NCT00731302

Aspirin Resistance in Systemic Lupus Erythematosus (SLE)

Vascular Damage in Systemic Lupus Erythematosus (SLE)

• Status: Completed
• Phase: Phase 1
• Study type: Interventional
• Enrollment: 70 (actual)
• Sponsor: Vanderbilt University · Academic / Other
• Sex: All
• Age: 18 Years
• Healthy volunteers: Accepted

Summary

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.

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.

Conditions

• Systemic Lupus Erythematosus

Interventions

Type	Name	Description
DRUG	aspirin and meloxicam	aspirin 81 mg daily then aspirin 81 mg plus meloxicam 7.5 mg daily

Timeline

• Start date: 2005-04-01
• Primary completion: 2017-04-01
• Completion: 2017-04-01
• First posted: 2008-08-08
• Last updated: 2017-08-07

Locations

2 sites across 1 country: United States