Aspirin Resistance in Systemic Lupus Erythematosus (SLE)

Systemic Lupus Erythematosus Clinical Trial

Official title:

Vascular Damage in Systemic Lupus Erythematosus (SLE)

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT00731302
• Other study ID #: HL65082
• Secondary ID: R01HL065082
• Status: Completed
• Phase: Phase 1
• First received: August 5, 2008
• Last updated: August 3, 2017
• Start date: April 2005
• Est. completion date: April 2017

Study information

• Verified date: August 2017
• Source: Vanderbilt University Medical Center
• Contact: n/a
• Is FDA regulated: No
• Study type: Interventional

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.

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.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 70
• Est. completion date: April 2017
• Est. primary completion date: April 2017
• Accepts healthy volunteers: Accepts Healthy Volunteers
• Gender: All
• Age group: 18 Years and older

Eligibility

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

Related Conditions & MeSH terms

• Lupus Erythematosus, Systemic
• Systemic Lupus Erythematosus

Intervention

Drug:
• aspirin and meloxicam
aspirin 81 mg daily then aspirin 81 mg plus meloxicam 7.5 mg daily

Locations

Country	Name	City	State
United States	Beth Israel Deaconess Medical Center	Boston	Massachusetts
United States	Vanderbilt University Medical School	Nashville	Tennessee

Sponsors (2)

Lead Sponsor	Collaborator
Vanderbilt University	National Heart, Lung, and Blood Institute (NHLBI)

Country where clinical trial is conducted

United States, 

References & Publications (1)

Kawai VK, Avalos I, Oeser A, Oates JA, Milne GL, Solus JF, Chung CP, Stein CM. Suboptimal inhibition of platelet cyclooxygenase 1 by aspirin in systemic lupus erythematosus: association with metabolic syndrome. Arthritis Care Res (Hoboken). 2014 Feb;66(2) — View Citation

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	thromboxane	a hormone of the prostacyclin type released from blood platelets. It induces platelet aggregation and arterial constriction.	after aspirin and after aspirin plus meloxicam