Tranexamic Acid Therapy in Hereditary Angioneurotic Edema

Abstract

HEREDITARY angioneurotic edema results from an inborn error in the biosynthesis of a serum alpha-2 globulin that inhibits the enzymatic activity of the first component of complement and is thus designated the C1 inhibitor (C1̄ INH).¹ As a consequence of this defect, there is unopposed action of the first component of complement (C1) in the plasma of affected patients and consequent consumption of the second and fourth components of complement (C4 and C2).^{2 , 3} It appears that the episodic activation of C1 is pathogenetically related to attacks of angioedema. Thus, a potential strategy for the suppression of attacks of angioedema might . . .