Surgical management of endometriosis does not affect oxidative damage in endometriotic tissue over time

Abstract

Oxidative stress has been considered as a potential factor involved in the pathology and progression of endometriosis. The objective of this study was to evaluate the natural progression of endometriosis by comparing oxidative damage in endometriotic tissue at two distinct time points. Retrospective cohort trial Women who had presented between 1999-2009 with pelvic pain and/or infertility between the ages of 18-45 years with a history of two distinct surgeries with biopsy proven endometriosis were included if there was banked blood and tissue samples available for review. Histopathochemistry was used to evaluate oxidative damage by measuring hydroxy deoxyguaninine (8OHdG) in endometriotic cells and to evaluate the cellular ability for DNA repair with 8-oxoguanine glycosylase 1 (OGG1). The markers were measured in a biopsy sample of pathology proven endometriosis for each patient at each surgery and compared to each other using Wilcoxan rank-sum tests. The pathologist was blinded to whether the samples were from the primary or secondary surgery. All surgeries were performed by the same surgeon. There were seven patients who met criteria and were included in the study. The average age at first surgery was 32.4 +/- 4.4 years. The average time between surgeries was 2.0 +/- 1.1 years. Stage of disease and marker intensity and presence in percentage of cells at first and second surgery are shown in table 1.Tabled 1Table 1: Stage of endometriosis and markers at first and second surgery.Stage8-OHdG Intensity8-OHdG % of cellsOGG1 IntensityOGG1 % of cells1IV/IV0/10/102/290/802IV/IV2/380/903/290/303IV/IV3/3100/802/310/804IV/IV2/280/602/250/805IV/IV3/275/753/395/956IV/IV2/240/53/390/907III/III2/360/803/395/90 Open table in a new tab Despite complete excision of all visible endometriosis at the time of first surgery, all patients had return of the disease to the same stage at their second surgery. Temporally, there was no significant difference between percentage of cells that expressed 8-OHdG (p = 0.79) or OGG1 (p = 0.81) between the two surgeries. There was a correlation of 8-OHdG percent of cells and intensity (r = 0.80, p < 0.01) and OGG1 percent of cells and intensity (r = 0.65, p < 0.01), but no temporal relationship between surgeries. Overall, There was no relationship of progression of oxidative damage over time. Based on these results, it appears that baseline oxidative damage in endometriotic cells is predictive of future cell damage and that surgical excision of endometriosis has no benefit in changing the underlying pathophysiology leading to oxidative damage.