<b><i>Objective:</i></b> The objective of this study was to evaluate cytokines related to natural killer and T-regulatory cells in endometriotic lesions, peritoneal fluid (PF) and the peripheral blood (PB) of patients with deep infiltrative endometriosis. <b><i>Study Design:</i></b> A case-control study was conducted in a tertiary referral hospital. Sixty-four consecutive patients after laparoscopy were divided into 2 groups: with endometriosis (Group A – <i>n</i> = 32) and without endometriosis (Group B – <i>n</i> = 32). <b><i>Main Outcome Measures:</i></b> Interleukin (IL)-2, IL-4, IL-7, IL-10, IL-12, IL-15, transforming growth factor β1, and IFNγ concentration was measured using a Luminex<sup>TM</sup> multiplex suspension bead array. Tissues from endometriotic lesions of patients with endometriosis and from eutopic endometrium were evaluated, as well as PF and PB of all patients. <b><i>Results:</i></b> Compared to the other analyzed groups, IL-15 concentration was significantly higher in the ectopic endometrium and IL-7 in the eutopic endometrium of the endometriosis group (<i>p</i> < 0.05). Compared to endometriosis group, IFNγ, IL-7, and IL-15 were observed to be significantly higher in the PF of the control group, and IL-10 was lower in the control group (<i>p</i> < 0.05). In PB, compared to endometriosis group, IL-4, IL-10, IL-12, IL-15, and IFNγ concentrations were significantly higher in the control group (<i>p</i> < 0.05). <b><i>Conclusions:</i></b> Our hypothesis is that deep endometriosis is a disease out of control. This disease’s nature is of progression and invasion of adjacent structures, and proof of this disease state is the disorganized secretion of cytokine regulation and inflammation, which seem to be among the factors responsible for the maintenance of the disease.
Endometriosis represents a common gynecological condition affecting 5%-15% of childbearing age women and up to 3% 5% of post-menopausal women. This disease is defined by the presence of stromal and/or endometrial glandular epithelium implants in extra-uterine locations possibly compromising several sites. Humans and animals are daily exposed to chemical pollutants that could adversely influence physiological processes and potentially cause diseases, including endometriosis. In this review, the authors aimed at settling the influence of environmental and dietary factors on endometriosis pathogenesis. The mechanism by which dioxin and its similes (TCDD/PCBs) act changing the endometrial physiology remains uncertain and is speculative due to the difficulty in assessing the exposure over intrauterine life, childhood and adulthood and its actual consequences, in addition to the limitations to its in vitro reproducibility. We need to better understand the mechanism of action of these environmental pollutants, not only on reproductive health, but also on overall health of individuals and so prevention strategies, including not only population education, but setting exposure limits, less polluting techniques and a better use of our natural resources, could be promoted.
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