Correspondence To

the editor: Eculizumab fails to inhibit generation of C5a in vivo Eculizumab is a monoclonal antibody (mAb) reputed to block C5 by preventing enzymatic generation of active components C5a and C5b.1 C5a is a proinflammatory mediator whereas C5b combines with C6, C7, C8, and C9 to form the membrane attack complex C5b-9, which contributes to procoagulant effects and cell lysis. Eculizumab has revolutionized treatment of paroxysmal nocturnal hemoglobinuria and atypical hemolytic uremic syndrome (aHUS),2,3 thus improving the hemolysis and thrombocytopenia seen in these disorders. Clinical studies of eculizumab efficacy in vivo have relied on parameters such as platelet count or lactate dehydrogenase (LDH) levels.2,3 Ex vivo studies rely on complement hemolytic assays, which test the functional capability of serum complement components to lyse sheep or chicken erythrocytes precoated with anti-sheep o