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Aspirin Resistance in Systemic Lupus Erythematosus (SLE)

This study has been completed.
Sponsor:
ClinicalTrials.gov Identifier:
NCT00731302
First Posted: August 8, 2008
Last Update Posted: August 7, 2017
The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details.
Collaborator:
National Heart, Lung, and Blood Institute (NHLBI)
Information provided by (Responsible Party):
C. Michael Stein, Vanderbilt University
  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 and meloxicam Phase 1

Study Type: Interventional
Study Design: Intervention Model: Single Group Assignment
Masking: None (Open Label)
Primary Purpose: Other
Official Title: Vascular Damage in Systemic Lupus Erythematosus (SLE)

Resource links provided by NLM:


Further study details as provided by C. Michael Stein, Vanderbilt University:

Primary Outcome Measures:
  • thromboxane [ Time Frame: after aspirin and after aspirin plus meloxicam ]
    a hormone of the prostacyclin type released from blood platelets. It induces platelet aggregation and arterial constriction.


Enrollment: 70
Study Start Date: April 2005
Study Completion Date: April 2017
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.
  Eligibility

Information from the National Library of Medicine

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Ages Eligible for Study:   18 Years and older   (Adult, Senior)
Sexes Eligible for Study:   All
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
Information from the National Library of Medicine

To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.

Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT00731302


Locations
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)
Investigators
Principal Investigator: C M Stein, M.D. Vanderbilt University
  More Information

Publications:
Responsible Party: C. Michael Stein, Dan May Professor of Medicine, Professor of Pharmacology, Associate Director of the Division of Clinical Pharmacology, Vanderbilt University
ClinicalTrials.gov Identifier: NCT00731302     History of Changes
Other Study ID Numbers: HL65082
R01HL065082 ( U.S. NIH Grant/Contract )
First Submitted: August 5, 2008
First Posted: August 8, 2008
Last Update Posted: August 7, 2017
Last Verified: August 2017

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
Anti-Inflammatory Agents
Antirheumatic Agents
Fibrinolytic Agents
Fibrin Modulating Agents
Molecular Mechanisms of Pharmacological Action
Platelet Aggregation Inhibitors
Cyclooxygenase Inhibitors
Enzyme Inhibitors
Antipyretics