Resumen
Angioedema (AE) is a heterogeneous syndrome of episodic, self-limited swelling of subcutaneous and submucosal tissues. Its two main mechanistic subtypes, mast-cell-mediated (histaminergic) and bradykinin-mediated, share clinical features but diverge in pathophysiology and entirely treatment. This carries life-or-death consequences: bradykinin-mediated AE does not respond to antihistamines, corticosteroids, or epinephrine, and misclassification delays access to effective therapy in a disease capable of causing fatal laryngeal obstruction. Among bradykinin-mediated variants, hereditary angioedema (HAE) due to C1-inhibitor deficiency (HAE-C1INH) and with normal C1-inhibitor levels (HAE-nC1INH) remain among the most underdiagnosed conditions in the region. HAE is a devastating disease; in addition to being potentially life-threatening, its recurrent and unpredictable nature imposes a substantial burden, keeping patients in a state of constant alertness that drastically impairs their quality of life and is associated with high rates of anxiety and depression, as documented in studies of health-related quality of life in this population.1 This letter offers a clinically grounded regional perspective that integrates epidemiological evidence and public health considerations to inform practice and policy at all levels of care.
Referencias
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Esta obra está bajo una licencia internacional Creative Commons Atribución-NoComercial 4.0.
Derechos de autor 2026 Revista Alergia México
