Lopez LR, Guyer KE, Torre IGDL, Pitts KR, Matsuura E, Ames PR. Platelet thromboxane (11-dehydro-Thromboxane B2) and aspirin response in patients with diabetes and coronary artery disease. World J Diabetes 2014; 5(2): 115-127 [PMID: 24748925 DOI: 10.4239/wjd.v5.i2.115]
Corresponding Author of This Article
Luis R Lopez, MD, Corgenix Medical Corporation, 11575 Main Street, # 400, Broomfield, CO 80020, United States. llopez@corgenix.com
Research Domain of This Article
Medicine, General & Internal
Article-Type of This Article
Topic Highlight
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Diabetes. Apr 15, 2014; 5(2): 115-127 Published online Apr 15, 2014. doi: 10.4239/wjd.v5.i2.115
Platelet thromboxane (11-dehydro-Thromboxane B2) and aspirin response in patients with diabetes and coronary artery disease
Luis R Lopez, Kirk E Guyer, Ignacio Garcia De La Torre, Kelly R Pitts, Eiji Matsuura, Paul RJ Ames
Luis R Lopez, Kelly R Pitts, Corgenix Medical Corporation, Broomfield, CO 80020, United States
Kirk E Guyer, Department of Chemistry, Indiana University, South Bend, IN 46634, United States
Ignacio Garcia De La Torre, Department of Immunology and Rheumatology, Hospital General de Occidente, Zapopan, Jalisco 45170, Mexico
Eiji Matsuura, Collaborative Research Center for Okayama Medical Innovation Center (OMIC) and Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama 700-8558, Japan
Paul RJ Ames, Queen Mary University of London, William Harvey Research Institute, Charterhouse Square, London EC1M 6BQ, United Kingdom
Author contributions: Lopez LR, Matsuura E and Ames PRJ contributed equally to this paper; Lopez LR and Guyer KE designed the studies; Garcia De La Torre I, Matsuura E and Ames PRJ contributed with patients and/or analytical tools; Lopez LR and Pitts KR wrote the review paper.
Supported by In part by the Senit Foundation, Scotland (United Kingdom); and grant-in-aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology (Japan)
Correspondence to: Luis R Lopez, MD, Corgenix Medical Corporation, 11575 Main Street, # 400, Broomfield, CO 80020, United States. llopez@corgenix.com
Telephone: +1-303-4538949 Fax: +1-303-4574519
Received: December 12, 2013 Revised: February 25, 2014 Accepted: March 11, 2014 Published online: April 15, 2014
Core Tip
Core tip: The effect of aspirin (ASA) on platelet thromboxane (11dhTxB2) generation in diabetes (DM) and symptomatic cardiovascular disease (CVD) was reviewed. Consistent with a heightened platelet hyperactive background, baseline 11dhTxB2 was significantly higher in DM and acute coronary syndrome (ACS) than healthy individuals. ASA ingestion inhibited 11dhTxB2 in all subjects, but there were more ASA poor-responders (ASA “resistant”) in DM (14.8%) and ACS (28.7%) than controls (8.4%). Only post-ASA 11dhTxB2 levels predicted adverse cardiovascular outcomes. ASA poor-responders had higher isoprostane (8-isoPGF2α) levels suggesting an underlying systemic oxidative inflammatory process not affected by ASA that may maintain platelet hyperactivity in DM and atherothrombotic CVD.
