Ace angioedema
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ACE Inhibitor-Induced Angioedema: Incidence, Pathophysiology, and Treatment
Incidence and Risk Factors of ACE Inhibitor-Induced Angioedema
Angiotensin-converting enzyme (ACE) inhibitor-induced angioedema is a rare but potentially life-threatening adverse effect, occurring in approximately 0.1% to 0.7% of patients treated with ACE inhibitors . The incidence is notably higher among certain populations, including African Americans, Hispanics, smokers, women, older individuals, and those with a history of drug rash or seasonal allergies . The risk is also elevated in patients using immunosuppressive therapy or other medications that affect the renin-angiotensin system.
Pathophysiology of ACE Inhibitor-Induced Angioedema
The pathogenesis of ACE inhibitor-induced angioedema primarily involves the accumulation of bradykinin, a peptide that causes vasodilation and increased vascular permeability . ACE inhibitors prevent the breakdown of bradykinin, leading to its accumulation and subsequent angioedema. Other mediators such as histamine, substance P, and prostaglandins may also play a role, although their exact contributions are not fully understood . Genetic factors, including polymorphisms in genes related to bradykinin metabolism, have been suggested to contribute to the susceptibility to this condition .
Clinical Manifestations
ACE inhibitor-induced angioedema typically presents with swelling of the face, lips, tongue, uvula, and upper airways, which can lead to airway obstruction and necessitate emergency interventions such as intubation or tracheotomy . In some cases, intestinal involvement with sub-occlusive symptoms has been reported. The onset of symptoms can occur within hours to years after starting ACE inhibitor therapy, making it a challenging condition to predict and diagnose .
Treatment and Management
Immediate withdrawal of the ACE inhibitor is crucial upon the onset of angioedema . Standard treatments include supportive care, corticosteroids, antihistamines, and epinephrine, although their efficacy is limited . Icatibant, a selective bradykinin B2 receptor antagonist, has shown promise in reducing the time to resolution of symptoms compared to standard therapy with glucocorticoids and antihistamines. However, its efficacy may vary among different ethnic groups, with some studies indicating less effectiveness in Black patients .
Recurrence and Alternative Therapies
Patients who experience ACE inhibitor-induced angioedema are at risk of recurrence if re-exposed to ACE inhibitors and should avoid this class of drugs permanently. Angiotensin receptor blockers (ARBs) are often considered as an alternative; however, there is a small risk of angioedema recurrence with ARBs, estimated between 2% and 17% . The incidence of angioedema with ARBs and direct renin inhibitors (DRIs) is significantly lower than with ACE inhibitors and is comparable to placebo.
Conclusion
ACE inhibitor-induced angioedema is a rare but serious condition that requires prompt recognition and management. Understanding the risk factors, pathophysiology, and effective treatment options is essential for minimizing the impact of this adverse effect. While icatibant offers a promising treatment, further research is needed to confirm its efficacy across different populations. Avoidance of ACE inhibitors in high-risk individuals and careful monitoring of alternative therapies are crucial steps in managing this condition.
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