Angiotensin-converting enzyme inhibitor induced angioedema: not always a class effect? A case report and short narrative review.

Guillaume Becker, Fabien Rougerie, Amelia-Naomi Sabo, Marie-Caroline Dalmas, Estelle Ayme-Dietrich, Laurent Monassier

Journal: Current medical research and opinion 2021;37(11):1855-1858

PMID: 34412518

Abstract

INTRODUCTION

Bradykinin-mediated angioedema is a rare but potentially fatal adverse event. Angioedema induced by angiotensin-converting enzyme (ACE) inhibitors is generally attributed to an inhibition of bradykinin degradation following ACE inhibition. Clinical studies on ACE inhibitors mainly focus on their efficacy. Few examine their potential to generate undesirable adverse effects, particularly with regard to angioedema.

CASE DESCRIPTION

We report here a case of angioedema occurring after ramipril initiation in a patient chronically treated with quinapril. Angioedema subsided spontaneously after ramipril discontinuation and quinapril reintroduction.

DISCUSSION AND CONCLUSIONS

Our clinical case suggests that despite similar pharmacodynamic properties, quinapril and ramipril do not have the same potential to generate angioedema. To explain this difference, we suggest a potentiation of the effect of bradykinin at the B2 receptor level by ramipril, which does not occur with quinapril. Consequently, angioedema may not always be a class effect of ACE inhibitors.

Address: Pôle pharmacie-pharmacologie, Hôpitaux Universitaires de Strasbourg, Strasbourg, France.; Laboratoire de Pharmacologie et Toxicologie NeuroCardiovasculaire UR7296, Département Universitaire de Pharmacologie, Addictologie, Toxicologie et Thérapeutique, Université de Strasbourg, Strasbourg, France.; Département de Médecine Générale, Faculté de Médecine, Université de Strasbourg, Strasbourg, France.; Service de Médecine Interne, Endocrinologie & Nutrition, Hôpital de Hautepierre, Hôpitaux Universitaires de Strasbourg, Strasbourg, France.

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