Cardiovascular and Diabetic Medications That Cause Bradykinin-Mediated Angioedema 22.08.18
Cardiovascular and Diabetic Medications That
Cause Bradykinin-Mediated Angioedema
Stephanie N. Hudey, MD, Emma Westermann-Clark, MD, MA, and Richard F. Lockey, MD
Division of Allergy and Immunology, Department of Internal Medicine, University of South Florida, Morsani College of Medicine, Tampa, Fla
Corresponding author: Emma Westermann-Clark, MD, MA, Division of Allergy and Immunology, Department of Internal Medicine, University of South Florida, Morsani College of Medicine, 13000 Bruce B. Downs Boulevard, Suite 111D, Tampa, FL 33612. E-mail: ewester1@health.usf.edu.
Abstract:
Medication-induced angioedema is a bradykinin-mediated process that results from increased production or decreased degradation of bradykinin. These reactions are documented for several cardiac medications including blockers of the reninangiotensin-aldosterone system (RAAS). Other cardiovascular and diabetes medications further increase the risk of medicationinduced angioedema, particularly with concomitant use of RAAS inhibitors. Dipeptidyl peptidase IV inhibitors are a class of oral diabetic agents that affect bradykinin and substance P degradation and therefore can lead to angioedema. Neprilysin inhibitors are a separate class of cardiac medications, which includes sacubitril, and can lead to drug-induced angioedema especially when used in combination with RAAS inhibitors. This article discusses the proposed mechanisms by which these medications cause angioedema and how medication-induced angioedema differs from mast cell-mediated angioedema. It also details how to recognize medication-induced angioedema and the treatment options available
Texto completo: http://dx.doi.org/10.1016/j.jaip.2017.03.017
Stephanie N. Hudey, MD, Emma Westermann-Clark, MD, MA, and Richard F. Lockey, MD
Division of Allergy and Immunology, Department of Internal Medicine, University of South Florida, Morsani College of Medicine, Tampa, Fla
Corresponding author: Emma Westermann-Clark, MD, MA, Division of Allergy and Immunology, Department of Internal Medicine, University of South Florida, Morsani College of Medicine, 13000 Bruce B. Downs Boulevard, Suite 111D, Tampa, FL 33612. E-mail: ewester1@health.usf.edu.
Abstract:
Medication-induced angioedema is a bradykinin-mediated process that results from increased production or decreased degradation of bradykinin. These reactions are documented for several cardiac medications including blockers of the reninangiotensin-aldosterone system (RAAS). Other cardiovascular and diabetes medications further increase the risk of medicationinduced angioedema, particularly with concomitant use of RAAS inhibitors. Dipeptidyl peptidase IV inhibitors are a class of oral diabetic agents that affect bradykinin and substance P degradation and therefore can lead to angioedema. Neprilysin inhibitors are a separate class of cardiac medications, which includes sacubitril, and can lead to drug-induced angioedema especially when used in combination with RAAS inhibitors. This article discusses the proposed mechanisms by which these medications cause angioedema and how medication-induced angioedema differs from mast cell-mediated angioedema. It also details how to recognize medication-induced angioedema and the treatment options available
Texto completo: http://dx.doi.org/10.1016/j.jaip.2017.03.017
Un articulo recomendado:
ResponderEliminarAngioedema
Luisa Holguín-Gómez 1, Luz Adriana Vásquez-Ochoa 2, Ricardo Cardona 3
1 Universidad de Antioquia. Medellín, Antioquia, Colombia
2 Hospital Pablo Tobón Uribe, Sección de Dermatología. Medellín,
Antioquia, Colombia
3 Universidad de Antioquia, Grupo de Alergología Clínica y Experimental,
IPS Universitaria. Medellín, Antioquia, Colombia
Abstract
Angioedema is defined as edema of the skin or mucosa, including the respiratory and the gastrointestinal mucosa, which is self-limiting, and in most cases is completely resolved in less than 72 hours. It occurs due to increased permeability of the mucosal and submucosal capillaries and postcapillary venules, with resulting plasma extravasation. There are different types of angioedema: histaminergic (which may be mediated by immunoglobulin E), hereditary, from acquired C1 inhibitor deficiency, from angiotensin converting enzyme inhibitor, bradykinin-mediated, and nonhistaminergic idiopathic angioedema. Treatment depends on the cause of angioedema, age, and
the frequency and severity of manifestations. The main measures are avoiding external triggers or causes, giving antihistamines, steroids, or adrenaline for histaminergic angioedema; replacing the deficient protein or blocking the action of bradykinin in C1 inhibitor deficiency and angioedema from angiotensin converting enzyme inhibitor
http://revistaalergia.mx/ojs/index.php/ram/article/view/220
Docentes presentes: Ruth H Ramírez, Ricardo Cardona Villa, Carlos F Chinchilla, Susana Díez.
ResponderEliminarResidentes presentes: Susana Uribe, Yurlani Gutierrez, Ana Maria Calle, Liliana Guevara, Luis Carlos Santamaria, July Ospina, Kaarem Gutierrez, Isabel Pareja.
• El prurito en el angioedema histaminergico, no es un signo que este presente en todos los casos ni lo defina.
• Estamos de acuerdo con el termino angioedema mediado por mastocitos para referirse al angioedema histaminergico.
• En ocasiones diferenciar un abdomen agudo y una crisis de angioedema herditario en pacientes ya diagnosticados con AHE puede ser muy dificil, aun cuando las imágenes pueden estar alteradas en ambas condiciones.
• En 2/3 de los paciente con angioedema por IECAs, los sintomas ocurren los primeros 3 meses de iniciar el tratamiento, pero va ligado a la predisposicion genética de los pacientes, aun cuando los episodios recurrentes de angioedema pueden ocurrir incluso semanas o meses después de suspender el IECA.
• En cuanto a los inhibidores de DPP-IV conocidos como "gliptinas", que incluyen sitagliptina, linagliptina y saxagliptina se desconoce el riesgo de angioedema con ellos en monoterapia, pero si puede haber un mayor riesgo cuando se combina con IECA.
• La falta de marcadores en esta enfermedad resaltan en la actualidad, es importante continuar en su busqueda. La bradicinina en plasma en sujetos con angioedema inducido por IECA, es un ejemplo de estos posibles marcadores futuros.
• Contemplar en pacientes con HTA que tienen angiodema por IECA administrar el ARA II con observación estrecha y teniendo siempre en cuenta que los ARA II también pueden causar angioedema.
• Nos cuestionamos si el angioedema por medicamentos pudiese ser dosis dependiente.
• En los pacientes con angioedema mediado por medicamentos que no mejoraran con esteroides, antihistaminicos ni adrenalina, en la actualidad se puede contemplar usar en ellos el Icatibant.
Relator: July Ospina