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Drug-induced angioedema is a known complication of the use of angiotensin-converting enzyme (ACE) inhibitors, angiotensin II antagonists (ARBs), and Angiotensin-Neprilysin Inhibitor LCZ969. [ 1 ] : 120 The angioedema appears to be dose dependent as it may resolve with decreased dose.
In people with ACE inhibitor angioedema, the drug needs to be discontinued and an alternative treatment needs to be found, such as an angiotensin II receptor blocker (ARB), [17] which has a similar mechanism but does not affect bradykinin. However, this is controversial, as small studies have shown some patients with ACE inhibitor angioedema ...
Angiotensin-converting-enzyme inhibitors (ACE inhibitors) are a class of medication used primarily for the treatment of high blood pressure and heart failure. [1] [2] This class of medicine works by causing relaxation of blood vessels as well as a decrease in blood volume, which leads to lower blood pressure and decreased oxygen demand from the heart.
In severe cases, the elevation of bradykinin may result in angioedema, a medical emergency. [13] People of African descent have up to five times increased risk of ACE inhibitor induced angioedema due to hereditary predisposing risk factors such as hereditary angioedema. [14] This refractory cough is a common cause for stopping ACE inhibitor ...
Lisinopril is an ACE inhibitor, meaning it blocks the actions of angiotensin-converting enzyme (ACE) in the renin–angiotensin–aldosterone system (RAAS), preventing angiotensin I from being converted to angiotensin II. Angiotensin II is a potent direct vasoconstrictor and a stimulator of aldosterone release.
Reflecting the critical role of zinc, ACE can be inhibited by metal-chelating agents. [14] ACE in complex with inhibitor lisinopril, zinc cation shown in grey, chloride anions in yellow. Based on PyMOL rendering of PDB 1o86. The picture shows that lisinopril is a competitive inhibitor, since it and angiotensin I are similar structurally.
Drug-induced AAE can be triggered by certain medications, including ACE inhibitors or angiotensin receptor blockers. [18] Furthermore, additional laboratory testing can be done to consider other causes of swelling that appear similar to angioedema. [2]
Inhibition of ACE with ACE inhibitors leads to decreased conversion of angiotensin I to angiotensin II (a vasoconstrictor) but also to an increase in bradykinin due to decreased degradation. This explains why some patients taking ACE inhibitors develop a dry cough, and some react with angioedema, a dangerous swelling of the head and neck region.