LMWH is less likely than UFH to cause HIT antibody formation as well as clinical HIT (Warkentin et al., 1995, 2003). Furthermore, LMWH binds less avidly to platelets than does UFH (Greinacher et al., 1993b). With functional assays employing platelet-rich plasma, several investigators reported a reduced cross-reactivity of HIT antibodies with LMWH compared with UFH (Ramakrishna et al., 1995; Slocum et al., 1996; Vun et al., 1996); however, with sensitive washed platelet functional assays, the cross-reactivity rate of LMWH is nearly 100% (Greinacher et al., 1992; Warkentin et al., 1995, 2005) (see Chapter 10).
Owing to the unavailability of other anticoagulant options during the 1980s, LMWH preparations were often used in Europe for further parenteral anticoagulation of HIT patients. No prospective cohort studies are available, but case reports (Roussi et al., 1984; Leroy et al., 1985; Vitoux et al., 1986; Gouault-Heilmann et al., 1987; Bauriedel et al., 1988; Kirchmaier and Bender, 1988) and a review (Reuter, 1987) suggest that LMWH may benefit some patients. Other case series, however, clearly show that LMWH is associated with disastrous complications in HIT patients (Horellou et al., 1984; Leroy et al., 1985; Gouault-Heilmann et al., 1987; Greinacher et al., 1992; Kleinschmidt et al., 1993). Unfortunately, no laboratory assay reliably predicts these differing treatment responses.
Treatment of HIT with LMWH is frequently unsuccessful. Of eight consecutive HIT patients who received LMWH, thrombocytopenia persisted in all, and new thromboembolic events occurred in two patients (Greinacher et al., 1992). After LMWH became available in North America, a similar experience was observed in seven HIT patients treated with LMWH (Warkentin, 1997). Another study has also shown a relatively high risk of adverse outcomes of treating HIT with LMWH (Ranze et al., 2000).
Recommendation. LMWH should not be used to treat patients with acute HIT (grade 1C).
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