Examination of baseline levels of carboxypeptidase N and complement components as potential predictors of angioedema associated with the use of an angiotensin-converting enzyme inhibitor

Sigler, C.

doi:10.1001/archderm.133.8.972

Cited by 13 publications

(8 citation statements)

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“…Plasma bradykinin has also been shown to be elevated during ACE inhibitor‐related episodes of angioedema (Figure 3). 48,49 An additional study has reported decreased levels of carboxypeptidase N (kininase I) and C1 esterase inhibitor in affected patients treated with an ACE inhibitor 50 . More recently, low levels of aminopeptidase P and dipeptidyl peptidase IV, enzymes known to catabolize bradykinin, have been observed in patients having developed angioedema in association with an ACE inhibitor 51,52 …”

Section: Mechanisms Involved In Ace Inhibitor‐induced Angioedemamentioning

confidence: 99%

Angioedema in Heart Failure: Occurrence With ACE Inhibitors and Safety of Angiotensin Receptor Blocker Therapy

Sica

Black

2002

Congestive Heart Failure

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Angioedema is a well-known side effect of treatment with an angiotensin-converting enzyme (ACE) inhibitor and one that we have been willing to accept in view of the incidence of the problem and the clear benefits of this class of agents in numerous clinical situations. Angioedema is also seen with angiotensin receptor blocker (ARB) therapy but much less frequently than with ACE inhibitors. The mechanism for angioedema with ARB therapy remains poorly defined. ACE inhibitor-related angioedema occurs more commonly in black patients. The basis for an increased risk of angioedema in black patients remains unclear. Angioedema can be life-threatening but more times than not it can be managed with conservative treatment measures including specifically the discontinuation of the medication and/or administration of an antihistamine and/or epinephrine. Occasionally, maneuvers to protect the integrity of the airway may be needed. In a heart failure patient having previously experienced ACE inhibitor-related angioedema, ARBs should be used cautiously since angioedema has been reported with ARB therapy in heart failure patients. The need to reduce renin-angiotensin aldosterone system activity in a heart failure patient would seem to justify the small risk of angioedema with ARB therapy in a patient having previously experienced ACE inhibitor-related angioedema.

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Section: Mechanisms Involved In Ace Inhibitor‐induced Angioedemamentioning

confidence: 99%

Angioedema in Heart Failure: Occurrence With ACE Inhibitors and Safety of Angiotensin Receptor Blocker Therapy

Sica

Black

2002

Congestive Heart Failure

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“…At present, ACEi‐induced angio‐oedema ia believed to result from alterations of bradykinin metabolism pathways causing increased concentrations of bradykinin, a mediator of inflammation, vasodilation and capillary leakage [6–12]. In general, changes of bradykinin steady‐state concentration in plasma and tissue can follow either diminished activity of degrading enzymes such as ACE or increased activity of generating enzymes such as kallikrein.…”

Section: Introductionmentioning

confidence: 99%

Potential genetic risk factors in angiotensin‐converting enzyme‐inhibitor‐induced angio‐oedema

Baş

Hoffmann

Tiemann

et al. 2010

Brit J Clinical Pharma

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KeywordsACE I/D polymorphism, angio-oedema, bradykinin, bradykinin B2 receptor polymorphism, serum ACE activity ---------------------------------------------------------------------- WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT• Angiotensin-converting enzyme inhibitor (ACEi)-induced angio-oedema is an underestimated clinical life-threatening problem.• The incidence of this non-allergic, bradykinin-induced drug side-effect is 1 : 4000.• Although most ACEi-treated patients probably have an increased bradykinin plasma concentration, only 0.5% of them develop an angio-oedema and nothing is known about potential risk factors. WHAT THIS STUDY ADDS• In our attempt to elucidate the unpredictable character of ACEi-induced angio-oedema, we investigated bradykinin B2 receptor 2/3 and c.C181T polymorphisms as well as the ACE insertion/deletion polymorphism in combination with serum ACE activity in 65 patients.• ACE insertion/deletion and bradykinin B2 receptor polymorphisms are not involved in the development of ACEi-induced angio-oedema.• Further studies should be carried out to clarify whether a combination of these polymorphisms might be a risk factor for ACEi-induced angio-oedema. AIMSThe pathophysiology of angiotensin-converting enzyme inhibitor (ACEi)-induced angio-oedema remains unclear. We have investigated the impact of ACE insertion/deletion (I/D) polymorphism in combination with serum ACE activity as well as the bradykinin B2 receptor 2/3 and c.C181T polymorphisms. METHODSWe analysed the ACE I/D as well as bradykinin B2 (2/3 and C181T) receptor polymorphisms in 65 patients with documented episodes of ACEi-induced angio-oedema and 65 patients matched for age and sex being under ACEi treatment without history of angio-oedema. Furthermore, we determined serum ACE activity in 47 of the 65 angio-oedema patients 3 months after the angio-oedema attack and compared these values with 51 healthy individuals (control II). ; P = 0.9). RESULTS No risk association was identified between ACE CONCLUSIONSOur data suggest that polymorphism of ACE I/D and the bradykinin B2 receptor polymorphisms are not involved in the development of ACEi-induced angio-oedema when considered individually. Further studies should be carried out to clarify whether a combination of these polymorphisms might be a risk factor for ACEi-induced angio-oedema.

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“…An additional study has reported decreased levels of carboxypeptidase N and C1 esterase inhibitor in affected patients treated with an ACE inhibitor 36 . More recently, low levels of aminopeptidase P and dipeptidyl peptidase IV, enzymes known to catabolize bradykinin, have been suggested as predisposing factors for development of angioedema in patients treated with ACE inhibitors 37,38 .…”

Section: Mechanisms Involved In Ace Inhibitor‐induced Angioedemamentioning

confidence: 98%

ACE Inhibitor‐Related Angioedema: Can Angiotensin‐Receptor Blockers Be Safely Used?

Sica

Black

2002

J of Clinical Hypertension

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Angioedema is a well‐recognized side effect of angiotensin‐converting enzyme (ACE) inhibitor therapy. Angioedema can also be seen with angiotensin receptor blocker therapy but much less frequently than is the case with ACE inhibitors. For unclear reasons, ACE inhibitor‐related angioedema occurs more commonly in black patients. Angioedema can be life threatening but more times than not its occurrence can be managed with conservative treatment measures including discontinuation of the medication and/or administration of an antihistamine. Occasionally, epinephrine and/or steroid therapy may be warranted. In a patient having experienced ACE inhibitor‐related angioedema, angiotensin receptor blockers should be used cautiously if at all. If angiotensin receptor blocker therapy is being considered in a patient with prior ACE inhibitor‐related angioedema there should be some justification for the use. Such justification might include the presence of heart failure or proteinuric nephropathic states among other considerations.

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Examination of baseline levels of carboxypeptidase N and complement components as potential predictors of angioedema associated with the use of an angiotensin-converting enzyme inhibitor

Cited by 13 publications

References 0 publications

Angioedema in Heart Failure: Occurrence With ACE Inhibitors and Safety of Angiotensin Receptor Blocker Therapy

Angioedema in Heart Failure: Occurrence With ACE Inhibitors and Safety of Angiotensin Receptor Blocker Therapy

Potential genetic risk factors in angiotensin‐converting enzyme‐inhibitor‐induced angio‐oedema

ACE Inhibitor‐Related Angioedema: Can Angiotensin‐Receptor Blockers Be Safely Used?

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