SEARCH · PubMed Health

Results for “ENDOMETRIOSIS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 649 records · Page 36Linked to original sources

PubMed1997

Peritoneal cellular immunity and endometriosis.

PROBLEM: An immunologic basis has long been considered to be very important in the pathogenesis of endometriosis. Interactions of the peritoneal cells, which comprise macrophages, B cells, T cells, natural killer (NK) cells, and retrograde endometrial cells, are critical, but remain controversial, for exploring the pathogenesis of endometriosis. METHOD OF STUDY: Accumulated data from the literature were reviewed, and our data were analyzed. RESULTS: The data show that peritoneal macrophages are activated by the recurrent reflux of menstrual shedding. Humoral and local endometrial autoantibodies are detected in patients with endometriosis, but B cells are not quantitatively increased. There is decreased NK cell activity in the peritoneal cavity and peripheral blood, and this decreased activity may be related to the failure to clear out the ectopic endometrial tissue. Peritoneal T cells are predominant by Th1 inflammatory cells, and these cells are impaired because of a decrease in activation (especially HLA-DR+CD4+CD3+ population) and in the production of interleukin-2. Inflammatory cytokines such as interleukin-1, interleukin-6, and tumor necrosis factor-alpha are elevated in the peritoneal fluid of women with endometriosis. CONCLUSIONS: The peritoneal NK and T lymphocytes are suppressed in women with endometriosis, but whether these immunologic deviations are the cause or the result of endometriosis is still unclear. Further studies are required to determine what role immunologic factors play in the pathophysiology of endometriosis.

B-Lymphocytes↗

PubMed1998

The peritoneal fluid levels of interleukin-12 in women with endometriosis.

PROBLEM: Interleukin-12 (IL-12) is produced mainly by monocytes/macrophages, and it induces proliferation and cytotoxicity of T-cells and natural killer cells. In women with endometriosis, natural killer cell activity in the peritoneal fluid is significantly decreased. We aimed to measure the peritoneal fluid level of IL-12 in endometriosis. METHOD OF STUDY: We measured IL-12 levels in peritoneal fluid samples from women with or without endometriosis and in supernatants from endometrial stromal, ovarian stromal, and mesothelial cell cultures, using a high-sensitivity enzyme-linked immunosorbent assay. RESULTS: The median concentration of IL-12 in the peritoneal fluid of women with endometriosis was 1.1 pg/ml (range, 0.2-5.5) and was 1.6 pg/ml (range, 0.4-2.8) in women without endometriosis, not a statistically significant difference. IL-12 was not detected in the supernatants of endometrial stromal, ovarian stromal, and mesothelial cell cultures. CONCLUSION: Concentrations of IL-12 in the peritoneal fluid of women with or without endometriosis are low, but they are detectable and are not affected significantly by the presence of endometriosis.

Adult↗

PubMed1998

Levels of antibodies to transferrin and alpha 2-HS glycoprotein in women with and without endometriosis.

PROBLEM: To establish an enzyme-linked immunosorbent assay (ELISA) for determining the levels of antibodies to transferrin and alpha 2-HS glycoprotein in the serum of women with and without endometriosis. METHOD OF STUDY: Serum samples were obtained from 105 normal women, who were randomly selected for a population-based epidemiologic study, and 123 patients with active endometriosis. An ELISA using transferrin and alpha 2-HS glycoprotein as antigens was established. RESULTS: The levels of antibodies to transferrin and alpha 2-HS glycoprotein in the serum of patients with endometriosis were approximately 21 times higher than those in the serum of control subjects without endometriosis. Only 2% of control subjects had false positive levels of these antibodies, and 5% of patients with endometriosis had false negative levels of these antibodies (specificity, 98.1 and 98.1, respectively, for anti-transferrin and anti-alpha 2-HS glycoprotein; sensitivity, 95 and 96.7, respectively, for anti-transferrin and anti-alpha 2-HS glycoprotein). CONCLUSIONS: Patients with endometriosis have significantly higher levels of antibodies to transferrin and alpha 2-HS glycoprotein than control subjects. Testing women for antibodies to transferrin and alpha 2-HS glycoprotein will provide a specific noninvasive diagnosis of endometriosis.

Adolescent↗

PubMed1999

Increase in the production of interleukin-6, interleukin-10, and interleukin-12 by lipopolysaccharide-stimulated peritoneal macrophages from women with endometriosis.

