| Abstract: | Substantial evidence now exists to associate platelet membrane glycoprotein Ib (GP Ib) with a receptor for quinine/quinidine-dependent platelet-specific antibodies. A direct relationship between GP Ib and this receptor activity has been difficult to establish for several reasons, including: the apparent existence of additional receptor activity not directly attributable to the presence of GP Ib; the variable reactivity of different sera observed by some investigators; the instability of receptor activity in semi-purified, soluble form; and differences in methods used by various laboratories to identify and quantitate either quinine/quinidine-dependent antibodies or platelet receptor activity. Moreover, little attention has been paid to the possibility that the Bernard-Soulier syndrome may represent a more heterogeneous collection of functional and molecular platelet abnormalities than hitherto supposed. As more patients are identified and studied, this possibility can also be addressed. A role for factor VIII-related antigen (VIIIR:Ag) in platelet destruction and/or clearance by drug-antibody complexes remains controversial. The observation that VIIIR:Ag is required for platelet activation in vitro (serotonin release, aggregation and increased platelet factor 3 availability) has been made, yet recent evidence indicates that VIIIR:Ag is not required for binding of antibody to platelets in the presence of drug or for complement-mediated lysis of platelets by antibody and drug. Evidence that VIIIR:Ag participates as part of the initial immunogenic complex is intriguing, yet still unconfirmed.(ABSTRACT TRUNCATED AT 250 WORDS) |
