title: Long-term effects of fenofibrate on carotid intima-media thickness and augmentation index in subjects with type 2 diabetes mellitus.
abstract: OBJECTIVE
  The aim of this substudy was to ascertain whether long-term treatment with fenofibrate reduces surrogate measures of atherosclerosis, biomarkers of inflammation, and endothelial activation in patients with type 2 diabetes.
  
  
  BACKGROUND
  Some fibrates may decrease cardiovascular events, improve endothelial function, and reduce levels of acute-phase proteins. In the FIELD (Fenofibrate Intervention and Event Lowering in Diabetes) study, fenofibrate failed to decrease the primary end point of coronary events in patients with type 2 diabetes.
  
  
  METHODS
  A total of 170 patients with type 2 diabetes of the FIELD Helsinki cohort were randomly assigned to micronized fenofibrate 200 mg/day or placebo in a double-blind design. Carotid intima-media thickness (IMT) and the augmentation index (a measure of large artery stiffness) were measured at baseline and at second- and fifth-year visits. Plasma levels of interleukin (IL)-6, C-reactive protein (CRP), serum amyloid A (SAA), secretory phospholipase A2 IIA (SPLA2), E-selectin, vascular cellular adhesion molecule (VCAM)-1, and intercellular adhesion molecule (CAM)-1 were determined by commercial enzyme-linked immunosorbent assay kits at the same visits.
  
  
  RESULTS
  IMT and the augmentation index increased similarly in both treatment groups during the study. Plasma levels of CRP, IL-6, SPLA2, SAA, VCAM-1, ICAM-1, and E-selectin remained unchanged in both groups.
  
  
  CONCLUSIONS
  Fenofibrate treatment was not associated with beneficial changes in IMT, augmentation index, or biomarkers of inflammation and endothelial function. (Fenofibrate Intervention and Event Lowering in Diabetes; NCT00132886).
authors.affiliation: Department of Medicine, University of Helsinki, Helsinki University Central Hospital and Biomedicum, Helsinki, Finland.
authors.forename: Anne
authors.initials: A
authors.lastname: Hiukka
authors.forename: Jukka
authors.initials: J
authors.lastname: Westerbacka
authors.forename: Eeva S
authors.initials: ES
authors.lastname: Leinonen
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Watanabe
authors.forename: Olov
authors.initials: O
authors.lastname: Wiklund
authors.forename: Lillemor Mattson
authors.initials: LM
authors.lastname: Hulten
authors.forename: Jukka T
authors.initials: JT
authors.lastname: Salonen
authors.forename: Tomi-Pekka
authors.initials: TP
authors.lastname: Tuomainen
authors.forename: Hannele
authors.initials: H
authors.lastname: Yki-Järvinen
authors.forename: Anthony C
authors.initials: AC
authors.lastname: Keech
authors.forename: Marja-Riitta
authors.initials: MR
authors.lastname: Taskinen
mesh_terms: D000209:Acute-Phase Proteins / Q000187:drug effects; D000368:Aged; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000187:drug effects; D002339:Carotid Arteries / Q000187:drug effects* / Q000473:pathology; D002340:Carotid Artery Diseases / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D048909:Diabetes Complications / Q000188:drug therapy* / Q000473:pathology; D003924:Diabetes Mellitus, Type 2 / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D004311:Double-Blind Method; D005260:Female; D011345:Fenofibrate / Q000494:pharmacology / Q000627:therapeutic use*; D006801:Humans; D000960:Hypolipidemic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D007249:Inflammation / Q000097:blood; D008297:Male; D008875:Middle Aged; D012720:Severity of Illness Index; D013997:Time Factors; D017211:Treatment Failure; D017539:Tunica Intima / Q000187:drug effects* / Q000473:pathology; D017540:Tunica Media / Q000187:drug effects* / Q000473:pathology
chemical_list: D000209:Acute-Phase Proteins; D015415:Biomarkers; D000960:Hypolipidemic Agents; D002097:C-Reactive Protein; D011345:Fenofibrate