Compare the changes of secretion of IL-2 and IL-6 in patients with endometriosis after the treatment of gonadotropin releasing hormone agonist (GnRHa) and estroprogestin

Objective To compare the changes of secretion of IL-2 and IL-6 in patients with endometriosis after the treatment of gonadotropin releasing hormone agonist and estroprogestin.Methods Using enzyme linked immunoabosorbent assay to detect the levels of interleukine-2(IL-2)and interleukine-6(IL-6)in supernatants of cultured PHA induced peripheral blood mononuclear cell(PBMC)and peritoneal fluid.Totally,28 endometriosis cases and 10 non-endometriosis cases were allocated and compared in this experiment.Endometriosis cases were randomly divided into two groups:GnRHa group(Group A)and GnRHa plus add-back therapy group(Group B).In both groups,the levels of IL-2 and IL-6 in supernatants of cultured PHA were detected after 3-month treatment.Results Compared with non-endometriosis cases group,the level of IL-6 in the supernatants of cultured PHA induced PBMC and peritoneal fluid of endometriosis groups were significantly increased(P 0.05);the ratio of IL-2/IL-6 in the supernatants and peritoneal fluid of both endometriosis groups was significantly lower than that of the non-endometriosis group(P 0.05).After 3-month treatment,in both endometriosis groups,the level of IL-6 in the supernatants was significantly decerased,while the radio of IL-2/IL-6 was remarkably increased(P 0.05,respectively).The difference between two endometriosis groups was not statistically significant.Conclusions The ascended levels of IL-6 in the supernatants and peritoneal fluid of both endometriosis groups infers that the increased level of IL-6 is possibly involved in the pathophysiology of endometriosis.The imbalance of Th1/Th2 leads to the depressed cell-mediated immune responses,which causes defect immunosurveillance and ectopic overgrowth of endometriotic tissues.Both the treatments of GnRHa alone and GnRHa plus add-back therapy lead to similar effects,which can be recognized as partly reverse the imbalance towards Th2.