Expired Study
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Boston, Massachusetts 02118


Purpose:

Experimental studies suggest that systemic inflammation leads to endothelial dysfunction and atherosclerosis. This study will examine the effects of the anti-inflammatory drug sulfasalazine on endothelial function in patients with coronary artery disease. Subjects will be treated with sulfasalazine or to placebo for six weeks. After a two-week rest period, subjects will cross over to the alternative treatment. Endothelium-dependent flow-mediated dilation of the brachial artery will be studied before and after each drug. We hypothesize that anti-inflammatory therapy will reverse endothelial dysfunction in patients with coronary artery disease.


Criteria:

Inclusion Criteria: - History of coronary artery disease Exclusion Criteria: - G6PD deficiency defined by red blood cell G6PD activity assay - Sulfa allergy - Aspirin allergy - Allergy to furosemide (lasix), hydrochlorthiazide, sulfonylureas, acetazolamide (Diamox) or other carbonic anhydrase inhibitors - SGOT, SGPT, alkaline phosphatase, total bilirubin greater than 2 times the upper limit of normal - WBC less than 4.0 or greater than 11.0 K/UL - Platelet count less than 150 K or greater than 450K - Hematocrit less than 30% 7 - Serum creatinine greater than 1.5 mg/dl - Unstable angina or acute MI within 2 weeks - Warfarin treatment - Immunosuppressive treatment (methotrexate, cyclosporine, etc.) - Digoxin treatment - Phenytoin (Dilantin) treatment - Methenamine (Mandelamine, Urex) treatment - Probenecid or sulfinpyrazone (Anturane, Aprazone) treatment - Porphyria - Symptomatic GI obstruction - GU obstruction (not including clinical evidence of benign prostatic hypertrophy) - Pregnancy


NCT ID:

NCT00554203


Primary Contact:

Principal Investigator
Joseph A Vita, MD
Boston Medical Center


Backup Contact:

N/A


Location Contact:

Boston, Massachusetts 02118
United States



There is no listed contact information for this specific location.

Site Status: N/A


Data Source: ClinicalTrials.gov

Date Processed: November 17, 2017

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