Immunomodulation in women with endometriosis receiving GnRH agonist

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Abstract
Objective: To assess the changes in the subpopulations of lymphocytes and in lymphocyte mitogenic activity in women with endometriosis receiving GnRH-agonist treatment. Methods: Twenty-six women with advanced endometriosis from the National Cheng Kung University Medical College were studied. Each received a total of six doses of GnRH agonist at 4-week intervals. Immunologic responses at various times after receiving GnRH-agonist treatment, including numbers of peripheral blood lymphocytes subsets and the lymphocyte proliferative activity, were analyzed using a repeated measures analysis of variance. Twenty-six healthy women who visited our gynecologic clinics for routine Papanicolaou smear examination at the time of the recruitment were enrolled as controls. The responses for each patient receiving GnRH agonist were normalized with respect to those of her matched control at each of the time points. The differences between post- and pretreatment data were estimated using generalized estimating equations. Results: There was no significant difference in the sizes of lymphocyte subsets between patients and controls before treatment. After GnRH-agonist treatment, there was a trend in the rise of natural killer cell numbers early in the treatment period, with P values of .05 and .07 at 1–2 weeks and 2–3 weeks, respectively. This rise in natural killer cell numbers was not significant until 3–4 weeks and the second month after the treatment. There were no significant changes in the CD4+ and CD8+ T-cell subsets and B cells, although a slight increase in total T cells (ie, CD3+ T) was observed 1–2 weeks after receiving GnRH agonist. The T-cell mitogenic activities at the end of 2 and 4 months after GnRH- agonist treatment were 1.5 and 1.8 times, respectively, of those before treatment. Conclusion: The increase in natural killer cell numbers and the upregulation of T-lymphocyte mitogenic activity, which might be caused by a direct effect of GnRH agonist or a consequence resulting from the depression of estradiol by GnRH agonist, may have implications in the clinical treatment of endometriosis.

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