Aspirin Resistance in Systemic Lupus Erythematosus (SLE)

The recruitment status of this study is unknown because the information has not been verified recently.

Verified February 2009 by Vanderbilt University. Recruitment status was Recruiting

First Received on August 5, 2008. Last Updated on February 18, 2009 History of Changes

Sponsor:	Vanderbilt University
Collaborator:	National Heart, Lung, and Blood Institute (NHLBI)
Information provided by:	Vanderbilt University
ClinicalTrials.gov Identifier:	NCT00731302

Purpose

This study examine whether patients with lupus respond to aspirin , and if not, if that is related to inflammation. We examine the ability of aspirin to inhibit the production of thromboxane in patients with lupus and controls and see if aspirin insensitive thromboxane production is inhibited by meloxicam.

Condition	Intervention	Phase
Systemic Lupus Erythematosus	Drug: aspirin, aspirin plus meloxicam	Phase I

Study Type:	Interventional
Study Design:	Endpoint Classification: Pharmacodynamics Study Intervention Model: Single Group Assignment Masking: Open Label

Resource links provided by NLM:

MedlinePlus related topics: Lupus

Drug Information available for: Acetylsalicylic acid Meloxicam

U.S. FDA Resources

Further study details as provided by Vanderbilt University:

Primary Outcome Measures:

thromboxane [ Time Frame: after aspirin and after aspirin plus meloxicam ] [ Designated as safety issue: No ]

Estimated Enrollment:	120
Study Start Date:	April 2005
Estimated Study Completion Date:	April 2010
Estimated Primary Completion Date:	April 2010 (Final data collection date for primary outcome measure)

Arms	Assigned Interventions
Experimental: I 81 mg aspirin followed by meloxicam 7.5 mg daily plus aspirin 81 mg daily	Drug: aspirin, aspirin plus meloxicam aspirin 81 mg daily then aspirin 81 mg plus meloxicam 7.5 mg daily

Detailed Description:

Premature cardiovascular disease is a major cause of mortality in patients with systemic lupus erythematosus (SLE) with the risk of myocardial infarction increased up to 50-fold. In addition to defining the mechanisms for accelerated atherosclerosis it is important to define the effects of drugs used to reduce cardiovascular risk in high-risk patients. Low dose aspirin, by inhibiting thromboxane A2 biosynthesis, has profound antiplatelet effects, but some patients have impaired thromboxane suppression - a phenomenon termed aspirin resistance. An explanation is that aspirin-independent thromboxane synthesis may occur through enhanced COX-2 activity, as would occur in an inflammatory condition such as lupus. However, little is known about the effects of low-dose aspirin in SLE. Thus, we propose to test the following hypothesis: 1) that aspirin insensitive thromboxane biosynthesis is increased in patients with lupus and is mediated by increased COX-2 activity.

Eligibility

Ages Eligible for Study:	18 Years and older
Genders Eligible for Study:	Both
Accepts Healthy Volunteers:	Yes

Criteria

Inclusion Criteria:

Written Informed consent.
Age >18 yrs.
SLE meeting ACR criteria {Tan, Cohen, et al. 1982 1482 /id} for at least 6 months.(SLE group)
Stable disease activity as evidenced by no change in immunosuppressive therapy in the past 1 month.
If female of childbearing potential must use an effective method of birth control

Exclusion criteria.

Renal disease (creatinine >1.5 mg/dL, dialysis, 2+ or more proteinuria)
Previous or current history of peptic ulcer disease or gastrointestinal bleed.
Previous or current thromboembolic or ischemic cardiovascular event (stroke, myocardial infarction, angina) - can do aspirin part of study.
Currently taking an anticoagulant or antiplatelet agent (besides aspirin).
Thrombocytopenia (platelet count <135,000)
Pregnancy
Allergy to aspirin, NSAIDs
NSAIDs in the previous week

Contacts and Locations

Please refer to this study by its ClinicalTrials.gov identifier: NCT00731302

Contacts

Contact: Charles M Stein

615 936 3420

michael.stein@vanderbilt.edu

Locations

United States, Massachusetts
Beth Israel Deaconess Medical Center	Recruiting
Boston, Massachusetts, United States, 02215
Contact: Ingrid Avalos 617-632-8998 iavalos@bidmc.harvard.edu
United States, Tennessee
Vanderbilt University Medical School	Recruiting
Nashville, Tennessee, United States, 37232
Contact: Charles M Stein 615-936-3420 michael.stein@vanderbilt.edu
Principal Investigator: Charles M Stein

Sponsors and Collaborators

Vanderbilt University

National Heart, Lung, and Blood Institute (NHLBI)

Investigators

Principal Investigator:

C M Stein, M.D.

Vanderbilt University

More Information

No publications provided

Responsible Party:	C. Michael Stein, Vanderbilt University
ClinicalTrials.gov Identifier:	NCT00731302 History of Changes
Other Study ID Numbers:	HL65082
Study First Received:	August 5, 2008
Last Updated:	February 18, 2009
Health Authority:	United States: Institutional Review Board

Additional relevant MeSH terms:

Lupus Erythematosus, Systemic
Connective Tissue Diseases
Autoimmune Diseases
Immune System Diseases
Aspirin
Meloxicam
Anti-Inflammatory Agents, Non-Steroidal
Analgesics, Non-Narcotic
Analgesics
Sensory System Agents
Peripheral Nervous System Agents
Physiological Effects of Drugs
Pharmacologic Actions

Anti-Inflammatory Agents
Therapeutic Uses
Antirheumatic Agents
Fibrinolytic Agents
Fibrin Modulating Agents
Molecular Mechanisms of Pharmacological Action
Cardiovascular Agents
Hematologic Agents
Platelet Aggregation Inhibitors
Cyclooxygenase Inhibitors
Enzyme Inhibitors
Antipyretics
Central Nervous System Agents

ClinicalTrials.gov processed this record on February 09, 2012