Printer Friendly

Aspirin 'resistance' connected to enteric coating.

FROM CIRCULATION

In a study of 400 healthy adults, measurements indicating the presence of what has been thought to be aspirin resistance were evident only with enteric-coated but not immediate-release aspirin, which the authors have described as aspirin "pseudoresistance."

The researchers used several measurements to evaluate responses reflecting the activity of cyclo oxygenase-1 (COX-l), the molecular target of aspirin, including platelet aggregation and serum thromboxane formation, which could indicate a genetic cause of aspirin resistance. Still, "we failed to find a single person who satisfied" the criteria for true aspirin resistance, reported Dr. Trio Grosser of the Institute for Translational Medicine and Therapeutics, University of Pennsylvania, Philadelphia, and his associates. "By contrast, pseudoresistance, due to delayed and reduced drug absorption, was common after ingestion of enteric-coated aspirin," they said. "These observations question the value of seeking to diagnose aspirin resistance with single point-of-care diagnostic approaches and support the finding of inconsistent platelet inhibition following enteric-coated preparations of aspirin," they concluded (Circulation 2012 [doi: 10.1161/CIRCULATIONAHA. 112.117283]). The study had several phases, which included screening the study participants, aged 18-55 years, for their response to a single 325-mg dose of immediate-release or enteric-coated aspirin, repeating testing among those who appeared to be resistant to aspirin, and comparing responses in responders and nonresponders.

Among the specific findings: All of the individuals who received a dose of immediate-release aspirin were responders, but up to 49% of those who received enteric aspirin were considered nonresponders. With repeated exposure, individuals categorized as nonresponders when given enteric-coated aspirin showed evidence of responses when administered immediate-release aspirin.

"What they have shown in an extremely elegant way is that aspirin resistance, at least in healthy volunteers, doesn't exist," Dr. Deepak Bhatt said in an interview.

Of great interest to physicians and patients is the finding that in the individuals who appeared to be aspirin resistant, enteric coating on aspirin was delaying and reducing absorption, he said. This may have been suspected as an explanation for so-called aspirin resistance, but "this is the first time someone has really nailed it down in a scientifically unassailable way," said Dr. Bhatt, professor of medicine at Harvard University, Boston, and chief of cardiology at VA Boston Healthcare System.

The results, however, raise further questions about more chronic administration of aspirin in patients who are not acutely ill and how many of these patients may not be fully absorbing aspirin if they are taking an enteric-coated formulation. "If there is a proportion of patients who are not getting the full anticlotting effect of aspirin ... that means potentially millions of patients are taking enteric-coated aspirin and not getting the protection they or their doctors are assuming they are getting," he said.

Dr. Bhatt's recommendation to clinicians, which predates the publication of this study, is to make sure that patients who are prescribed the immediate-release aspirin get the correct formulation, and not end up with an enteric-coated formulation unintentionally.

Dr. Sanjay Kaul, director of the vascular physiology and thrombosis research laboratory at the Burns and Allen Research Institute, Cedars-Sinai Medical Center, Los Angeles, also advised caution about extrapolating the results of a study of healthy volunteers to patients with heart disease or chronic illnesses that may affect how aspirin works in the body.

In an interview, he said that testing for aspirin resistance is "of dubious value," and the concept, like resistance to clopidogrel, "is driven to a large extent by marketing considerations," and the development of tests to assess aspirin responsiveness.

The study was funded by the National Heart, Lung, and Blood Institute; the National Center for Research Resources; the American Heart Association; and Bayer HealthCare. Coauthor Dr. Garret FitzGerald received research funding from Bayer HealthCare to support partial funding of this study, and Dr. Grosser received consultancy fees from PLx Pharma. The four remaining coauthors had no conflicts.

Dr. Bhatt said his disclosures include being an unpaid consultant to PLx Pharma. Dr. Kaul said he had no relevant disclosures.

e.mechcatie@elsevier.com
COPYRIGHT 2013 International Medical News Group
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2013 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Title Annotation:CARDIOVASCULAR MEDICINE
Author:Mechcatie, Elizabeth
Publication:Family Practice News
Geographic Code:1USA
Date:Jan 1, 2013
Words:662
Previous Article:Late-life epilepsy diagnosis brings unique challenges.
Next Article:Vitamin D lowered aldosterone in heart failure patients.
Topics:

Terms of use | Privacy policy | Copyright © 2019 Farlex, Inc. | Feedback | For webmasters