Table 2 lists some common features of APLAS and HIT. Both clinicopathologic disorders are characterized by thrombocytopenia, a paradoxical risk for venous and arterial thrombosis, and associated antibodies that can be detected by either functional or antigen assays (see Chapter 10). Moreover, for both APLAS and HIT, positive functional assays are more strongly associated with thrombosis than positive antigen assays (Ginsberg et al., 1995; Warkentin et al., 2000; Galli et al., 2003). The parallels between these disorders led Arnout (1996) to hypothesize that IgG-mediated platelet activation could explain thrombosis in APLAS. Supportive experimental data include the observations that antiphospholipid antibodies enhance platelet activation induced by other agonists (Martinuzzo et al., 1993). Furthermore, Arvieux et al. (1993) observed murine monoclonal antibodies reactive against b2GPI induced platelet activation in the presence of subthreshold concentrations of ADP and epinephrine, an effect dependent on binding to platelet FcgIIa receptors. However, other workers were unable to demonstrate enhanced platelet activation in the presence of IgG antiphospholipid antibodies (Shi et al., 1993; Ford et al., 1998) or showed no role for platelet FcgIIa receptors (Lutters et al., 2001; Jankowski et al., 2003).
Was this article helpful?