Severe Angioedema Related to ACE Inhibitors in Patients With a History of Idiopathic Angioedema

Orfan, Nicholas; Patterson, Roy; Dykewicz, Mark S.

doi:10.1001/jama.1990.03450100077030

Cited by 67 publications

(16 citation statements)

References 16 publications

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“…It is also advisable to check the complement C'4 level as patients with preexisting angioedema, including HAE as a result of C'1 esterase inhibitor deficiency, are predisposed to develop angioedema in response to ACE inhibitors. 40 In general, angiotensin II receptor antagonists are tolerated by patients who have reacted to ACE inhibitors.…”

Section: Treatment Of Angioedema As a Results Of Ace Inhibitorsmentioning

confidence: 99%

Angioedema

Kaplan

Greaves

2005

Journal of the American Academy of Dermatology

308

235

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Section: Treatment Of Angioedema As a Results Of Ace Inhibitorsmentioning

confidence: 99%

Angioedema

Kaplan

Greaves

2005

Journal of the American Academy of Dermatology

308

235

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“…Female gender, a history of smoking and age > 65 years also seem to be risk factors (13,20). In patients suffering from other forms of angioedema (hereditary, acquired or idiopathic) ACEi seems to have a precipitating effect on the disease (21)(22)(23). Especially patients with hereditary angioedema (HAE) have a greatly increased risk of angioedema when treated with ACEi; this class of pharmaceuticals is thus contraindicated in these patients (24,25).…”

Section: Epidemiology and Risk Factorsmentioning

confidence: 99%

Angiotensin-converting Enzyme Inhibitor-induced Angioedema – A Dangerous New Epidemic

Rasmussen

Mey²,

Bygum³

2014

Acta Derm Venerol

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Angioedema is a sudden localised and often asymmetric swelling of the skin or mucous membranes caused by transient increased endothelial permeability causing plasma extravasation. In the last decades the incidence of severe angioedema involving the upper airways and even fatal outcome due to asphyxia has increased. This is mainly due to pharmaceuticals such as angiotensin converting enzyme-inhibitors, which are extensively used worldwide. Some aspects of the pathophysiology have been elucidated and the vasoactive molecule bradykinin is shown to be one of the main causative agents. The diagnosis is often delayed and traditional treatment usually ineffective. Complement C1 inhibitor concentrate and bradykinin receptor antagonists, normally used to treat patients with hereditary angioedema, have shown good results when used in patients with bradykinin-mediated angioedema. This review discusses the disease, prognosis and treatment options.

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“…For example, in aspirin-induced asthma, cyclooxygenase inhibition is associated with enhanced release of leukotrienes from pulmonary mast cells (115,116), although one group has claimed to have identified anti-drug IgE antibodies in hypersensitive patients (96,117). ACE inhibitors can cause angioedema through exacerbation of the pharmacological effects of mediators (118), while studies have demonstrated greater hazards associated with anaphylaxis in patients receiving -blockers which can influence the release of mediators by modulation of adenylate cyclase (119). The incidence of severe anaphylactoid reactions during anaesthesia is 1 in 10 000 cases (105).…”

Section: Role Of Cellular Disposition Inmentioning

confidence: 99%