Angiotensin-converting Enzyme Inhibitor-induced Angioedema Research Articles

Angiotensin-Converting Enzyme (ACE) Inhibitor-Induced Angioedema in an African American Male With Coronavirus Disease 2019 (COVID-19)

Angiotensin-Converting Enzyme (ACE) Inhibitor-Induced Angioedema in an African American Male With Coronavirus Disease 2019 (COVID-19)

Five-Membered Nitrogen Heterocycles Angiotensin-Converting Enzyme (ACE) Inhibitors Induced Angioedema: An Underdiagnosed Condition.

Angiotensin-converting enzyme (ACE) inhibitors are used primarily in the treatment of hypertension, heart failure, and in the acute phase of myocardial infarction. Lisinopril [N2-[(1S)-1-car-boxy-3-phenylpropyl]-L-lysyl-L-proline], enalapril [(S)-1-[N-[1-(ethoxycarbonyl)-3-phenylpropyl]-L-alanyl]-L-proline] and ramipril [2-aza-bicyclo-[3.3.0]-octane-3-carboxylic acid] are all five-membered heterocycles and three of the most prevalent ACE inhibitors in clinical use worldwide. ACE inhibitor-induced angioedema (AE) is clinically characterized by self-limited edema of the dermis and subcutaneous lipid tissue, localized on face skin, oral mucosa and tongue in most cases. However, severe episodes of intestinal AE misdiagnosed as acute appendicitis and laryngeal AE requiring incubation have been reported. The pathophysiology of ACE inhibitor-induced angioedema is attributed to the accumulation of bradykinin, which is a potent vasodilator with proinflammatory activity that is normally degraded by angiotensin-converting enzyme (ACE) and aminopeptidase P; however, a small proportion of treated patients is affected. Given that patients do not respond to anti-H1 antihistamines and steroids, early clinical recognition and discontinuation of the ACE inhibitors are the treatments of choice for the long-term management of ACE inhibitor- induced angioedema. The search period of the present review was set up until November 2023, and its aim is to shed light on the broader context of ACE inhibitor-induced angioedema, exploring aspects such as clinical presentation, pathophysiology, and therapeutic considerations in this potentially life-threatening condition. The exploration of alternative drug options such as angiotensin II receptor blockers, the potential association of coadministration of DPP-4 inhibitors with ACE inhibitors, the presentation of angioedema and the significant clinical importance of this condition are also discussed. By focusing on the chemical structure of ACE inhibitors, specifically their nitrogen-based heterocycles-an attribute shared by over 880 drugs approved by the FDA within the pharmaceutical industry-this review emphasizes the pivotal role of nitrogen scaffolds in drug design and underscores their relevance in ACE inhibitor pharmacology.

Meta-analysis of ACE inhibitor–induced angioedema identifies novel risk locus

Angioedema is a rare but potentially life-threatening adverse drug reaction in patients receiving angiotensin-converting enzyme inhibitors (ACEis). Research suggests that susceptibility to ACEi-induced angioedema (ACEi-AE) involves both genetic and nongenetic risk factors. Genome- and exome-wide studies of ACEi-AE have identified the first genetic risk loci. However, understanding of the underlying pathophysiology remains limited. We sought to identify further genetic factors of ACEi-AE to eventually gain a deeper understanding of its pathophysiology. By combining data from 8 cohorts, a genome-wide association study meta-analysis was performed in more than 1000 European patients with ACEi-AE. Secondary bioinformatic analyses were conducted to fine-map associated loci, identify relevant genes and pathways, and assess the genetic overlap between ACEi-AE and other traits. Finally, an exploratory cross-ancestry analysis was performed to assess shared genetic factors in European and African-American patients with ACEi-AE. Three genome-wide significant risk loci were identified. One of these, located on chromosome 20q11.22, has not been implicated previously in ACEi-AE. Integrative secondary analyses highlighted previously reported genes (BDKRB2 [bradykinin receptor B2] and F5 [coagulation factor 5]) as well as biologically plausible novel candidate genes (PROCR [protein C receptor] and EDEM2 [endoplasmic reticulum degradation enhancing alpha-mannosidase like protein 2]). Lead variants at the risk loci were found with similar effect sizes and directions in an African-American cohort. The present results contributed to a deeper understanding of the pathophysiology of ACEi-AE by (1) providing further evidence for the involvement of bradykinin signaling and coagulation pathways and (2) suggesting, for the first time, the involvement of the fibrinolysis pathway in this adverse drug reaction. An exploratory cross-ancestry comparison implicated the relevance of the associated risk loci across diverse ancestries.

