Background: There is clinical evidence that the surgical insult experienced by patients who undergo laparoscopic cholecystectomy (LC) differs significantly from that experienced by those undergoing open cholecystectomy (OC). LC is accompanied by less pain, better ventilatory function and almost total absence of secondary paralytic ileus. The aim of the present study was to investigate the endocrine and immune response to the injury induced by both types of surgery. To this end, the relationship between levels of hormones of the hypothalamus-hypophysis-adrenal axis (indicators of stress) and cytokine levels was analyzed.
Methods: Blood samples from subjects undergoing either OC (n = 14) or LC (n = 14) were obtained 24 h before surgery and 24 h and 7 days after surgery. Serum concentrations of interleukin-6 (IL-6), interleukin-1 (IL-1), interleukin-10 (IL-10) and prolactin were determined using enzyme-linked immunosorbent assay. Cortisol and GH concentrations were determined by radioimmunoassay.
Results: Twenty-four hours after surgery, prolactin, GH and cortisol levels were higher than preoperative values in both OC and LC groups. Seven days after surgery, cortisol and GH levels had normalized but prolactin levels were maintained. No significant differences in hormone levels were detected between OC and LC groups. IL-6 levels were significantly higher in the OC group 7 days after intervention. Correlation analysis between levels of cytokines and hormones indicated that prolactin, at concentrations exceeding physiological values, regulates levels of IL-1 (p 0.3271, p < 0.05) and IL-6 (p = 0.3765, p < 0.01). Although levels were similar in both groups, cortisol was shown to exert weak but significant, linear control on IL-6 levels (r = 0.4569, p < 0.001).
Conclusions: A similar hormonal response to surgical insult was produced in patients subjected to OC and LC. IL-6 levels seem to be the most indicative of injury. Prolactin is the main hormone involved in the regulation of cytokines produced in response to this type of stress and is thought to exert control over the production of IL-6.