Kwoun MO, Ling PR, Lydon E, et al. Immunologic effects of acute hyperglycemia in nondiabetic rats. JPEN. Journal of Parenteral and Enteral Nutrition. 1997;21:91–95.

This article explores the influence of hyperglycemia on immune function in phagocytic cells.

Dandona P, Aljada A, Mohanty P, et al. Insulin inhibits intranuclear nuclear factor kappa-B and stimulates I-kappa-B in mononuclear cells in obese subjects: Evidence for an anti-inflammatory effect? Journal of Clinical Endocrinology and Metabolism. 2001;86:3257–3265.

This study examines insulin's anti-inflammatory properties.

Carr ME. Diabetes mellitus: A hypercoagulable state. Journal of Diabetes and its Complications. 2001;15:44–54.

This article reviews the factors contributing to increased rates of thrombotic death among patients with diabetes mellitus.

Hansen TK, Thiel S, Wouters PJ, et al. Intensive insulin therapy exerts anti-inflammatory effects in critically ill patients and counteracts the adverse effect of low mannose-binding lectin levels. Journal of Clinical Endocrinology and Metabolism. 2003;88:1082–1088.

This article explores the aintiinflammatory effect of intensive insulin therapy during critical illness and finds an improvement in morbidity and mortality.

Das UN. Is insulin an antiinflammatory molecule? Nutrition. 2001;17:409–413.

This article proposes a role for the glucose-insulin-potassium regimen in care of critically ill patients.

Satomi N, Sakurai A, Haranaka K. Relationship of hypoglycemia to tumor necrosis factor production and antitumor activity: Role of glucose, insulin, and macrophages. Journal of the National Cancer Institute. 1985;74:1255–1260.

This study examines hypoglycemia's contribution to tumor necrosis factor production.

Fourrier F. Recombinant human activated protein C in the treatment of severe sepsis: An evidence-based review. Critical Care Medicine. 2004;32(Suppl.):S534–S541.

This article details the Surviving Sepsis Campaign's recommendations for managing severe sepsis.

Dhainaut JF, Laterre PF, Janes JM, et al. Drotrecogin alfa (activated) in the treatment of severe sepsis patients with multiple organ dysfunction: data from the PROWESS trial. Intensive Care Medicine. 2003;29:894–903.

This study finds that drotrecogin alfa (activated) therapy reduces 28-day mortality and speeds recovery of cardiovascular and respiratory organ function.  The increased risk of bleeding associated with this therapy appears to be outweighed by treatment benefits.

Laterre PF, Heiselman D. Management of patients with severe sepsis treated by drotrecogin alfa (activated). American Journal of Surgery. 2002;184:39S–46S.

This article outlines principles to consider in managing drotrecogin alfa (activated) therapy for critically ill patients.

Macias WL, Dhainaut JF, Yan BS, et al. Pharmacokinetic-pharmacodynamic analysis of drotrecogin alfa (activated) in patients with severe sepsis. Clinical Pharmacology and Therapeutics. 2002;72:391–402.

This study finds that plasma concentration of drotrecogin alfa (activated) becomes steady soon after infusion begins, and remains so throughout infusion.  After infusion is stopped, plasma concentration declines rapidly.