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I thank Dr Wilkerson for his valuable comments. The treatment of acquired angioedema is shaped after that of hereditary angioedema. However, the acquired form is even less prevalent than the hereditary form, precluding large-scale studies. Thus, current experience is mainly based on case reports and case series. It should be kept in mind that acquired angioedema or C1 inhibitor deficiency is immune-mediated. Thus, in contrast to patients with the hereditary form, patients with acquired angioedema may be partially resistant to C1 inhibitor substitution (given as a concentrate or as fresh frozen plasma) because of hypercatabolism. Theoretically, the problem of C1-inhibitor catabolism can be bypassed by products that inhibit the bradykinin pathway. However, to my knowledge, studies on these new agents in acquired C1-inhibitor deficiency are currently nonexistent.