for the body to synthesise vitamin K-dependent coagulation factors, factor II, VII, IX, and X, leading to prolonged prothrombin time. Due to the bulky aromatic sidechains, superwarfarins have a much longer half-life when compared to warfarin, and exposure to superwarfarins results in a prolonged period of anticoagulation which can result in clinical bleeding. Diagnosis is straightforward in patients with known history of superwarfarin exposure but has proved difficult for patients who did not report superwarfarin intake. Superwarfarin poisoning should therefore be suspected in all patients with unexplained prolongation of prothrombin time, and can be confirmed by their detection in serum. Treatment for superwarfarin poisoning includes rapid correction of factor deficiencies with either 4-factor prothrombin complex concentrate or fresh frozen plasma in patients with active bleeding, and high dose vitamin K therapy given multiple times per day for a prolonged period of weeks to months.

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Language: en