Aspirin Resistance in Systemic Lupus Erythematosus (SLE)

Systemic Lupus Erythematosus Clinical Trial

Official title: Vascular Damage in Systemic Lupus Erythematosus (SLE)

Status Completed

Clinical Trial 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.

Clinical Trial 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. ;

Related Conditions & MeSH terms

• Lupus Erythematosus, Systemic
• Systemic Lupus Erythematosus

• NCT number: NCT00731302
• Study type: Interventional
• Source: Vanderbilt University Medical Center
• Status: Completed
• Phase: Phase 1
• Start date: April 2005
• Completion date: April 2017