Isolated Laryngeal Angioedema in a Patient with Long-term ACE Inhibitor Use: A Case Report.

Angiotensin converting enzyme (ACE) inhibitor-associated angioedema is the most common cause of angioedema seen in the emergency department (ED) and can be associated with a high morbidity. Most cases occur within months of initiation of an ACE inhibitor and are associated with facial and/or oropharyngeal swelling. We present a case of isolated laryngeal edema requiring intubation following 10years of ACE inhibitor therapy. An 82-year-old female, who was on lisinopril therapy for 10years, presented to the ED with shortness of breath and a sensation that her throat was swelling. She appeared to be in mild respiratory distress and could only speak in one-word sentences. On the physical exam, there was no swelling in the tongue, lips, or face, and the uvula was midline. There was mild posterior pharyngeal edema and swelling noted, but the airway was not visibly obstructed. She was tachypneic and stridor was present. After no improvement with medications, anesthesia successfully intubated her in the operating room. It was deemed a difficult airway secondary to posterior pharyngeal erythema and edema. She was diagnosed with ACE inhibitor-associated angioedema and was extubated four days later. Her lisinopril was discontinued, and she has not had a recurrence of angioedema. ACE inhibitor-induced angioedema commonly presents with facial and oropharyngeal swelling. Its recognition, even years after starting an ACE inhibitor, is necessary to ensure swift and appropriate treatment of potentially life-threatening posterior pharyngeal edema.

Tranexamic acid for angiotensin-converting enzyme inhibitor-induced angioedema.

Approximately 0.7% of patients taking angiotensin-converting enzyme inhibitors (ACEIs) develop ACEI-induced angioedema (ACEI-IA). With no approved treatments for ACEI-IA, the risk of complications is concerning. Tranexamic acid (TXA) has the potential to prevent intubations and resolve ACEI-IA by inhibiting the downstream production of bradykinin. In this review, we aim to evaluate the safety and efficacy of TXA use in ACEI-IA. We queried the PubMed database for studies involving TXA for ACEI-IA from January 2003 to January 2023. Seven studies met the study inclusion criteria. Our results demonstrate that TXA may improve angioedema symptoms and prevent intubation. In addition, its availability, low cost, and safety profile support its use for improving the symptoms and complications of ACEI-IA in an emergency setting.

Unresolved Chronic Diarrhea: A Case of Angiotensin-Converting Enzyme Inhibitor-Induced Mesenteric Angioedema.

The occurrence of angiotensin-converting enzyme inhibitors (ACEI)-induced visceral angioedema is infrequent, frequently overlooked, and presents a diagnostic challenge due to its wide range of non-specific symptoms.While ACEI-induced visceral angioedema is more frequently observed in females and African Americans, it is crucial not to overlook the possibility of this phenomenon in other demographic groups as well.Its rarity emphasizes the importance of including it in the list of potential conditions to be considered, thus preventing unnecessary tests and procedures.

Concomitant medication in patients with bradykinin-mediated angioedema - there's more than ACE inhibitors.

Bradykinin-mediated angioedema is a rare, non-allergic, potentially life-threatening disease. ACE inhibitor-induced angioedema and hereditary angioedema (HAE) are the two most common presentations. Therapeutic options, pathophysiology and diagnosis continue to be investigated, with considerable progress in HAE over the last few decades. For all patients with bradykinin-mediated angioedema, there are several medications that should be avoided or administered with caution. Some of the triggering medications are well known, while others are suspected or of unknown significance. A common denominator is that there is no approved therapy for bradykinin-mediated angioedema as a drug side effect. Some medications, such as tissue plasminogen activator, have a higher incidence of angioedema with potential airway compromise than ACE inhibitors, although this fact is widely underappreciated. In this review, we aim to summarize what is currently known and recommended about concomitant medication in HAE patients and the interaction of other bradykinin-influencing drugs.

Geriatric Pharmacotherapy Case Series: Recurrent Angioedema Following Discontinuation of ACE Inhibitor Therapy.

