The role of intensive insulin therapy in increasing superoxide dismutase (SOD) and normalizing hyperglycemia in critically ill patients.
OBJECTIVE
To find out the difference between intensive insulin therapy and conventional insulin therapy in influencing the increase of superoxide dismutase (SOD), decrease of cytokine production (TNF-alpha and IL-6), increase of albumin level, and occurrence of SIRS.


METHODS
The study design was randomized pre and post control group design involving 40 adult patients admitted to the ICU of Sanglah Hospital, Denpasar. The study subjects were randomly allocated into two groups: the first group to receive intensive insulin therapy in which blood glucose was set at a level between 80 - 110 mg/dL; the second group to receive conventional insulin therapy, which was given if the blood glucose level exceeded 215 mg/dL and to be maintained at the level of between 180 - 200 mg/dL.


RESULTS
This study showed: (1) There was a significant increase of SOD in the group receiving intensive insulin therapy as compared to the conventional insulin therapy (370.70 vs. 98.50 U/gHb, p=0.001), (2) There was no significant decrease in the TNF-alpha level, (3) There was a significant decrease of IL-6 level (10.25 vs. 2.02; p=0.023); (4) There was a significant decrease in the event of SIRS (10% vs. 45%, p=0.000) in the intensive insulin therapy group as compared to the conventional insulin therapy group.


CONCLUSIONS
Increase of insulin dose in the intensive insulin therapy can maintain blood glucose at normoglycemic level between 80 - 110 mg/dL faster than that in the conventional insulin therapy. On the other hand, intensive insulin therapy can increase the SOD level, decrease IL-6 level, and decrease the events of SIRS in the ICU critically ill patients compared to conventional insulin therapy.
Wiryana
Made
M
Department of Anaesthesiology and Reanimation Medical Faculty, Udayana University-Sanglah Hospital, Denpasar, Bali, Indonesia. ijim@inaactamedica.org
D000328:Adult; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D016638:Critical Illness / Q000628:therapy*; D004305:Dose-Response Relationship, Drug; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D006943:Hyperglycemia / Q000097:blood* / Q000188:drug therapy; D007004:Hypoglycemic Agents / Q000008:administration & dosage* / Q000627:therapeutic use; D007262:Infusions, Intravenous; D007328:Insulin / Q000008:administration & dosage* / Q000627:therapeutic use; D007332:Insulin Infusion Systems; D015850:Interleukin-6 / Q000096:biosynthesis / Q000097:blood; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D013482:Superoxide Dismutase / Q000097:blood* / Q000187:drug effects; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000097:blood; D055815:Young Adult
D015415:Biomarkers; D001786:Blood Glucose; D007004:Hypoglycemic Agents; D007328:Insulin; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D013482:Superoxide Dismutase