Therapy of “the Neurotic Edema”

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Abstract
Episodic swellings of hereditary angioneurotic edema (HANE) are apparently secondary to deficient function of serum inhibitor of C1 esterase, inherited as an autosomal dominant trait in this syndrome. As another consequence of deficient inhibitor function, the behavior of the first component of complement, C1, is poorly regulated and its activation is strikingly enhanced during bouts of HANE so forming free C1 esterase in plasma.1 , 2 Normally, if C1 in plasma were converted to C1 esterase, its enzymatic activity would be obscured by the inhibitor. Frank et al. report in this issue of the Journal that episodes of HANE may be prevented . . .