Background. Morbid obesity is believed to be an extreme of the metabolic spectrum. Moreover, diabetes is hypothesized to be associated with a chronic inflammatory state that is not observed in nondiabetic healthy individuals. We investigated the differences in expression of inflammatory cytokines induced by surgical stress between diabetic and nondiabetic individuals. Method. 39 morbidly obese patients undergoing laparoscopic Roux-en-Y gastric bypass (9 with type 2 diabetes mellitus) were compared with 8 nonobese euglycemic patients undergoing laparoscopic antireflux surgery. Cytokine levels for IL-6, IL-10, and IL-18 were measured 15 minutes before surgery and immediately after surgery. Results. IL-6 and IL-10 levels were elevated from baseline following surgery, but morbidly obese patients exhibited a much higher elevation than lean patients. Individuals with type 2 diabetes had the most pronounced IL-6 and IL-10 elevations. Baseline IL-18 levels were significantly higher in diabetic patients compared with nondiabetic or lean patients. However, IL-18 levels were not changed in response to surgery. Conclusions. Diabetes and morbid obesity are associated with augmented cytokine expression in response to surgical trauma that is several folds higher than in nonobese euglycemic patients. Diabetic patients exhibit a chronic elevation in IL-18 that is not changed by surgical stress. 1. Introduction Surgical stress induces an appropriate systemic inflammatory response that has been extensively characterized [1]. The initial inflammatory response is inherently designed to eradicate microorganisms, promote healing following injury, and restore homeostasis. However, perpetual or excessive inflammatory response may overwhelm the compensatory capacities of the host, eventuating in multiple-organ failure and patient demise. Cytokines, produced by immunoactive cells, are critical mediators of the inflammatory process and the response of tumor necrosis factor-α, interleukin- (IL-) 6, and IL-10 have all been described in the context of sepsis, surgical injury, and trauma [2]. Patients with severe obesity also have significant comorbidities that include, but are not limited to, coronary artery disease, type 2 DM, and pulmonary diseases. These patients represent an extreme in metabolic and physiologic dysfunctions, which under conditions of stress may portend deleterious outcomes. Indeed, there is mounting evidence suggesting that the condition of severe obesity is a chronic systemic inflammatory state with cytokine mediators contributing to the pathophysiology of the
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