PROBLEM: To verify whether the peritoneal macrophage (PM) is activated in endometriosis. METHOD OF STUDY: We examined the synthesis of nitric oxide (NO), total antioxidant, interleukin (IL)-6, IL-10, and IL-12 by cultured PMs, which were either unstimulated or stimulated with lipopolysaccharide (LPS), from women with endometriosis (early, n = 12; advanced, n = 11) or without endometriosis (n = 13). RESULTS: After stimulation with 2 ng/mL LPS for 24 hr, PMs from women with early-stage endometriosis secreted more NO, IL-6, and IL-10 than the controls. Higher IL-12 levels were noted in women with advanced endometriosis when compared with the controls. After 2 ng/mL-LPS stimulation for 24 hr, we also detected higher total antioxidant levels in the advanced-endometriosis group than those in the early-endometriosis group. CONCLUSION: The increased production of IL-6, IL-10, and IL-12 by stimulated PMs confirmed previous observations that the PM is the principle source of these cytokines in peritoneal fluid.

Endometriosis↗

PubMed2004

Killer inhibitory receptor CD158a overexpression among natural killer cells in women with endometriosis is undiminished by laparoscopic surgery and gonadotropin releasing hormone agonist treatment.

PROBLEM: Natural killer (NK) dysfunction is considered to contribute to the pathogenesis of endometriosis. In this study, we investigated the host immune response to endometriosis in terms of killer inhibitory receptor (KIR) expression by NK cells. METHOD OF STUDY: We compared cells from Japanese women laparoscopically diagnosed with endometriosis and treated with laparoscopic surgery (n = 98), 1 month after laparoscopic surgery (n = 36), and 12 weeks after gonadotropin releasing hormone agonist (GnRHa) treatment (n = 18) to cells from 104 women with other laparoscopic diagnoses. KIR expression by NK cells was assessed in peripheral blood and peritoneal fluid samples by flow cytometry. RESULTS: In women with endometriosis, the percentage of CD158a-expressing cells among CD16-expressing NK (CD158a(+)NK) cells in both peritoneal fluid and peripheral blood was significantly higher than in control subjects. No significant differences in proportion of CD158a(+)NK cells were identified between peripheral blood NK cells sampled before and 1 month after laparoscopic surgery, or 12 weeks after initiating GnRHa treatment. CONCLUSIONS: Increased percentage of CD158a(+)NK cells in peripheral blood from women with endometriosis was undiminished by laparoscopic surgery and GnRHa treatment; the persistence of CD158a(+)NK cell excess is probably related to NK cell suppression in endometriosis. This overexpression may represent a risk factor for development of endometriosis and its recurrence after treatments.

Adult↗

PubMed2004

Increased numbers of activated mast cells in endometriosis lesions positive for corticotropin-releasing hormone and urocortin.

PROBLEM: Mast cells are critical in allergic and inflammatory diseases such as interstitial cystitis, which is often clinically associated with or mistaken as endometriosis. Mast cells had previously been reported to be increased at sites of endometriosis, and tryptase may contribute to the fibrosis and inflammation characterizing endometriosis. METHOD OF STUDY: This is a pilot study of mast cell numbers and its activation in endometriosis biopsies (n = 10) by immunostaining for mast cell tryptase, corticotropin-releasing hormone (CRH) and urocortin (Ucn). RESULTS: This is the first report that tryptase positive mast cells were not only increased (64-157 mast cells/mm(2)) in human endometriosis, but also highly activated (89%) in areas strongly stained positive for CRH/Ucn. Normal endometrium was weakly positive for both CRH/Ucn. CONCLUSION: High numbers of activated mast cells are present in endometriosis sites that were strongly positive for CRH/Ucn. CRH and Ucn may activate mast cells and contribute to the fibrosis and inflammation in endometriosis.

Adult↗

PubMed2005

Increase of activated mast cells in human endometriosis.

PROBLEM: The proliferation of stromal cells in endometriosis promotes extensive adhesion; therefore, the morphological analysis of stromal lesions is important in the investigation of the pathogenesis of endometriosis. METHOD OF STUDY: In this study, the morphological and numeric comparisons of degranulated mast cells were performed between endometriotic lesions and comparative regions (eutopic endometrium and normal uterine serosa) of patients with and without endometriosis. RESULTS: In cases of endometriosis, diffuse infiltration of numerous mast cells was observed throughout the stromal lesions. These mast cells exhibited degranulation, and scattered granules were also observed. In the eutopic endometrium and normal uterine serosa of both the endometriosis patients and the controls, mast cells were rarely detected. CONCLUSIONS: These results suggest that an abnormal immune response, specifically a hypersensitivity reaction, is strongly related to endometriosis; our findings will be helpful in the development of methods for the treatment of endometriosis.

Adult↗

PubMed2006

Synergistic effect of interleukin-6 promoter (IL6 -634C/G) and intercellular adhesion molecule-1 (ICAM-1 469K/E) gene polymorphisms on the risk of endometriosis in Japanese women.

