Lack of Drug Specific Antibody

Prolonged or repeated exposure to argatroban does not result in the generation of antibodies that alter its anticoagulant activity (Walenga et al., 2002). This has been shown in healthy volunteers, HIT patients, and HIT patients undergoing PCI, and in the postmarketing safety surveillance of over 4800 patients treated in Japan between 1991 and 1998 with argatroban anticoagulation (Walenga et al., 2002). In contrast, approximately 50% of lepirudin-treated patients develop drug-specific antibodies that can occasionally increase plasma lepirudin concentrations, requiring careful monitoring and dose adjustments to avoid bleeding complications (Song et al., 1999; Eichler et al., 2000) (see Chapter 14). An estimated 0.2% of patients re-exposed to lepirudin experience anaphylactoid reactions, possibly death (Greinacher et al., 2003). Bivalirudin cross-reacts in vitro with approximately 51% of anti-lepirudin antibodies (Eichler et al., 2004). Argatroban does not cross-react with anti-lepirudin antibodies and has been used successfully in patients with a history of HIT and anti-lepirudin antibodies (Harenberg et al., 2005).

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