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Aspirin Resistance in Systemic Lupus Erythematosus (SLE)

This study is ongoing, but not recruiting participants.
National Heart, Lung, and Blood Institute (NHLBI)
Information provided by (Responsible Party):
C. Michael Stein, Vanderbilt University Identifier:
First received: August 5, 2008
Last updated: October 31, 2016
Last verified: October 2016
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 and meloxicam
Phase 1

Study Type: Interventional
Study Design: Intervention Model: Single Group Assignment
Masking: Open Label
Official Title: Vascular Damage in Systemic Lupus Erythematosus (SLE)

Resource links provided by NLM:

Further study details as provided by Vanderbilt University:

Primary Outcome Measures:
  • thromboxane [ Time Frame: after aspirin and after aspirin plus meloxicam ]

Estimated Enrollment: 120
Study Start Date: April 2005
Estimated Study Completion Date: April 2017
Estimated Primary Completion Date: April 2017 (Final data collection date for primary outcome measure)
Arms Assigned Interventions
Experimental: Aspirin and Meloxicam
Arm: Aspirin and Meloxicam Each participant will receive 81 mg aspirin per day for 7 days, followed by meloxicam 7.5 mg daily plus aspirin 81 mg daily for 5 days
Drug: aspirin and meloxicam
aspirin 81 mg daily then aspirin 81 mg plus meloxicam 7.5 mg daily
Other Name: generic, not applicable

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.

Ages Eligible for Study:   18 Years and older   (Adult, Senior)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   Yes

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
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Please refer to this study by its identifier: NCT00731302

United States, Massachusetts
Beth Israel Deaconess Medical Center
Boston, Massachusetts, United States, 02215
United States, Tennessee
Vanderbilt University Medical School
Nashville, Tennessee, United States, 37232
Sponsors and Collaborators
Vanderbilt University
National Heart, Lung, and Blood Institute (NHLBI)
Principal Investigator: C M Stein, M.D. Vanderbilt University
  More Information

Publications automatically indexed to this study by Identifier (NCT Number):
Responsible Party: C. Michael Stein, Dan May Professor of Medicine, Professor of Pharmacology, Associate Director of the Division of Clinical Pharmacology, Vanderbilt University Identifier: NCT00731302     History of Changes
Other Study ID Numbers: HL65082
R01HL065082 ( US NIH Grant/Contract Award Number )
Study First Received: August 5, 2008
Last Updated: October 31, 2016

Additional relevant MeSH terms:
Lupus Erythematosus, Systemic
Connective Tissue Diseases
Autoimmune Diseases
Immune System Diseases
Anti-Inflammatory Agents, Non-Steroidal
Analgesics, Non-Narcotic
Sensory System Agents
Peripheral Nervous System Agents
Physiological Effects of Drugs
Anti-Inflammatory Agents
Antirheumatic Agents
Fibrinolytic Agents
Fibrin Modulating Agents
Molecular Mechanisms of Pharmacological Action
Platelet Aggregation Inhibitors
Cyclooxygenase Inhibitors
Enzyme Inhibitors
Antipyretics processed this record on April 25, 2017