PROBLEM: Endometriosis is an immune-related, chronic inflammatory disease with a polygenic predisposition. The aim of this study was to investigate whether the interleukin-6 (IL-6) gene promoter region polymorphism (-634C/G) and the intercellular adhesion molecule-1 (ICAM-1) gene 469K/E polymorphism are responsible in part for the genetic susceptibility to endometriosis. METHODS OF STUDY: The IL-6 -634C/G and ICAM-1 469K/E genotypes were determined in 202 patients with endometriosis and 236 control women by polymerase chain reaction-restriction fragment length polymorphism. RESULTS: There were no differences in the IL-6 -634C/G or the ICAM-1 469K/E genotypes and allele frequencies between control women and endometriosis patients collectively, or between control women and each clinical subgroup of endometriosis patients. Interestingly, the frequency of ICAM-1 EE homozygotes who concomitantly carried the IL-6 -634G allele was significantly higher in patients with endometriosis (chi(2) = 6.458, P = 0.0396, d.f. = 2). CONCLUSION: Our results suggest that the IL-6 -634C/G and ICAM-1 469K/E polymorphisms synergistically affect the susceptibility for endometriosis in the Japanese population.

Adult↗

PubMed2002

Clinical aspects of endometriosis.

Endometriosis is one of the most commonly encountered gynecologic diseases requiring medical and/or surgical therapy. It is a leading cause of hysterectomy in the United States and has significant associated morbidity. The most frequent symptoms of genital tract endometriosis are dysmenorrhea, dyspareunia, chronic pelvic pain, and infertility. Endometriosis occurs in the pelvis, most commonly the ovaries and the dependent areas covered with peritoneum. Diagnosis requires surgical intervention and is usually made by laparoscopy. In women being evaluated for pelvic pain, the diagnosis of endometriosis is made frequently (40-60%) and varies with the population being studied. Infertility and endometriosis have long been associated. Although women with infertility may have pelvic pain, subfertility (20-30%) can be the only presenting symptom. In asymptomatic women, the diagnosis of endometriosis ranges from 2% to 22% of reproductive-age women. Its true incidence and natural history remain to be clarified. Endometriosis is a significant public health issue because of the large number of women it affects and the significant morbidity associated with this disease.

Diagnosis, Differential↗

PubMed2002

Local cytokines in endometrial tissue: the role of interleukin-8 in the pathogenesis of endometriosis.

Endometriosis, defined by the presence of viable endometrial tissue outside the uterine cavity, is among the most common gynecologic disorders affecting women of reproductive age. Endometriosis is associated with an inflammatory peritoneal environment, where multiple cytokines and growth factors are found at elevated levels. Interleukin-8 (IL-8) is a cytokine that induces chemotaxis of neutrophils and is a potent angiogenic agent. In addition, IL-8 was recently found to stimulate proliferation of various cells. We have observed that IL-8 is elevated in the peritoneal fluid of women with endometriosis and the levels correlate with the severity of the disease. We hypothesized that IL-8 may play a role in the growth and maintenance of ectopic endometrial tissue not only by chemoattracting and stimulating leukocytes to secrete growth factors and cytokines, but also by directly affecting endometrial cell proliferation. We found that IL-8 mRNA and protein levels in the endometrium were significantly higher during early proliferative and late secretory phases than during the mid-cycle. IL-8 receptors A and B are also expressed in the endometrium mostly localized in the stroma. Interestingly, IL-8 receptor expression is higher in the eutopic endometrium of women with endometriosis compared to the endometrium of women without endometriosis. Endometrial cells in culture proliferate significantly when treated with IL-8, which is inhibited by anti-IL-8 neutralizing antibody. More convincingly, IL-8 antisense oligonucleotide treatment decreases IL-8 production by endometrial cells as well as cell proliferation when compared to non-sense oligonucleotide treatment. The addition of IL-8 reverses the inhibitory effect of IL-8 antisense oligonucleotides on cell proliferation. These findings suggest that IL-8 may act as an autocrine growth factor in the endometrium. We have also studied the effect of endometrial cell adhesion on IL-8 expression and observed that IL-8 stimulates the adhesion of endometrial cells to fibronectin. Treatment of the cells with anti-IL-8 neutralizing antibody inhibited partially the cell adhesion. Thus, IL-8 may also be relevant for stimulating the attachment of endometrial implants in the pathogenesis of endometriosis. In addition, adherence of endometrial cells induced further IL-8 expression by an integrin-dependent mechanism. In summary, IL-8 may act as an autocrine growth factor in the endometrium and may also play a role in the pathogenesis of endometriosis by promoting the vicious circle of endometrial cell attachment, cell growth, and further secretion of this cytokine.

