ACE inhibitor-induced cough
Chronic cough is a well-described class effect of angiotensin converting enzyme (ACE) inhibitors.
The cough is typically dry and is associated with a tickling or scratching sensation in the throat. Reports vary; 5 –35% of patients who receive ACE inhibitors develop a dry cough, sometimes severe enough to require discontinuation of the drug.
ACE inhibitor cough is considered a class effect that may occur with any ACE inhibitors and is not dose-dependent. Cough may occur within hours of the first dose of medication, or its onset can be delayed for weeks to months after the initiation of therapy.
Treatment with ACE inhibitors may sensitise the cough reflex, thereby potentiating other causes of chronic cough. 3 Although cough usually resolves within 1 –4 weeks of cessation of therapy with the offending drug, in a subgroup of individuals cough may linger for up to 3 months. Women and those of black or Asian ethnicity have been reported to be at increased risk of ACE inhibitor cough. Mechanisms of cough from ACE inhibitors The inhibition of ACE prevents the conversion of angiotensin I to angiotensin II, with consequent salutary benefits via the renin– angiotensin system in pathological states. ACE inhibitor cough is thought to be linked to the suppression of ACE, which is proposed to result in an accumulation of substances normally metabolised by ACE: bradykinin and substance P. However, the development of cough may result from a more complex cascade of events than originally believed. Bradykinin has been shown to induce the production of arachidonic acid metabolites and nitric oxide, and there is some evidence that these products, which are subject to regulation by other pathways, may promote cough through proinflammatory mechanisms.
Can angiotensin II receptor blockers be used in patients with a history of ACE inhibitor cough?
Theoretically, angiotensin II receptor blockers (ARBs) should not induce cough as they do not directly inhibit ACE activity or inhibit the breakdown of bradykinin. Indeed, ARBs have been associated with a low incidence of cough in patients with a history of ACE inhibitor cough, e.g. the frequency of cough with losartan was lower than with lisinopril (29 versus 72%, P < 0.01), and similar to hydrochlorothiazide (34%). 5 CPPC c01.tex V2 - 11/18/2015 1:44 P.M.
A Treatment of ACE inhibitor cough
The only uniformly effective intervention for ACE inhibitor-induced cough is the cessation of therapy with the offending agent. In cases in which the continuation of an ACE inhibitor is necessary despite cough, cromoglicate, baclofen, theophylline and local anaesthetics have been reported to be of some benefit, although none has been subjected to large-scale trials.
Since the use of ACE inhibitors is now widespread, it is vitally important that practitioners consider identifying cases of ACE inhibitor-induced cough.
Available studies indicate that, in the great majority of patients, those who develop these adverse reactions from ACE inhibitors can tolerate ARBs. The cardiovascular benefits and potential reduction in mortality from use of these drug classes are important and significant.
Therefore, in a risk–benefit assessment, consideration should be given to the cautious alternative use of ARBs in the management of patients who develop cough from ACE inhibitors.
Chronic cough is a well-described class effect of angiotensin converting enzyme (ACE) inhibitors.
The cough is typically dry and is associated with a tickling or scratching sensation in the throat. Reports vary; 5 –35% of patients who receive ACE inhibitors develop a dry cough, sometimes severe enough to require discontinuation of the drug.
ACE inhibitor cough is considered a class effect that may occur with any ACE inhibitors and is not dose-dependent. Cough may occur within hours of the first dose of medication, or its onset can be delayed for weeks to months after the initiation of therapy.
Treatment with ACE inhibitors may sensitise the cough reflex, thereby potentiating other causes of chronic cough. 3 Although cough usually resolves within 1 –4 weeks of cessation of therapy with the offending drug, in a subgroup of individuals cough may linger for up to 3 months. Women and those of black or Asian ethnicity have been reported to be at increased risk of ACE inhibitor cough. Mechanisms of cough from ACE inhibitors The inhibition of ACE prevents the conversion of angiotensin I to angiotensin II, with consequent salutary benefits via the renin– angiotensin system in pathological states. ACE inhibitor cough is thought to be linked to the suppression of ACE, which is proposed to result in an accumulation of substances normally metabolised by ACE: bradykinin and substance P. However, the development of cough may result from a more complex cascade of events than originally believed. Bradykinin has been shown to induce the production of arachidonic acid metabolites and nitric oxide, and there is some evidence that these products, which are subject to regulation by other pathways, may promote cough through proinflammatory mechanisms.
Can angiotensin II receptor blockers be used in patients with a history of ACE inhibitor cough?
Theoretically, angiotensin II receptor blockers (ARBs) should not induce cough as they do not directly inhibit ACE activity or inhibit the breakdown of bradykinin. Indeed, ARBs have been associated with a low incidence of cough in patients with a history of ACE inhibitor cough, e.g. the frequency of cough with losartan was lower than with lisinopril (29 versus 72%, P < 0.01), and similar to hydrochlorothiazide (34%). 5 CPPC c01.tex V2 - 11/18/2015 1:44 P.M.
A Treatment of ACE inhibitor cough
The only uniformly effective intervention for ACE inhibitor-induced cough is the cessation of therapy with the offending agent. In cases in which the continuation of an ACE inhibitor is necessary despite cough, cromoglicate, baclofen, theophylline and local anaesthetics have been reported to be of some benefit, although none has been subjected to large-scale trials.
Since the use of ACE inhibitors is now widespread, it is vitally important that practitioners consider identifying cases of ACE inhibitor-induced cough.
Available studies indicate that, in the great majority of patients, those who develop these adverse reactions from ACE inhibitors can tolerate ARBs. The cardiovascular benefits and potential reduction in mortality from use of these drug classes are important and significant.
Therefore, in a risk–benefit assessment, consideration should be given to the cautious alternative use of ARBs in the management of patients who develop cough from ACE inhibitors.
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