Immunomodulation in women with endometriosis receiving GnRH agonist
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GnRH agonist treatment for endometriosis showed a trend of increasing natural killer cell numbers and significantly upregulated T-lymphocyte mitogenic activity.
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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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Cited by (27)
- Use of gonadotropic releasing hormone agonists in hyperplastic syndrome in gynecology 2025
- Endometriosis 2025
- Immunosuppression and immunotherapy in endometriosis 2021
- Recombinant IL-2: clinical efficacy and pathogenetic rationale for use in external genital endometriosis 2021
- O inibidor Btk Ibrutinib limita o desenvolvimento da endometriose em camundongos 2021
- Immunology of endometriosis 2018
- Roles of regulatory T cells in endometriosis-associated infertility 2014
- Immune interactions in endometriosis 2011
- Natural killer cells and telomerase in the endometrium of patients with endometriosis 2010
- Natural Killer Cells and Telomerase in the Endometrium of Patients with Endometriosis 2010
- Lymphocytes in Endometriosis 2010
- Effects of Bee Venom Acupuncture on Surgically Induced Endometriosis in Rats 2006
- Role of immunologic and inflammatory factors in the development of endometriosis: indications for treatment strategies 2005
- Role of immunologic and inflammatory factors in the development of endometriosis: indications for treatment strategies 2005
- In vitro effect of gonadotropin-releasing hormone agonist on natural killer cell cytolysis in women with and without endometriosis 2004
- Killer Inhibitory Receptor CD158a Overexpression Among Natural Killer Cells in Women With Endometriosis is Undiminished by Laparoscopic Surgery and Gonadotropin Releasing Hormone Agonist Treatment* 2004
- The Differential Expression of Intercellular Adhesion Molecule‐1 (ICAM‐1) and Regulation by Interferon‐Gamma during the Pathogenesis of Endometriosis 2004
- Immunology of Endometriosis and Immunotherapy 2003
- The involvement of T lymphocytes in the pathogenesis of endometriotic tissues overgrowth in women with endometriosis 2003
- Immunology and Endometriosis 2003
- Pathogenesis of endometriosis: natural immunity dysfunction or autoimmune disease? 2003
- New considerations for the pathogenesis of endometriosis 2002
- Secretory Leukocyte Protease Inhibitor in Ovarian Endometriomas Following GnRH Agonist Therapy 2001
- Secretory leukocyte protease inhibitor in ovarian endometriomas following GnRH agonist therapy 2001
- Treating endometriosis as an autoimmune disease 2001
- Macrophage derived growth factors m odulate Fas ligand expression in cultured endometrial stromal cells: a role in endometriosis 1999
- Immunology of endometriosis 1999
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