Barry S. Coller

Potential application of labeled antibodies for thrombus detection.

Labeling platelets with monoclonal antibodies in whole blood for imaging thrombi is less cumbersome than the established 111In-oxine method.. 7E3, a murine monoclonal antibody directed against glycoprotein IIb and/or IIIa on both human and dog platelets was used to label canine platelets. Thrombi were induced by transcatheter placement of a copper coil followed by electrocoagulation. 7E3 was iodinated with 131I and labelled with 111In using 7E3-DTPA conjugate. Whole blood was incubated with 0.5-1.0 micrograms labeled 7E3/mL blood. In 4/4 dogs, experimental deep vein thrombi were identified using both 131I- and In 1/3 dogs, experimental coronary thrombus could be identified ex vivo at 4 h. Clot to blood ratios ranged between 7 to 13:1. Using the 111In-oxine method, 0/3 coronary thrombi were seen. Thus, 131I- and 111In-labeled 7E3 may be used to readily identify peripheral venous thrombi. For reliable and prompt identification of coronary thrombi, more rapid clearance of the labeled platelets is required.

IgA inhibitor to factor VIII/von Willebrand factor

Summary. A 60‐year‐old Black female presented with a haemorrhagic diathesis and an acquired factor VIII/von Willebrand factor (VIII/vWf) inhibitor. This inhibitor was classified as an IgA immunoglobulin and was active not only against factor VIII coagulant (VIII:C) activity but also against plasma von Willebrand factor (vWf). The purified IgA also interacted with normal platelets to inhibit ristocetin‐induced platelet aggregation (RIPA). In contrast, studies with haemophilia A plasma and platelets revealed that the inhibitor did not react significantly with these plasmas or platelets. The significant differences in the inhibition of vWf assay both of the plasma and the platelets of the haemophilia A patients suggests that part of the haemorrhagic diathesis may be related not only to the inhibition of VIII: C but also to interference with platelet function. In addition, these studies suggest that there may be significant differences in the factor VIII‐related antigen (VIII R: Ag) on platelets in haemophilia A patients compared to normal.