ACE Inhibitor-Induced Angioedema: a Review

Kostis, William J.; Shetty, Mrinali; Chowdhury, Yuvraj S.; Kostis, John B.

doi:10.1007/s11906-018-0859-x

Cited by 90 publications

(93 citation statements)

References 57 publications

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“…Both KK inhibitors and BK2 receptor antagonists showed no improvement over placebo or usual treatment despite several positive case reports. Two important factors to take into account is that ACE is only one of the many enzymes involved in the elimination of BK and that earlier reports have shown that patients with ACEia have lower activity of APP as well as DPP-IV [43]. Moreover, ACE not only breaks down BK but also substance P, which is also vasoactive.…”

Section: Discussionmentioning

confidence: 99%

Current Treatment of Angioedema Induced by ACE Inhibitors

Terreehorst

Reitsma

Cohn

2019

Curr Treat Options Allergy

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Purpose of Review Angioedema is a well-known side effect of ACE inhibitors. Current knowledge shows that the underlying pathophysiological mechanism is an excess of bradykinin, most likely due to ineffective breakdown pathways. Since C1 inhibitor deficiency has the same pathophysiological background, it would be logical to assume that C1 inhibitor deficiency treatments could be of use in ACE inhibitor-induced angioedema. The objective of this review was to evaluate the evidence for treatment of ACE inhibitorinduced angioedema by means of drugs intervening in the bradykinin system. Recent Findings We searched in the literature for double-blind placebo-controlled trials using either inhibitors of production of kallikrein, bradykinin receptor antagonists, C1 inhibitor concentrate, or fresh frozen plasma as treatment for ACE inhibitor-induced angioedema. The reference list of retrieved articles was checked for articles with the same subject (snowballing). The evidence for each treatment was evaluated by IT and DMC. Summary Double-blind placebo-controlled trials were only found for ecallantide and icatibant. Both treatments did not show superiority over conventional treatment with histamine receptor antagonists and steroids. No double-blind placebo-controlled trials were found of fresh frozen plasma or C1 inhibitor concentrate. To date, there is insufficient evidence for the use of bradykinin receptor antagonists and kallikrein production inhibitors. Although case reports regarding the use of fresh frozen plasma and C1 inhibitor concentrate are positive, well-designed trials are lacking. Drug Allergy (L Mayorga, Section Editor)

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Section: Discussionmentioning

confidence: 99%

Current Treatment of Angioedema Induced by ACE Inhibitors

Terreehorst

Reitsma

Cohn

2019

Curr Treat Options Allergy

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“…The blockade of ACE by specific inhibitors (i.e., captopril, enalapril, benazepril, zofenopril, lisinopril, etc.) mediates arterial and venous vasodilatation, inducing the hypotensive effect (Kostis, Shetty, Chowdhury, & Kostis, ).…”

Section: Chemical Agentsmentioning

confidence: 99%

The role of teratogens in neural crest development

Cerrizuela

Vega-Lopez

Aybar

2020

Birth Defects Research

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The neural crest (NC), discovered by Wilhelm His 150 years ago, gives rise to a multipotent migratory embryonic cell population that generates a remarkably diverse and important array of cell types during the development of the vertebrate embryo. These cells originate in the neural plate border (NPB), which is the ectoderm between the neural plate and the epidermis. They give rise to the neurons and glia of the peripheral nervous system, melanocytes, chondrocytes, smooth muscle cells, odontoblasts and neuroendocrine cells, among others. Neurocristopathies are a class of congenital diseases resulting from the abnormal induction, specification, migration, differentiation or death of NC cells (NCCs) during embryonic development and have an important medical and societal impact. In general, congenital defects affect an appreciable percentage of newborns worldwide. Some of these defects are caused by teratogens, which are agents that negatively impact the formation of tissues and organs during development. In this review, we will discuss the teratogens linked to the development of many birth defects, with a strong focus on those that specifically affect the development of the NC, thereby producing neurocristopathies.Although increasing attention is being paid to the effect of teratogens on embryonic development in general, there is a strong need to critically evaluate the specific role of these agents in NC development. Therefore, increased understanding of the role of these factors in NC development will contribute to the planning of strategies aimed at the prevention and treatment of human neurocristopathies, whose etiology was previously not considered.

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“…It's benign when limited to skin but can cause respiratory distress when present in the mouth, pharynx or larynx [1] [2]. It's estimated that over 40 million people around the world are prescribed ACE-Is (angiotensin-converting enzyme inhibitors), with the most common being lisinopril [2] [3]. Drug-induced angioedema has implicated multiple classes of drugs, the most common being Angiotensin-converting enzyme-inhibitor induced angioedema (AIIA) [4].…”

Section: Introductionmentioning

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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ACE Inhibitor-Induced Angioedema: a Review

Abstract: ACE-I are frequently used therapeutic agents that are associated with angioedema. Their use should be avoided in high-risk individuals and early diagnosis, tracheal intubation in cases of airway compromise, and absolute avoidance of re-challenge are important.

Cited by 90 publications

References 57 publications

Current Treatment of Angioedema Induced by ACE Inhibitors

Current Treatment of Angioedema Induced by ACE Inhibitors

The role of teratogens in neural crest development

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

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