IMMUNOMODULATION IN WOMEN WITH ENDOMETRIOSIS RECEIVING GNRH AGONIST

Objective: To assess the changes in the subpopulations of lymphocytes and in lymphocyte mitogenic activity in women with endometriosis recei ving GnRH-agonist treatment. Methods: Twenty-six women with advanced e ndometriosis from the National Cheng Kung University Medical College w ere studied. Each received a total of six doses of GnRH agonist at 4-w eek intervals. Immunologic responses at various times after receiving GnRH-agonist treatment, including numbers of peripheral blood lymphocy tes subsets and the lymphocyte proliferative activity, were analyzed u sing a repeated measures analysis of variance. Twenty-six healthy wome n who visited our gynecologic clinics for routine Papanicolaou smear e xamination at the time of the recruitment were enrolled as controls. T he responses for each patient receiving GnRH agonist were normalized w ith respect to those of her matched control at each of the time points . The differences between post- and pretreatment data were estimated u sing generalized estimating equations. Results: There was no significa nt difference in the sizes of lymphocyte subsets between patients and controls before treatment. After GnRH-agonist treatment, there was a t rend 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, resp ectively. 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 c ells, although a slight increase in total T cells (ie, CD3(+) T) was o bserved 1-2 weeks after receiving GnRH agonist. The T-cell mitogenic a ctivities at the end of 2 and 4 months after GnRH-agonist treatment we re 1.5 and 1.8 times, respectively, of those before treatment. Conclus ion: 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 tr eatment of endometriosis. (C) 1997 by The American College of Obstetri cians and Gynecologists.