Targeting Inflammation using SALsalate in Patients with Type 2 Diabetes: Effects on Flow Mediated Dilation (TINSAL-FMD)
6/9/2012 11:30:00 AM
6/9/2012 1:30:00 PM
ALLISON B. GOLDFINE, STEWART BUCK, KATHLEEN A. JABLONSKI, CYRUS V. DESOUZA, GUILLERMO E. UMPIERREZ,
, LAURA TIPTON, STEVEN E. SHOELSON, MARK A. CREAGER, TINSAL-FMD STUDY TEAM,
Sub-acute inflammation participates in the pathogenesis of diabetes and cardiovascular disease. Previous studies found the anti-inflammatory drug, salsalate, improves glycemia in patients with T2D. To test the hypothesis that inhibition of inflammation will improve endothelial function in patients with T2D, we conducted an ancillary study to the NIH-sponsored, multicenter, randomized double-masked, placebo controlled trial evaluating safety and efficacy of targeting inflammation using salsalate to improve glycemia in patients with T2D (TINSAL-T2D). Flow mediated, endothelium dependent dilation (FMD) and endothelial independent nitroglycerin mediated dilation (NTG) of the brachial artery were assessed at baseline, and 3 and 6 months following randomization to salsalate, 3.5 g/d or placebo. The primary endpoint was change in FMD at 6 months.
88 participants were enrolled, and post randomization data was available in 75. Treatment and control groups were of similar age (56 yr), BMI (33 kg/m2), gender (64% male), ethnicity, current treatment, and baseline HbA1c (7.7%). HbA1c was reduced by 0.32% (
=0.003), fasting glucose by 12.5 mg/dl (
<0.001), and WBC count by 330 cells/µL (P<0.02) in salsalate vs placebo treated patients. There was no difference in change in FMD (+0.55 vs -0.16%, P=NS, salsalate vs placebo, respectively) or NTG induced dilation (-0.16 vs +0.39%, P=NS) between groups at 6 months. There was no difference in the change in systolic or diastolic blood pressure; while total and LDL cholesterol were respectively 9 mg/dl and 12 mg/dl higher and urinary albumin was 1.6 µg/mg creatinine higher in salsalate vs placebo.
Salsalate does not improve FMD in peripheral conduit arteries in T2D despite lowering HbA1c and markers of inflammation. This finding suggests either salicylate targeted inflammatory pathways do not cause endothelial dysfunction in T2D or confounding effects of salsalate mitigate favorable effects on endothelial function.
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