Introduction Angiotensin-converting enzyme inhibitors (ACEIs) are first-line pharmaceutical agents in common chronic conditions such as hypertension and heart failure with reduced ejection fraction. When angioedema occurs, if secondary to ACEIs, discontinuation of the ACEI is necessary to mitigate the risk of recurrent angioedema. While angioedema is a well-known adverse effect of ACEIs, it is not well-known that angioedema may recur even after ACEI discontinuation. Additionally, only few reports in the literature describe this phenomenon. This case describes an older man with a history of chronic obstructive pulmonary disease, hypothyroidism, diabetes mellitus, hypertension, and heart failure who presented from an assisted living facility with recurrent angioedema 12 days after an initial episode of angioedema where his ACEI therapy (enalapril) was discontinued. Assessment Empiric methylprednisolone, diphenhydramine, intramuscular epinephrine, intravenous C1 esterase inhibitor Berinert®, and two units of fresh frozen plasma was given in the emergency department. The patient was monitored in the intensive care unit because of mild airway compromise but did not require invasive airway protection. Serum C4 level was normal, ruling out hereditary angioedema. Outcome Patient was discharged after five days in stable condition with resolution of symptoms. Conclusion ACEIs are the most common cause of drug-induced angioedema in the United States. Angioedema is self-limiting swelling that requires close airway monitoring. While health professionals recognize the risk for angioedema with active ACEI use, it is not well known that the risk of angioedema may occur for months following cessation of ACEI therapy. Increased awareness of delayed ACEI-induced angioedema following ACEI discontinuation is important for both providers and pharmacists to provide appropriate diagnosis and monitoring. Improved awareness would also allow patients with a history of ACEI-induced angioedema to be cognizant of the potential for recurrence following drug discontinuation.

Icatibant in reverting angiotensin-converting enzyme inhibitor-induced angioedema: a case report

Icatibant in reverting angiotensin-converting enzyme inhibitor-induced angioedema: a case report

Taming the Tongue: The Surgical Approach to Macroglossia.

While traditionally in the realm of otorhinolaryngology or oral maxillofacial surgery, conditions involving the tongue may also be managed by plastic surgeons. The authors present an unusual case of acquired macroglossia resulting from angiotensin-converting enzyme inhibitor-induced angioedema and review the literature to discuss its surgical management from a plastic surgery perspective. A 62-year-old female suffered severe airway obstruction, respiratory arrest, and anoxic brain injury from angioedema-associated macroglossia. After tracheostomy, the patient was managed nonsurgically, with bite wound care and medications to minimize angioedema to marginal effect. Ultimately, a partial glossectomy was planned. The edematous distal tongue was amputated and closed primarily. On postoperative day 2, she was successfully weaned off mechanical ventilation and no longer suffers trauma from tongue biting. The simple anterior tongue resection described in this paper was an appropriate approach for our patient. More research is needed to guide plastic surgeons in an optimal approach for clinical scenarios.

S3458 Often Reported, Rarely Considered: A Case of ACEI-Induced Mesenteric Angioedema

S3458 Often Reported, Rarely Considered: A Case of ACEI-Induced Mesenteric Angioedema

Use of C1 esterase inhibitor (Berinert®) for ACE inhibitor-induced angioedema at the Emergency Department

article: Use of C1 esterase inhibitor (Berinert®) for ACE inhibitor-induced angioedema at the Emergency Department - Italian Journal of Emergency Medicine 2022 August;11(2):119-22 - Minerva Medica - Journals

A Rare Case of ACE Inhibitor-Induced Intestinal Angioedema Presenting as a Delayed Complication in a Heart Transplant Recipient

<h3>Introduction</h3> ACE inhibitor-induced intestinal angioedema is a rare side effect of ACEi that presents with nonspecific signs and symptoms. Although the risk of occurrence is greater early in therapy, angioedema can present at any time and thus a high index of suspicion is needed to avoid delays in diagnosis, unnecessary testing, and considerable morbidity. <h3>Case Report</h3> Our patient is a 54-year-old male with past medical history of orthotopic heart transplantation 3 years prior for history of end-stage ischemic cardiomyopathy, heparin-induced thrombocytopenia, and hypertension who presented with 3 days of crampy abdominal pain rated 4 out of 10. He also had bloating and watery diarrhea. He had no fever, nausea or vomiting. The patient had rebound tenderness on physical examination. Labs were unremarkable. GI pathogen panel was negative including C. difficile. CT showed a moderate segment of distal ileum which demonstrated acute inflammatory changes including mucosal hyperemia and mural edema on a background of moderate ascites. GI were consulted and performed colonoscopy that revealed no significant abnormalities. The patient had been on lisinopril for 3 years to treat hypertension. This was subsequently stopped due to suspicion of intestinal angioedema. His symptoms resolved within 72 hours of discontinuation. <h3>Summary</h3> Isolated intestinal angioedema secondary to ACEi is a diagnosis of exclusion that necessitates awareness among physicians, particularly in vulnerable subgroups such as heart transplant patients. Symptoms classically subside within 24 to 48 hours after discontinuation of the ACEi.

