Perioperative response of leptin and the tumor necrosis factor alpha system in morbidly obese patients. Influence of cortisol inhibition by etomidate.

Abstract

Leptin, tumor necrosis factor alpha (TNFalpha) and soluble TNFalpha receptors are secreted by the adipose tissue. Surgery induces a complex cytokine and neurohormonal response. The aim of our study was to investigate the perioperative response of leptin and the TNFalpha system in morbidly obese patients submitted to gastroplasty, and the possible involvement of cortisol in their responses. Serum cortisol, adrenocorticotropic hormone (ACTH), leptin, TNFalpha and soluble TNFalpha receptor I were measured in 22 morbidly obese women (11 anesthetized with thiopental and 11 with etomidate, a well known inhibitor of cortisol synthesis). Samples were collected before anesthesia induction, just before surgical incision, and 2, 4, 6, 12, 24 and 48 h after the start of surgery. Baseline serum leptin correlated with body mass index (r=0.567, P=0.007). Baseline serum leptin and TNFalpha were higher than normal. Cortisol release was inhibited in the etomidate group with a subsequent higher stimulation of ACTH release. A statistically significant decrease in serum leptin levels was observed in both groups at 2, 4, 6 and 48 h, compared with basal values. A similar decrease in serum TNFalpha levels was observed in both groups, but the decrease reached significance only in the etomidate group. Serum soluble TNFalpha receptor I did not decrease. No differences were found between the two groups in leptin, TNFalpha or soluble TNFalpha receptor I concentrations at any time. Serum leptin and TNFalpha levels decrease in obese patients during gastroplasty. Transitory inhibition of cortisol release does not alter this response.