title: Inflammatory and oxidative stress markers after intravenous insulin in percutaneous coronary intervention with stent in type 2 diabetes mellitus: a randomized controlled trial.
abstract: OBJECTIVE
  The objective of the study was to evaluate the effects of normalizing glycemia through iv insulin per 24 h on markers of oxidative stress and inflammation in patients with diabetes submitted to percutaneous coronary intervention (PCI) with stent.
  
  
  METHODS
  This was a prospective, open-label, randomized controlled trial, comparing continuous iv insulin per 24 h targeting glycemia less than 110 mg/dl iv insulin treatment (IIT; n = 35) to standard treatment (ST; n = 35, regular insulin if glycemia was greater than 200 mg/dl). Blood samples for glycemia, glycated hemoglobin, lipids, inflammatory markers [C-reactive protein (CRP), soluble CD40 ligand, IL-6, and endothelin 1 (ET-1)] and oxidative stress (total antioxidant status, carbonyl) were collected immediately after and 24 h after PCI.
  
  
  RESULTS
  Seventy patients were included. Mean age was 60.5 ± 10 yr, 60% were men, glycated hemoglobin was 8.1 ± 1.8 (IIT) vs. 7.6 ± 1.6% (ST) (P = 0.39). The intensive insulin group had lower glycemia (P = 0.006) and higher insulinemia (P < 0.001). Insulin did not change CRP [4.5 (2.1-11.7) vs. 6.8 (2.4-10.3), P = 0.35], soluble CD40 ligand [402 (191-843) vs. 610 (230-1200), P = 0.68], IL-6 [6.21 (3.1.-10.4) vs. 10.37 (5.9-15.3), P = 0.09], and ET-1 [1.02 (0.7-1.8) vs. 1.10 (0.7-1.9), P = 0.657]. CRP, IL-6, and ET-1 increased after PCI in both groups (P < 0.05). No change was observed on protein oxidation (carbonyl, P = 0.70; total antioxidant status, P = 0.33). There was a positive correlation between CRP and glycemia (r = 0.29, P = 0.002).
  
  
  CONCLUSIONS
  Continuous iv insulin for 24 h increased insulin levels and prevented hyperglycemia. Insulin infusion did not prevent the rise in inflammatory and oxidative stress markers, and no differences were observed between IIT and ST after PCI with a stent.
authors.affiliation: Graduate Program in Cardiology, Hospital de Clínicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, 90035-003 Porto Alegre, Brazil.
authors.forename: Simone de Souza
authors.initials: Sde S
authors.lastname: Fantin
authors.forename: Marco Vugman
authors.initials: MV
authors.lastname: Wainstein
authors.forename: Carísi Anne
authors.initials: CA
authors.lastname: Polanczyk
authors.forename: Priscila
authors.initials: P
authors.lastname: Ledur
authors.forename: Carmen Maria
authors.initials: CM
authors.lastname: Lazzari
authors.forename: Cristini
authors.initials: C
authors.lastname: Klein
authors.forename: Fernanda Schäfer
authors.initials: FS
authors.lastname: Hackenhaar
authors.forename: Mara Silveira
authors.initials: MS
authors.lastname: Benfato
authors.forename: Beatriz D'Agord
authors.initials: BD
authors.lastname: Schaan
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D000975:Antioxidants / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism; D001786:Blood Glucose / Q000378:metabolism; D003324:Coronary Artery Disease / Q000150:complications / Q000601:surgery; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000150:complications*; D004305:Dose-Response Relationship, Drug; D005260:Female; D006801:Humans; D007004:Hypoglycemic Agents / Q000008:administration & dosage / Q000494:pharmacology*; D007249:Inflammation / Q000378:metabolism*; D018836:Inflammation Mediators / Q000378:metabolism; D007275:Injections, Intravenous; D007279:Injections, Subcutaneous; D007328:Insulin / Q000008:administration & dosage / Q000494:pharmacology*; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000502:physiology*; D011446:Prospective Studies; D015607:Stents; D016896:Treatment Outcome
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D001786:Blood Glucose; D007004:Hypoglycemic Agents; D018836:Inflammation Mediators; D007328:Insulin