of Clinical Pharmacology, Department of Medicine, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA Biology Institute, Department of Medicine Winthrop-University Hospital, 222 Station Plaza, North, Mineola, NY 11501, USA 3Division of Rheumatology, Allergy and Immunology, Department of Medicine Winthrop-University Hospital, 222 Station Plaza, North, Mineola, NY 11501, USA 2Vascular Corresponding author: Allison B Reiss, AReiss@ Received: 11 Oct 2006 Revisions requested: 23 Nov. | Available online http content 9 1 R4 Open Access Research article Effect of cyclooxygenase inhibition on cholesterol efflux proteins and atheromatous foam cell transformation in THP-1 human macrophages a possible mechanism for increased cardiovascular risk Edwin SL Chan1 Hongwei Zhang2 Patricia Fernandez1 Sari D Edelman3 Michael H Pillinger1 Louis Ragolia2 Thomas Palaia2 Steven Carsons2 3 and Allison B Reiss2 Division of Clinical Pharmacology Department of Medicine New York University School of Medicine 550 First Avenue New York NY 10016 USA 2Vascular Biology Institute Department of Medicine Winthrop-University Hospital 222 Station Plaza North Mineola NY 11501 USA 3Division of Rheumatology Allergy and Immunology Department of Medicine Winthrop-University Hospital 222 Station Plaza North Mineola NY 11501 USA Corresponding author Allison B Reiss AReiss@ Received 11 Oct 2006 Revisions requested 23 Nov 2006 Revisions received 18 Dec 2006 Accepted 23 Jan 2007 Published 23 Jan 2007 Arthritis Research Therapy 2007 9 R4 doi ar21 09 This article is online at http content 9 1 R4 2007 Chan et al. licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Both selective cyclooxygenase COX -2 inhibitors and nonsteroidal anti-inflammatory drugs NSAIDs have been beneficial pharmacological agents for many patients suffering from arthritis pain and inflammation. However selective COX-2 inhibitors and traditional NSAIDs are both associated with heightened risk of myocardial infarction. Possible pro-atherogenic mechanisms of these inhibitors have been suggested including an imbalance in prostanoid production leaving the pro-aggregatory prostaglandins unopposed but the precise .
