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• W2071755711 abstract "RationaleType I and Type II hereditary angioedema syndromes have been well characterized, and multiple treatment options exist. However, comparatively little is known about Type III hereditary angioedema (with normal C1 esterase inhibitor levels and function). We present a case of Type III hereditary angioedema successfully treated with ecallantide, a plasma kallikrein inhibitor.MethodsOur patient was referred for evaluation and treatment of recurrent idiopathic angioedema symptoms.ResultsA 72 year old woman with a family history of angioedema presented with a two year history of recurrent angioedema of lips, tongue, and throat. Symptoms started after discontinuing tamoxifen, an estrogen receptor antagonist, which was used for a period of 10 years. She had been treated with multiple antihistamines, steroids, and epinephrine with no significant benefit. The patient had normal C1 inhibitor protein level (24 mg/dL), normal C1 inhibitor function (100%), normal C1Q level (5.3 mg/dL), and low-normal C4 level (16 mg/dL, range: 16-47). Based upon the positive family history, female gender, and association with estrogen, a clinical diagnosis of type III hereditary angioedema was made. As previous therapies had no clinical effect, the patient was started on ecallantide 30 mg subcutaneously during acute attacks. Within one hour of therapy, the angioedema resolves completely. The frequency of episodes has decreased from monthly to once every 6 months. The patient has had no side effects with ecallantide.ConclusionsThis case demonstrates a successful treatment of Type III Hereditary Angioedema with ecallantide. Future studies would be useful in assessing the efficacy of ecallantide in other angioedema syndromes. RationaleType I and Type II hereditary angioedema syndromes have been well characterized, and multiple treatment options exist. However, comparatively little is known about Type III hereditary angioedema (with normal C1 esterase inhibitor levels and function). We present a case of Type III hereditary angioedema successfully treated with ecallantide, a plasma kallikrein inhibitor. Type I and Type II hereditary angioedema syndromes have been well characterized, and multiple treatment options exist. However, comparatively little is known about Type III hereditary angioedema (with normal C1 esterase inhibitor levels and function). We present a case of Type III hereditary angioedema successfully treated with ecallantide, a plasma kallikrein inhibitor. MethodsOur patient was referred for evaluation and treatment of recurrent idiopathic angioedema symptoms. Our patient was referred for evaluation and treatment of recurrent idiopathic angioedema symptoms. ResultsA 72 year old woman with a family history of angioedema presented with a two year history of recurrent angioedema of lips, tongue, and throat. Symptoms started after discontinuing tamoxifen, an estrogen receptor antagonist, which was used for a period of 10 years. She had been treated with multiple antihistamines, steroids, and epinephrine with no significant benefit. The patient had normal C1 inhibitor protein level (24 mg/dL), normal C1 inhibitor function (100%), normal C1Q level (5.3 mg/dL), and low-normal C4 level (16 mg/dL, range: 16-47). Based upon the positive family history, female gender, and association with estrogen, a clinical diagnosis of type III hereditary angioedema was made. As previous therapies had no clinical effect, the patient was started on ecallantide 30 mg subcutaneously during acute attacks. Within one hour of therapy, the angioedema resolves completely. The frequency of episodes has decreased from monthly to once every 6 months. The patient has had no side effects with ecallantide. A 72 year old woman with a family history of angioedema presented with a two year history of recurrent angioedema of lips, tongue, and throat. Symptoms started after discontinuing tamoxifen, an estrogen receptor antagonist, which was used for a period of 10 years. She had been treated with multiple antihistamines, steroids, and epinephrine with no significant benefit. The patient had normal C1 inhibitor protein level (24 mg/dL), normal C1 inhibitor function (100%), normal C1Q level (5.3 mg/dL), and low-normal C4 level (16 mg/dL, range: 16-47). Based upon the positive family history, female gender, and association with estrogen, a clinical diagnosis of type III hereditary angioedema was made. As previous therapies had no clinical effect, the patient was started on ecallantide 30 mg subcutaneously during acute attacks. Within one hour of therapy, the angioedema resolves completely. The frequency of episodes has decreased from monthly to once every 6 months. The patient has had no side effects with ecallantide. ConclusionsThis case demonstrates a successful treatment of Type III Hereditary Angioedema with ecallantide. Future studies would be useful in assessing the efficacy of ecallantide in other angioedema syndromes. This case demonstrates a successful treatment of Type III Hereditary Angioedema with ecallantide. Future studies would be useful in assessing the efficacy of ecallantide in other angioedema syndromes." @default.
• W2071755711 created "2016-06-24" @default.
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• W2071755711 date "2014-02-01" @default.
• W2071755711 modified "2023-10-16" @default.
• W2071755711 title "Ecallantide In Treatment Of Type III Hereditary Angioedema" @default.
• W2071755711 doi "https://doi.org/10.1016/j.jaci.2013.12.161" @default.
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