Angioedema Caused by Drugs That Prevent the Degradation of Vasoactive Peptides: A Pharmacovigilance Database Study.

Angioedema results from the decreased degradation of vasoactive peptides such as substance P and bradykinin. In this study, we sought to clarify whether dipeptidyl peptidase-4 (DPP-4) and angiotensin-converting enzyme (ACE) inhibitors that suppress the degradation of substance P and bradykinin are involved in angioedema onset. We calculated information coefficients (ICs) by performing a disproportionality analysis to evaluate DPP-4/ACE inhibitor-induced angioedema using the Japanese Adverse Drug Event Report (JADER) database. No angioedema signals were detected for DPP-4 inhibitors; however, a signal was detected for ACE inhibitors (IC: 2.42, 95% confidence interval (CI): 2.19 to 2.65). Of the patients treated with DPP-4 inhibitors, four developed drug-induced angioedema in combination with ACE inhibitors, and all were taking vildagliptin. Signals were detected for enalapril (IC: 2.39, 95% CI: 2.06 to 2.71), imidapril (IC: 2.83, 95% CI: 2.38 to 3.27), lisinopril (IC: 2.28, 95% CI: 1.55 to 3.00), temocapril (IC: 1.35, 95% CI: 0.29 to 2.40), and trandolapril (IC: 1.57, 95% CI: 0.19 to 2.95). Both inhibitors inhibited the degradation of substance P and bradykinin and were thus expected to cause angioedema. However, no signal of angioedema was detected with the DPP-4 inhibitors, in contrast to some ACE inhibitors. This study found that ACE inhibitors and DPP-4 inhibitors, which inhibit the degradation of substance P and bradykinin, tended to have different effects on the onset of angioedema in clinical practice.

Angiotensin-Converting Enzyme Inhibitor-Induced Non-allergic Perioral Angioedema: A Case-Based Scoping Review.

Patients with angiotensin-converting enzyme inhibitor (ACEI)-induced angioedema (ACEIIA) may visit family physicians. The aim of this article was to describe a case of delayed-onset ACEIIA and to present a concise scoping review. Using a case report and a scoping review study design, we report a case of ACEIIA, with clinically confirmed diagnosis. The symptoms resolved after replacing the offending ACEI with another antihypertensive agent. After excluding other causes of perioral swelling and discontinuation of ACEI, the patient was symptom-free within a few days thereafter. Based on this case presentation, we performed a meta-narrative scoping review including up-todate diagnosis and management of ACEIIA, based on published data in English, French, and German from inception to April 1, 2021. Patients with angioedema of unknown origin should be cautiously examined to rule out oral diseases, including allergy to dental materials and drug-induced angioedema. Clinicopathological aspects and current treatment guidelines for ACEI-associated angioedema are also presented.

