title: [Influence and mechanism of a tight control of blood glucose by intensive insulin therapy on human sepsis].
abstract: OBJECTIVE
  To investigate the effect of a tight control of blood glucose by intensive insulin therapy on human sepsis, and to explore the potential mechanism of the intensive insulin therapy.
  
  
  METHODS
  Eligible patients were randomized by a blinded pharmacist to receive tight control of blood glucose by intensive insulin therapy (maintenance of blood glucose at a level between 4.4 and 6.1 mmol/L) or to receive conventional treatment (maintenance of glucose at a level between 10.0 and 11.1 mmol/L). The expression of HLA-DR on peripheral monocytes was measured in 54 patients by flow cytometry on 24 h, 3 d, 5 d, 7 d, 10 d and 14 d of intensive care in parallel with serum c-reactive protein (CRP), severity of the disease (APACHE II score, SOFA score) and clinical data collection.
  
  
  RESULTS
  Patients receiving intensive insulin therapy were less likely to require prolonged mechanical ventilation. Tight control of blood glucose significantly reduced the number of days during which leukopenia or leukocytosis and the days with hypo- or hyperthermia (P < 0.05). Hypoglycemia occurred in 3 patients (10.7%) in the tight control of blood glucose group. There were no instance of hemodynamic deterioration or convulsions. Compared with the conventional treatment, tight control of blood glucose also increased the HLA-DR expression of peripheral monocytes, and there were significantly difference on 3 d, 5 d and 7 d (P < 0.05). Whereas it suppressed the elevated serum CRP concentrations, there was significantly difference on 7 d (P < 0.05).
  
  
  CONCLUSIONS
  Tight control of blood glucose by intensive insulin therapy expedited healing of human sepsis, and increased the HLA-DR expression of peripheral and suppressed the elevated serum CRP. So, it is necessary to use insulin to strict control the glucose levels in human sepsis.
authors.affiliation: Research Institute of General Surgery, General Hospital of Nanjing Military Area, Nanjing 210002, China. yudrnj@163.com
authors.forename: Wen-kui
authors.initials: WK
authors.lastname: Yu
authors.forename: Wei-qin
authors.initials: WQ
authors.lastname: Li
authors.forename: Xiao-dong
authors.initials: XD
authors.lastname: Wang
authors.forename: Xiao-wen
authors.initials: XW
authors.lastname: Yan
authors.forename: Xiao-ping
authors.initials: XP
authors.lastname: Qi
authors.forename: Ning
authors.initials: N
authors.lastname: Li
authors.forename: Jie-shou
authors.initials: JS
authors.lastname: Li
mesh_terms: D001786:Blood Glucose / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism; D006684:HLA-DR Antigens / Q000096:biosynthesis; D006801:Humans; D006943:Hyperglycemia / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D007328:Insulin / Q000627:therapeutic use*; D018805:Sepsis / Q000150:complications*
chemical_list: D001786:Blood Glucose; D006684:HLA-DR Antigens; D007004:Hypoglycemic Agents; D007328:Insulin; D002097:C-Reactive Protein