Antibodies as a Cause for Platelet Functional Defects

The Luc. antibody occurring in a polytransfused thrombasthenic patient is an IgG which agglutinates all human platelets except thrombasthenic ones. At sub-agglutinating doses, ADP, Adrenaline, Collagen, Thrombin and arachidonic acid-induced aggregations but not ristocetin and bovine factor VIII mediated platelet aggregations are inhibited. It does not modify ADP binding to normal human platelet membranes. The antibody strongly reduced thrombus formation on rabbit aorta subendothelium. Its activity is consumed after incubation with normal human platelet membranes but not with thrombasthenic ones. It inhibits thromboxane formation with all inducers but not with arachidonic acid and PGG2. This antibody reacts with a component present on human platelet membranes 120.000 MW.

The Por. antibody occurring in a polytransfused Bernard-Soulier patient is an IgG which agglutinates all human platelets except those of Bernard-Soulier and thrombasthenia. The activity is consumed after incubation with normal and thrombasthenic platelet membranes but not with platelet membranes of Bernard-Soulier patients. At sub-agglutinating doses only ristocetin, bovine factor VIII aggregation and adhesion of human platelets to rabbit aorta subendothelium are inhibited. Purified neuraminidase, chymotrypsin or trypsin destroy the reaction of normal platelets with this antibody. This IgG reacts with a component of human platelet membrane 155.000 MW.

 

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