RECURRENT ANGIOEDEMA FOLLOWING ANGIOTENSIN CONVERTING ENZYME INHIBITOR DISCONTINUATION

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Angiotensin converting enzyme inhibitors (ACEIs) are guideline recommended first-line treatment for hypertension. Angioedema is a recognized side effect of ACEI therapy, yet clinicians are often unaware that limited case reports describe recurrent angioedema following ACEI discontinuation. This is a case of ACEI-induced angioedema occurring after discontinuing ACEI therapy. CASE PRESENTATION: An elderly male with medical history of hypothyroidism, hypertension, and heart failure presented from his long-term care facility complaining of face, tongue, and throat swelling with dysphagia and voice changes starting 24 hours prior. Examination showed normal vital signs and edema of aforementioned areas. He denied family history of similar occurrences. It was reported 12 days prior he was seen for unilateral lip swelling and his enalapril was discontinued without further treatment. Medication administration record review showed ACEI was appropriately discontinued by his care facility. He was given methylprednisolone, diphenhydramine, intramuscular epinephrine, C1 esterase inhibitor, and 2 units of fresh frozen plasma prior to admission. The patient was monitored in the intensive care unit due to mild airway compromise but did not require invasive airway protection. A serum complement factor 4 level was checked and returned normal. He was discharged after 5 days in stable condition with resolution of symptoms. DISCUSSION: ACEIs are the most common cause of drug induced angioedema in the United States. ACEI-induced angioedema is a self-limiting swelling that may involve the lips, tongue, upper airway, and rarely intestinal wall. Swelling is said to occur because of ACEI inhibition on the angiotensin converting enzyme preventing degradation of vasoactive substances such as bradykinin (1). Recurrence of angioedema after ACEI discontinuation was reported in 46% of cases in one retrospective study (2). The precise etiology of this delayed reaction is not well described, though it is reasonable to hypothesize in part, a drug washout period must occur. The adverse drug reaction probability scale score was 5 (probable) in this patient (3). Recurrence has been documented more commonly in elderly male patients (2). The mainstay of treatment for non-allergic angioedema caused by ACEIs is discontinuation of the offending drug and acute airway management if needed. No drug therapy has been proven effective in the treatment of this condition (1). CONCLUSIONS: Increased awareness of delayed ACEI-induced angioedema following ACEI discontinuation is important among health care providers for appropriate diagnosis and monitoring. While self-limiting without a known effective treatment, close airway monitoring is critical for patient survival. Improved awareness would also allow patients with a history of ACEI-induced angioedema to be cognizant of the potential for recurrence early following drug discontinuation. REFERENCE #1: Erickson DL, Coop CA. Angiotensin-converting enzyme inhibitor-associated angioedema treated with c1-esterase inhibitor: A case report and review of the literature. Allergy Rhinol (Providence). 2016;7(3):168-171. REFERENCE #2: Beltrami L, Zanichelli A, Zingale L, Vacchini R, Carugo S, Cicardi M. Long-term follow-up of 111 patients with angiotensin-converting enzyme inhibitor-related angioedema. J Hypertens. 2011 Nov;29(11):2273-7. REFERENCE #3: LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet]. Bethesda (MD): National Institute of Diabetes and Digestive and Kidney Diseases; 2012-. Adverse Drug Reaction Probability Scale (Naranjo) in Drug Induced Liver Injury. [Updated 2019 May 4]. DISCLOSURES: No relevant relationships by Mark Malesker, source=Web Response No relevant relationships by Shraddha Narechania, source=Web Response No relevant relationships by Bryton Perman, source=Web Response

