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Acquired Angioedema With Anti-C1-inhibitor Autoantibodies During Assisted Reproduction Techniques.

C1-inhibitor (C1-INH) deficiency activates the contact system, resulting in increased bradykinin, vascular hyperpermeability, and recurrent, localized, and self-limiting acute angioedema attacks [1]. Angioedema is classified as hereditary (C1-INH-HAE) or acquired (C1-INH-AAE) [1]. C1-INH-HAE is an autosomal dominant inherited disorder caused by mutations in the C1-INH gene, with an estimated prevalence of approximately 1/50 000 inhabitants [1]. C1-INHAAE is much less prevalent (around 1/500 000) and is often associated with the presence of anti-C1-INH autoantibodies and/or lymphoproliferative disorders [1,2]. Estrogens and pregnancy can worsen the clinical expression of C1-INH-HAE [3-5], whereas the fertility rate is similar in patients with C1-INH-HAE and in the general population [3]. However, to our knowledge, there are no previous reports on pregnancy and C1-INH-AAE. We present the case of a 38-year-old woman who attended our clinic wishing to become pregnant. She underwent 3 intrauterine insemination cycles with sperm from a donor, which were unsuccessful. Five months after having initiated assisted fertilization techniques, she experienced a first episode of nonerythematous, nonpruriginous angioedema affecting her feet. The patient had previously tolerated oral contraceptives containing estrogens (drospirenone/ ethinylestradiol). Thereafter, she underwent ovarian stimulation with recombinant human luteinizing hormone, recombinant human follicle-stimulating hormone, recombinant human chorionic gonadotropin, and micronized natural progesterone for in vitro fertilization (IVF). The embryos were cryopreserved owing to her high progesterone levels. During this period, she experienced several self-limiting acute edema episodes affecting the upper/lower limbs. One of these episodes also affected the glottis and required admission Manuscript received June 21, 2017; accepted for publication October 20, 2017.