Cardiovascular and Diabetic Medications That Cause Bradykinin-Mediated Angioedema

Hudey, S.; Westermann-Clark, Emma; Lockey, Richard F.

doi:10.1016/j.jaip.2017.03.017

Cited by 20 publications

(23 citation statements)

References 41 publications

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“…This risk assessment of neoplasm incidence would also become important for favouring ARBs over ACEIs. ACEIs accelerate the activity of bradykinin in tissues, and angiogenesis might be stimulated (4). In addition, increase in substance P by ACEIs could partially explain the higher incidence of cancer (5).…”

Section: Angiotensin Receptor Blockers and Angiotensin-converting Enzmentioning

confidence: 99%

Angiotensin Receptor Blockers and Angiotensin-Converting Enzyme Inhibitors for the Treatment of Hypertensive Patients With Type 2 Diabetes Mellitus

Kawada

2020

Canadian Journal of Diabetes

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Section: Angiotensin Receptor Blockers and Angiotensin-converting Enzmentioning

confidence: 99%

Angiotensin Receptor Blockers and Angiotensin-Converting Enzyme Inhibitors for the Treatment of Hypertensive Patients With Type 2 Diabetes Mellitus

Kawada

2020

Canadian Journal of Diabetes

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“…It is self-evident that patients with HAE should not be treated with ACEIs, which inhibit the degradation of bradykinin [67, 68]. Caution should be taken when prescribing gliptins, neprilysin, and mTOR inhibitors [2, 5, 69, 70]. Furthermore, infections, e.g., Helicobacter pylori , might precipitate angio-oedema attacks [56, 71].…”

Section: Clinical Presentationmentioning

confidence: 99%

“…Aspirin and other non-steroidal anti-inflammatory drugs can induce angio-oedema through their ability to inhibit cyclooxygenase favouring leukotriene production [92]. Drug-induced angio-oedema related to ACEIs, gliptins, neprilysin, and mTOR inhibitors seems to be bradykinin mediated and is normally not accompanied by urticaria [2, 5, 68-70, 95]. Abdominal attacks are very painful and might mimic acute abdomen with a risk of surgery being performed [96].…”

Section: Differential Diagnosesmentioning

confidence: 99%

“…Among patients with primary angio-oedema, i.e., angio-oedema without associated urticaria, the bradykinin-mediated angio-oedema subtypes should be considered [2, 3]. Most of these patients develop angio-oedema due to medications [4, 5], especially angiotensin-converting enzyme inhibitors (ACEIs); however, others may have hereditary angio-oedema (HAE).…”

Section: Introductionmentioning

confidence: 99%

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Hereditary Angio-Oedema for Dermatologists

Bygum¹

2019

Dermatology

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Among angio-oedema patients, hereditary angio-oedema (HAE) should not be overlooked. Besides skin swellings, these patients might have very painful abdominal attacks and potentially life-threatening angio-oedema of the upper airway. They will not respond to traditional anti-allergic therapy with antihistamines, corticosteroids, and adrenaline, and instead need specific drugs targeting the kallikrein-kinin pathway. Classically, patients with HAE have a quantitative or qualitative deficiency of the C1 inhibitor (C1INH) due to different mutations in SERPING1, although a new subtype with normal C1INH has been recognised more recently. This latter variant is diagnosed based on clinical features, family history, or molecular genetic testing for mutations in F12, ANGPT1,or PLG.The diagnosis of HAE is often delayed due to a general unfamiliarity with this orphan disease. However, undiagnosed patients are at an increased risk of unnecessary surgical interventions or life-threatening laryngeal swellings. Within the last decade, new and effective therapies have been developed and launched for acute and prophylactic therapy. Even more drugs are under evaluation in clinical trials. It is therefore of utmost importance that patients with HAE are diagnosed as soon as possible and offered relevant therapy with orphan drugs to reduce morbidity, prevent mortality, and improve quality of life.

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“…A complete understanding of how ARBs cause angioedema is still uncertain. Research in human subjects suggests that ARBs increase bradykinin levels via indirect mechanisms which can lead to specific treatments . However, case reports (not described here due to inherent design limitations) and rare studies emerged on the incidence of angioedema with ARBs therapy after treatment was switched from an ACE‐I or was introduced without switch (Table ).…”

Section: Review Of Studies Of Arb‐induced Angioedemamentioning

confidence: 99%