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The paroxysmal nocturnal hemoglobinuria (PNH) platelet differs from the normal human platelet in its interaction with activated complement components: (a) when complement is activated by the alternative pathway, greater amounts of C3 are fixed to the PNH platelet than to the normal platelet; (b) the platelet-release reaction, as measured by serotonin release, occurs after C3 fixation to the PNH platelet. This reaction does not occur with normal platelets; (c) although serotonin release mediated by antibody alone was the same for normal and PNH platelets, antibody-initiated complement activation resulted in the fixation of greater amounts of C3 to PNH platelets and greater consequent serotonin release; and (d) nearly maximal serotonin release; and (d) nearly maximal serotonin release from PNH platelets occurs after the fixation of C3 (or perhaps C5) to the membrane without completion of the terminal sequence. In contrast, completion of the terminal complement sequence beyond C5 is required for maximal serotonin release from normal platelets. These abnormalities of interaction of complement components and PNH platelets may explain the occurrence of thromboses in this disease.

Mechanism of complement-mediated activation of human blood platelets in vitro: comparison of normal and paroxysmal nocturnal hemoglobinuria platelets.