ALTEPLASE-ASSOCIATED ANGIOEDEMA: NEW TREATMENT OPTIONS

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Alteplase (recombinant tissue plasminogen activator or tPA) has revolutionized the management of acute ischemic stroke since its FDA approval in 1995. Intracerebral bleed is the most known and feared complication after tPA administration. tPA-associated orolingual angioedema (TAOA) is a less common but potentially fatal complication of tPA. We report a patient who developed hemi-orolingual angioedema after receiving tPA. CASE PRESENTATION: A 79-year-old female presented with sudden onset right-sided weakness with initial National Institutes of Health Stroke Scale score of 4. CT head was negative for intracranial bleed and a CT angiogram with perfusion of the head showed occlusion of P2 segment of the left posterior cerebral artery. She received tPA bolus followed by infusion and was transferred to the intensive care unit. She developed right hemi-orolingual angioedema without evidence of airway compromise one and half hours after tPA initiation. Administration of intravenous corticosteroids and antihistamines failed to improve angioedema. She was subsequently treated with 2 units of fresh frozen plasma (FFP) with complete resolution of swelling within 2 hours. DISCUSSION: Alteplase cleaves plasminogen to plasmin which degrades thrombus-bound fibrin. Plasmin also activates the kinin and complement pathways causing increased bradykinin and histamine release respectively. Bradykinin-mediated vasodilation appears to be the primary cause of TAOA. TAOA has an incidence of 0.2-5.1%. It usually develops hemi-lingually and tends to be contralateral to the ischemic side possibly due to autonomic dysfunction from insular cortex ischemia. However, this may not always be true since our patient had contralateral angioedema without insular cortex involvement. Initial management includes corticosteroids and antihistamines which are less effective for bradykinin-mediated angioedema. FFP contains kininase 2 which degrades bradykinin and hence is effectively used off label for angiotensin-converting enzyme inhibitor-induced angioedema. As TAOA also follows the bradykinin pathway, we treated our patient with FFP. To our knowledge, this is the first-ever case of TAOA treated with FFP. Other potential treatment options include C1 esterase inhibitor, icatibant (bradykinin receptor antagonist), and ecallantide (kallikrein inhibitor) which are being used for hereditary angioedema and need to be studied for TAOA. CONCLUSIONS: TAOA is a life-threatening complication that typically occurs in the first 4 hours after tPA administration. Physicians should be aware of this uncommon side effect for early recognition and treatment. Treatment targeting the bradykinin pathway like FFP might be more effective and needs further investigation. REFERENCE #1: Rathbun KM. Angioedema after thrombolysis with tissue plasminogen activator: an airway emergency. Oxf Med Case Reports. 2019;2019(1):omy112. Published 2019 Jan 24. doi:10.1093/omcr/omy11 REFERENCE #2: Hemi-orolingual angioedema and ACE inhibition after alteplase treatment of stroke. M. D. Hill, T. Lye, H. Moss, P. A. Barber, A. M. Demchuk, N. J. Newcommon, T. L. Green, C. Kenney, A. Cole–Haskayne, A. M. Buchan. Neurology May 2003, 60 (9) 1525-1527; DOI: 10.1212/01.WNL.0000058840.66596.1A DISCLOSURES: No relevant relationships by Robert Caldera, source=Web Response No relevant relationships by Kristin Fless, source=Web Response No relevant relationships by Bilal Khan, source=Web Response No relevant relationships by Nirav Mistry, source=Web Response No relevant relationships by Vagram Ovnanian, source=Web Response No relevant relationships by Fariborz Rezai, source=Web Response No relevant relationships by Aditi Saha, source=Web Response No relevant relationships by Sohaib Tariq, source=Web Response No relevant relationships by Lalithaa Thirunavukarasu Murugan, source=Web Response No relevant relationships by Paul Yodice, source=Web Response

Tranexamic Acid for the Emergency Treatment of Angiotensin-Converting Enzyme Inhibitor-Induced Angioedema.

Introduction: Angioedema is a rare but potentially life-threatening adverse effect associated with the use of angiotensin-converting enzyme (ACE) inhibitors. Various therapies, including ecallantide, icatibant, complement-1 esterase inhibitors, and fresh frozen plasma, have been used for treatment with inconsistent results and significant adverse effects. Tranexamic acid (TXA) is used as an alternative for the treatment of hereditary angioedema and it may be an attractive option for the treatment of ACE inhibitor-induced angioedema (ACEi-AE) in the emergency department (ED). The purpose of this study was to evaluate the impact of TXA administration on rates of intubation in patients presenting to the ED with suspected ACEi-AE.Methods: This was an institutional review board-approved, retrospective cohort study conducted at a single-site ED. All patients who received TXA for ACEi-AE in the ED between January 1, 2019 and March 31, 2021 were eligible for inclusion. The primary outcome was the proportion of patients who required intubation for suspected ACEi-AE.Results: A total of 16 patients received TXA in the ED for suspected ACEi-AE during the study timeframe. Of these, two patients were intubated prior to administration of TXA. The remaining 14 patients did not require intubation following TXA administration.Conclusion: Administration of TXA was associated with a low rate of adverse effects and did not contribute to further morbidity when added to standard care in patients presenting to the ED with suspected ACEi-AE.

Use of Tranexamic Acid Prevents Intubation in ACE Inhibitor-Induced Angioedema

ACE-I, a common antihypertensive medication, regulates blood pressure by inhibiting angiotensin-converting enzyme (ACE). This inhibition prevents the formation of angiotensin II from angiotensin I, a peptide hormone that causes vasoconstriction

Incidence and risk factors of angiotensin-converting enzyme inhibitor–induced angioedema: A large case-control study

The prevalence of angiotensin-converting enzyme inhibitor–induced angioedema (ACEI-IA) ranges from 0.2% to 0.7%.1-5 Risk factors include being African American, a woman, or an adult aged more than 65 years.1-6 Previous studies are limited to epidemiologic data from single-center studies or risk factors collected from large clinical trials. The objective for this study was to evaluate the incidence of ACEI-IA in a sample of patients from 3 distinct geographic regions of the United States, analyzing patients’ characteristics and comparing possible associated risk factors.