Superwarfarin poisoning

Superwarfarin poisoning should be suspected when there is a severe deficiency of vitamin K-dependent clotting factors of unknown aetiology with a transient or no response to standard doses of vitamin K. Management of such patients typically involves prolonged administration of high doses of vitamin K. The anticoagulant effect (indicated by elevated descarboxyprothrombin and vitamin K^sub 1^O 2,3-epoxide concentrations) may persist in the absence of detectable brodifacoum. Although it has been over 20 years since the first descriptions of Superwarfarin rodenticide poisoning in humans,1 awareness of the problem among physicians remains minimal. Superwarfarins are potent, highly lipophilic 4-hydroxycoumarin derivatives and like warfarin they exert their anticoagulant effect by inhibiting the vitamin K epoxide reductase enzyme complex that recycles vitamin K 2,3-epoxide to vitamin K hydroquinone, the cofactor required by γ-glutamyl carboxylase for the post-translational modification of coagulation factors II, VII, IX, X, and other polypeptides.2 These compounds are available without restrictions and are used with increasing frequency to control infestation of warfarin-resistant rats. In the UK there is no statutory obligation that requires reporting of poisoning by brodifacoum (or other Superwarfarin type rodenticides) to the public health authorities or to the police. Self-administration by adults with Munchausen syndrome or those attempting suicide, or accidental ingestion by children, account for the majority of reported episodes of poisoning with vitamin K antagonists.3 Incidences of malicious poisoning are also known.4 Reporting without patients' consent would represent a breach of confidentiality. Legal judgments have established that patients' right to privacy may be breached but only when there is an overriding public interest.5 We question whether the unrestricted availability of superwarfarin-type compounds should continue.