Abstract
ObjectiveDexmedetomidine has sympatholytic, anti-inflammatory, and analgesic effects and may exert anti-tumor effect by acting on α2A adrenoreceptor. We investigated whether perioperative dexmedetomidine preserves immune function in patients undergoing uterine cancer surgery.MethodsOne hundred patients were randomly assigned to the control or dexmedetomidine groups (50 patients each). Dexmedetomidine was infused at rates of 0.4 μg/kg/h intraoperatively and 0.15 μg/kg/h during the first 24 h postoperatively. The primary outcome was natural killer (NK) cell activity, which was measured preoperatively and 1, 3, and 5 days postoperatively. The inflammatory response was measured by interleukin-6, interferon-γ, and neutrophil/lymphocyte ratio, and pain scores and opioid consumption were assessed. Cancer recurrence or metastasis and death were evaluated 2 years postoperatively.ResultsNK cell activity decreased postoperatively in both groups and changes over time were not different between groups (P=0.496). Interferon-γ increased postoperatively in the dexmedetomidine group, whereas it maintained at the baseline value in the control group. Change in interferon-γ differed significantly between groups (P=0.003). Changes in interleukin-6 and neutrophil-lymphocyte ratio were comparable between groups. Both pain score with activity during the first 1 h and opioid consumption during the first 1–24 h postoperatively were lower in the dexmedetomidine group. Rates of cancer recurrence/metastasis (16.3% vs. 8.7%, P=0.227) and death within 2 years postoperatively (6.7% vs. 2.2%, P=0.318) were not different between groups.ConclusionsPerioperative dexmedetomidine had no favorable impacts on NK cell activity, inflammatory responses, or prognosis, whereas it increased interferon-γ and reduced early postoperative pain severity and opioid consumption in uterine cancer surgery patients.
Highlights
Surgical resection is the main and curative treatment for solid tumors, the spread of tumor cells in the blood and lymphatic system might occur by surgical manipulation [1]
In the dexmedetomidine group (DEX group), dexmedetomidine was infused at 0.4 mg/kg/h from anesthetic induction to the end of surgery and continued at 0.15 mg/kg/h for the first 24 h postoperatively
Dexmedetomidine administration in patients undergoing uterine cancer surgery did not demonstrate a favorable impact on immunity in terms of perioperative changes of natural killer (NK) cell activity, IL-6, and NLR
Summary
Surgical resection is the main and curative treatment for solid tumors, the spread of tumor cells in the blood and lymphatic system might occur by surgical manipulation [1]. Surgical traumainduced systemic stress and inflammatory responses and the use of anesthetics and opioid analgesics impair immune function [2]. This perioperative immunosuppression may predispose already immunocompromised cancer patients further vulnerable to tumor growth and spread. Perioperative immunosuppression is characterized by suppressed cell-mediated immunity and excessive pro-inflammatory responses [8]. Dexmedetomidine has been demonstrated to preserve natural killer (NK) cell function, which is a critical part of innate immunity, and reduce pro-inflammatory cytokines in both experimental and clinical settings [4, 7]. Despite possible beneficial effects of dexmedetomidine on immunity, its immunomodulatory role in cancer surgery has not been established
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
