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Review
. 2014 Sep 29;4(4).
doi: 10.3402/jchimp.v4.25260. eCollection 2014.

Drug-induced visceral angioedema

Prashanth M Thalanayar  1 , Ibrahim Ghobrial  1 , Fritz Lubin  1 , Reena Karnik  1 , Robin Bhasin  1
Affiliations
Review

Drug-induced visceral angioedema

Prashanth M Thalanayar et al. J Community Hosp Intern Med Perspect. .

Abstract

Angioedema associated with angiotensin converting enzyme inhibitors (ACEIs) is due to the accumulation of bradykinin and its metabolites. Angiotensin receptor blockers (ARBs) produce anti-hypertensive effects by blocking the angiotensin II AT1 receptor action; hence bradykinin-related side effects are not expected. However, we notice the occurrence of ARB-induced angioedema as not a very rare side effect. Visceral drug-induced angioedema has been reported with ACEIs, not with ARBs. This underlying review will help educate readers on the pathophysiology and recent guidelines pertaining to ACEI- and ARB-induced visceral angioedema.

Keywords: angiotensin converting enzyme inhibitor; angiotensin receptor blocker; intestinal angioedema; visceral angioedema.

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Figures

Fig. 1
Fig. 1
Renin-angiotensin system. Mechanisms behind ARB-induced angioedema. Flow diagram showing feedback-induced increase in Angiotesin II levels and subsequent ACE self-inhibition. Also shown is an illustration of feedback-induced AT2 receptor-mediated bradykinin stimulation associated with ARB administration. ACEI=angiotensin converting enzyme inhibitor; ARB=angiotensin receptor blocker; AT=angiotensin.
Fig. 2
Fig. 2
Contrast CT findings of visceral angioedema. (a) Peri-hepatic fluid accumulation. (b, c) Small bowel wall edema, Target sign.
Fig. 3
Fig. 3
Flowchart depicting the algorithmic approach to episodic abdominal pain that was used in the described case.
Fig. 4
Fig. 4
Mechanism of bradykinin accumulation associated with ACEI use. ACE inhibition leads to diversion of substrates toward secondary enzymes rather than primary metabolizing enzymes thereby producing physiologically active metabolites. LMW=low molecular weight; HMW=high molecular weight; B1=bradykinin 1; B2=bradykinin 2.
See this image and copyright information in PMC

References

    1. Hoover T, Lippmann M, Grouzmann E, Marceau F, Herscu P. Angiotensin converting enzyme inhibitor induced angio-oedema: A review of the pathophysiology and risk factors. Clin Exp Allergy. 2010;40:50–61. - PubMed
    1. The use of medicines in the United States: Review of 2011 Report by the IMS Institute for Healthcare Informatics April 2012. Available from: http://www.imshealth.com/ims/Global/Content/Insights/IMS Institutefor He... [cited 12 September 2013].
    1. Paul M, Poyan Mehr A, Kreutz R. Physiology of local renin-angiotensin systems. Physiol Rev. 2006;86(3):747–803. - PubMed
    1. Dendorfer A, Wolfrum S, Wagemann M, Qadri F, Dominiak P. Pathways of bradykinin degradation in blood and plasma of normotensive and hypertensive rats. Am J Physiol Heart Circ Physiol. 2001;280(5):H2182–8. - PubMed
    1. Urich K. Toxic proteins and peptides: Enzymes and other protein components. Comparative animal Biochemistry. In: Urich K, editor. Munsingen, Germany: Springer; 1994. pp. 323–4. 9.1.2 Available from: http://books.google.com/books?id=GLbcWyeaCGQC&323#v=onepage&q=323&f=false [cited 30 August 2014].

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