Treatment of Life-Threatening ACE-Inhibitor–Induced Angioedema

Hirschy, RaeAnn; Shah, Tanvi; Davis, Tamara M.; Rech, Megan A.

doi:10.1097/tme.0000000000000211

Cited by 3 publications

(4 citation statements)

References 54 publications

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“…This supports the assumption that single-area intraabdominal AE is underreported due to the difficulty in diagnostics. 17,44 Hospitalization and ER visit were observed in 43.2% and 40.3% of cases, respectively, establishing how AE is a patient group that requires acute resources in the medical care system. A study revealed increased annual number of admissions and costs due to AE during the period of 1998 to 2005.…”

Section: Discussionmentioning

confidence: 99%

“…Anti-allergic standard treatment (antihistamines, corticosteroids, adrenaline) was most frequently administered to patients in this cohort, despite the fact that these drugs are ineffective for patients with non-histaminergic AE. 17 Treatment of AE is based on pathophysiology, but this is rarely possible in the acute setting to determine the underlying mediator of AE. Many of the patients in this study were reported with good effect of antihistamines and corticosteroids even though none showed clinical signs of urticaria.…”

Section: Discussionmentioning

confidence: 99%

“…1 Even though there are different pathophysiological causes of AE, many cases have overlapping clinical manifestations, which makes diagnosis and treatment difficult. 17,18 Overall the treatment of AE depends on the symptoms. AE attacks are self-limiting and last 1-7 days without medical treatment.…”

Section: Introductionmentioning

confidence: 99%

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<p>Clinical Features and Disease Course of Primary Angioedema Patients in a Tertiary Care Hospital</p>

Pall¹,

Lomholt²,

Buchwald³

et al. 2020

JAA

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Purpose: To give a better understanding of primary AE, the clinical characteristics and the possible therapeutic approaches. Background: Angioedema (AE) is a non-pitting, non-itching swelling of skin or mucosa. The symptom can become life-threatening if located in the airways. Primary (monosymptomatic) AE is a manifestation of several different diseases and the diagnosis is not always straightforward. The aetiological and pathophysiological factors of primary AE are not completely clarified. There is a need for further investigation. Patients and Methods: This was a retrospective cohort study of patients referred to an outpatient dermatology clinic in a tertiary care hospital for clinical assessment due to primary AE in the period from 1996 to 2014. Results: A total of 315 patients were identified with primary AE. The most frequent subtype was idiopathic AE (42.5%) and the second most common was angiotensin-converting enzymeinhibitor (ACEi)-induced AE (31.1%). Three patients were diagnosed with hereditary AE and one patient was diagnosed with acquired C1-inhibitor deficiency. At least 107 (34.0%) patients had established histaminergic AE. More than 1/3 of the patients were treated in an emergency room or hospitalized due to AE. A 98.1% of patients had experienced AE in the head and neck area. Seven patients were in the need of acute airway intervention. Six of these had ACEi-induced AE. Female sex and smoking were found to be risk factors for developing AE. Conclusion: The most frequent diagnoses were histaminergic-, non-histaminergic idiopathic AE and ACEi-induced AE, whereas complement C1-inhibitor deficiency was rare. Histaminergic AE made up a substantial group of patients with primary AE. Even though there are different pathophysiological causes of AE, many cases have overlapping clinical manifestations, which make diagnosis and treatment difficult.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

<p>Clinical Features and Disease Course of Primary Angioedema Patients in a Tertiary Care Hospital</p>

Pall¹,

Lomholt²,

Buchwald³

et al. 2020

JAA

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“…In addition to icatibant, ecallantide, tranexamic acid, purified C1 inhibitor concentrate, and possibly fresh frozen plasma are other therapies that are effective for aborting attacks of angioedema in hereditary angioedema (HAE). In theory, these treatments could be helpful in ACE inhibitor-induced angioedema, but available studies are greatly limited [19].…”

Section: Discussionmentioning

confidence: 99%

Angiotensin-Converting Enzyme Inhibitor Induced Angioedema Occurring after 8 Years of Taking Lisinopril: A Case Report

Jodeh¹,

Stone²

2020

CRCM

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Angiotensin-converting enzyme inhibitor induced angioedema (AIIA) can vary from mild to life-threatening. A vast majority of cases of AIIA occur within a month of starting an angiotensin-converting enzyme-inhibitor (ACE-I).We present a 48-year-old male who presented with respiratory failure secondary to AIIA, after being on lisinopril for over 8 years. He had no previous complications secondary to lisinopril and aside from smoking, carried no risk factors for AIIA. Despite conventional treatment for angioedema, he had a prolonged stay in the Medical Intensive Care Unit (MICU). Following discharge, there hasn't been a recurrence of AIIA since the discontinuation of lisinopril. The case is intended to caution that AIIA remains possible even late into a chronic regimen of ACE-I. This is a risk that shouldn't be neglected, even with sparse risk factors or longer duration of ACE-I use. Conventional treatment is not currently in line with proposed etiologies of AIIA. We advocate for more clinical trials involving pharmaceutical agents targeting bradykinin accumulation.

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