Lingual angioedema after perindopril use.

A enzyme (ACE) inhibitors are commonly used in the treatment of hypertension.1 Inflammatory manifestations have been previously reported after ACE inhibitor use, whereas true allergic reactions are uncommon. We report a case of severe lingual edema and airway compromise associated with ACE inhibitor use. • • • A 56-year-old woman with a history of chronic alcoholism, tobacco consumption, systemic hypertension, chronic respiratory disease, a recent humerus fracture, and penicillin allergy was receiving chronic oral treatment with dextropropoxyphene (390 mg/day), salicylate (200 mg/ day), nifedipine (30 mg/day), zolpidem (10 mg/day), and budenoside and terbutaline spray. Treatment with nifedipine was stopped and the patient was prescribed a new treatment for hypertension, perindopril (Coversyl®), an ACE inhibitor, during hospitalization for alcohol withdrawal. Four hours after taking the first tablet, her tongue began to swell. Two hours later, the macroglossia had reached such a point that it was complicated by obstructive and positional dyspnea accompanied by wheezing. She was transferred to the intensive care unit (Figure 1). Arterial blood pressure was 120/80 mm Hg, heart rate was 95 beats/min. The patient was afebrile with no cutaneous lesions. Treatment included noninvasive mask ventilation, epinephrine 1 mg/hour intravenously by infusion, and hydrocortisone hemisuccinate 800 mg/day. The macroglossia diminished and assisted ventilation was stopped 5 hours after admission. Epinephrine was stopped 24 hours after admission and the patient was discharged from the intensive care unit 6 hours later. • • • Based on the rapid onset of symptoms and the temporal relation to the administration of perindopril, a syndrome of angioedema induced by perindopril appears to be the most likely cause for this patient’s macroglossia. Other known causes of macroglossia, including tumor, myxoedema, congenital hypertrophy, amyloidosis, acromegaly, and inflammatory disease2 can be eliminated based on the absence of previous similar manifestations, with rapid onset and prompt response to treatment. All other medications, including dextropropoxyphene, salicylate, zolpidem, budenoside, and terbutaline were taken chronically by the patient, and were reintroduced after intensive care unit discharge without complication. Thus, imputability for perindopril as the causative agent is strong. Furthermore, ACE inhibitors are known to induce angioedema.3,4 Angioedema is estimated to occur at rate of 1 per 3,000 patients per week. It can occur with all agents of this class but we found no similar report after perindopril use. It may be fatal.5 Angioedema is characterized by edema of the skin and subcutaneous fat. Tongue edema, as well as face, lip, glottic, and pharyngeal edema are frequently described. Three mechanisms are postulated to be responsible for this complication: deficiency of a mediator of the complement cascade, bradykinin dysequilibrium, and development of immunoglobin A or G antibodies.3