Class of 2010 Abstract / OBJECTIVES: To comprehensively review medical literature and report angiotension converting enzyme inhibitors (ACE-‐I) adverse drug reactions including, incidences, mechanism of action, predisposing conditions, and report prevention and treatments. METHODS: This was a descriptive retrospective study of data related to ACE-‐I adverse drug reactions other than ACE-‐I induced cough. It was to review the ADR that accompany with the use of ACE-‐I. Literature obtained through search engines MEDLINE and OVID SP available through the Arizona Health and Science Library at the University of Arizona.
RESULTS: This comprehensive literature review looked at angioneurotic edema, orthostatic hypotension, hyperkalemia, and increased risk of bleeding and anaphylaxis with tPA and to a minor extent Elevated serum creatinine, and Teratogenicity. Angioneurotic edema (angioedema) reports initially estimated an incidence of 0.1 to 0.7%. A comprehensive review suggested the incidence was even lower at 0.1 to 0.2%, but the OCTAVE trial that specifically looked at angioedema as an endpoint estimated an incidence of ~0.7% although the study only had a 24-‐week follow up. Most patients that discontinued treatment due to angioedema experienced symptom relief within 72 hours. The incidence of orthostatic hypotension from a study that followed patients on lisinopril was only 0.25%;moreover, a meta-‐analysis by Agusti et al included 51 RCT that reported a relative risk of developing OH on an ACE-‐I alone was 1.95. Hyperkalemia incidence reporeted varied from 1.1% to 10%; the more recent literature suggests a value near the lower end of this range. Elevated serum creatinine appears to occur early in ACE-‐I treatment with discontinuation resolving in resolution. ACE-‐I have been shown to be teratogenic during any trimester and should generally be avoided in pregnancy. There appears to be an increased risk of bleeding and anaphylactoid typer reactions when alteplase and ACE-‐I are used simultaneously. Muravyov et al reported the viscosity of whole blood and plasma to be decreased after only three weeks of ACE-‐I administration. CONCLUSIONS: With the continued increasing use of ACE-‐Is and the drug class' ability to achieve therapeutic outcomes in a wide array of patient populations, it is important to better understand the processes and mechanisms behind the ADRs associated with ACE-‐I therapy. A basic understanding of incidence rates and physiologic mechanisms will allow clinicians to properly assess the probability of causation and better treat patients who have experienced an ACE-‐I induced ADR. However, an in-‐depth level of understanding can help guide clinicians in making decisions that will hopefully decrease the amount of ADRs their patients experience or prevent their patients from developing ACE-‐I related ADR altogether. It is important to note that, in most of the aforementioned ADR situations, treatment consists of ACE-‐I discontinuation and avoidance of future exposures.
| Identifer | oai:union.ndltd.org:arizona.edu/oai:arizona.openrepository.com:10150/623789 |
| Date | January 2010 |
| Creators | Monaco, Dominick, Romero, Jose, Solis, Jesus |
| Contributors | Herrier, Richard, College of Pharmacy, The University of Arizona |
| Publisher | The University of Arizona. |
| Source Sets | University of Arizona |
| Language | en_US |
| Detected Language | English |
| Type | text, Electronic Report |
| Rights | Copyright © is held by the author. |
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