Abstract
Acquired angioedema resulting from the deficiency of the C1-inhibitor (AAE-C1-INH) was first described by Caldwell et al1 in 1972. In 1986, Jackson et al2 discovered autoantibodies against the C1-inhibitor (C1-INH). AAE-C1-INH often accompanies lymphoproliferative—and occasionally—autoimmune disorders, neoplasms, and infections. Low C1-INH level is associated with activation of the kinin-bradykinin cascade, leading to the formation of bradykinin, increasing capillary permeability, and tissue swelling.
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