D2.236 - Drug-induced angioedema by racecadotril in a patient treated with angiotensin-converting enzyme inhibitors
Case report
Introduction
Angioedema (AE), a subcutaneous or submucosal swelling, might occur due to drugs (AE-DI). Angiotensin-converting enzyme inhibitors (ACEIs) are well-known triggers of AE. Racecadotril, an oral enkephalinase inhibitor used in the management of acute diarrhoea, is less commonly associated with AE. We present a rare case of a patient with AE associated with the combined use of an ACEI and racecadotril.
Material and methods
A 74-year-old male with no previous history of allergies or AE who had been on enalapril for over 4 years was now prescribed racecadotril for a prolonged episode of diarrhoea.
Within 3 days of treatment, the patient exhibited signs of progressive, painless tongue swelling with respiratory compromise. In the emergency department administration of adrenaline, hydrocortisone, methylprednisolone and dexchlorpheniramine yielded no response and resulted in further progression of the swelling. A nasal laryngoscopy revealed AE at the base of the tongue. Icatibant was administered, with no significant clinical improvement. Due to compromised respiration, sedation was induced with and subsequent nasotracheal intubation. After >6 hours, due to no improvement a second dose of icatibant was administered. The patient’s condition gradually improved and extubation succeeded after 48 hours
Results
In the event study, no personal or family history of urticaria, AE or recurrent abdominal pain was reported. Complement studies (C3, C4, C1 inhibitor levels, activity, and C1q) revealed no abnormalities.Skin tests with inhalant and food allergens were positive only for dust mites. After excluding other potential causes of acute AE, such as bleeding, infection, or systemic inflammation, the AE episode was finally attributed to the combined use of racecadotril with ACE inhibitors.. Anti-hypertensive treatment was switched to calcium channel blockers and diuretics. Advice was provided regarding the avoidance of ACEIs and racecadotril.
Conclusion
This case highlights a rare but potentially severe interaction between ACEIs and racecadotril. Although the Spanish technical sheet for racecadotril advises against its use in patients on ACEIs, a review of the literature reveals limited reports of such interactions, and racecadotril is not listed in the DANCE classification as a cause of AE-DI.
Although unknown, one proposed mechanism is a bradykinin mediated increase in vascular permeability, for both ACEIs and racecadotril result in bradykinin increase. The patient showed an incomplete response to icatibant, likely due to delayed administration.
