Abstract

While surgery is commonly the management of symptomatic endometriosis when patients do not respond to medical or supportive therapy, recurrence after surgery poses a serious challenge, and repeat surgery increases the risk of premature ovarian failure, adhesion and organ injury. Conceivably, the recurrent endometriotic lesions could arise from minimal residual lesions (MRLs) or from de novo lesions. However, several lines of evidence suggest that the former is more likely. So far, most, if not all, efforts to combat recurrence have been focused on postoperative medication of hormonal drugs to reduce recurrence risk through lesional dormancy and possibly atrophy. However, the perioperative period may exert a disproportionally high impact on the risk of recurrence; it is likely to be amendable for possible intervention but has been generally neglected. Indeed, many perioperative factors are known to or conceivably could facilitate the recurrence of endometriosis through the suppression of cell-mediated immunity due to the activation of adrenergic signaling and the release of prostaglandins. Perioperative use of β-blockers and/or nuclear factor κB/jCycloxygenase 2 (NF-κB/COX-2) inhibitors may boost the cell-mediated immunity suppressed by surgery, resulting in the partial or even complete removal of MRLs and reduced recurrence risk. This is both biologically plausible and supported by a recent experimental study. We call for more research on possible perioperative interventions to reduce the recurrence risk of endometriosis. The potential payoff might be a substantial reduction in the risk of recurrence and cost when compared with the traditional approach of postoperative intervention.

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