Cell Adhesion↗

PubMed2002

The potential role of exposure to environmental toxicants in the pathophysiology of endometriosis.

Humans and animals are exposed daily to a complex mixture of polyhalogenated aromatic hydrocarbons (PHAHs). Previous work has shown that exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is associated with a dose-dependent increase in the incidence and severity of endometriosis in the rhesus monkey. Dioxin-like chemicals can also exert effects in combination with TCDD via the aryl hydrocarbon receptor. Using a rhesus model of chronic TCDD exposure and endometriosis, serum concentrations of TCDD and 19 dioxin-like PHAHs were quantified 13 years after termination of exposure to TCDD. In additional studies, the immune status of TCDD-exposed monkeys was evaluated. For TCDD-exposed and unexposed animals, TCDD exposure correlated with an increased serum TCDD concentration. Furthermore, TCDD exposure and an elevated serum TCDD concentration were associated with increased serum levels of triglycerides, 1,2,3,6,7,8-hexachlorodibenzofuran (HxCDF), PCB77, and PCB126. Importantly, the animals with elevated serum levels of PCB77 and PCB126 and increased total serum TCDD equivalents (TEQs) had a high prevalence of endometriosis, and the severity of disease correlated with the serum concentration of PCB77. In immune studies, TCDD exposure correlated with increased tumor necrosis factor alpha (TNFalpha) production by peripheral blood mononuclear cells (PBMC) in response to stimulation by T cell mitogen and decreased NK cytolytic activity. Elevated serum concentrations of TCDD, 1,2,3,6,7,8-HxCDF, and PCB126 correlated with increased numbers of CD3+/CD25- and CD3-/CD25+ leukocytes and enhanced secretion of TNFalpha by mitogen-stimulated PBMC. This evidence suggests that TCDD exposure and endometriosis in the rhesus monkey may be associated with increased serum concentrations of specific coplanar PCB compounds and long-term alterations in systemic immunity. Furthermore, the data suggest a potential involvement of an increased body burden of PCB compounds in the etiology of endometriosis in the rhesus. Recent advances in the detection and assay of individual PHAH congeners in biological samples have made it possible to assess total PHAH body burden in humans and animals. Future studies are expected to exploit this advance to assess the health impact of PHAH body burdens in both exposed individuals and the general population. Serum PHAH concentrations and TEQs in TCDD-exposed monkeys with endometriosis are similar to or lower than blood levels in the general human population; thus, it is important to consider the implications of these findings for human health and the prevalence of endometriosis in humans. Additional studies are warranted, particularly in human subjects, to explore the potential implications of these data.

Animals↗

PubMed2002

The molecular basis for implantation failure in endometriosis: on the road to discovery.

Endometriosis is a benign gynecologic disorder associated with pelvic pain and infertility, with the latter being due, in part, to failure of embryonic implantation in the maternal endometrium. Adequacy of the endometrium for fertility has been classically investigated by histologic evaluation of a mid-late luteal phase biopsy and, historically, normal histology has been reassuring. However, recent studies demonstrate histologically normal, but biochemically abnormal, endometrium during the window of implantation in some women with endometriosis. In the pregenomic era, a "one-by-one" approach has been adopted to investigate proteins and genes expressed in the window of implantation, and several genes or gene products have been found to be aberrantly expressed in endometrium of women with endometriosis either during the implantation window or at other times of the cycle. Some of these are related to failure of implantation, while others likely contribute to the establishment and growth of endometriotic lesions. The time has come for a genome-wide approach to evaluate uterine endometrium for embryonic implantation. Knowing the biochemical mechanisms underlying normal implantation and the abnormalities in endometriosis will facilitate development of new diagnostic criteria beyond histologic evaluation and will permit identification and validation of molecular targets for future drug discovery. This monograph reviews (a) some of the evidence of compromised fertility in women with endometriosis and treatments targeted to improve their fertility; (b) the concept of the window of implantation; (c) genes/gene products aberrantly expressed in endometrium during the window of implantation or other times of the cycle in women with endometriosis; and (d) the use of microarray technology to investigate endometrial gene expression in human endometrial stromal cells and preliminary data resulting from a collaborative consortium effort of a genome-wide investigation of gene expression in the window of implantation of women with versus without endometriosis.

Embryo Implantation↗

PubMed2002

Role of endometriosis in cancer and tumor development.

Endometriosis, like cancer, is characterized by cell invasion and unrestrained growth. Furthermore, endometriosis and cancer are similar in other aspects, such as the development of new blood vessels and a decrease in the number of cells undergoing apoptosis. In spite of these similarities, endometriosis is not considered a malignant disorder. The possibility that endometriosis could, however, transform and become cancer has been debated in the literature since 1925. Mutations in the genes that encode for metabolic and detoxification enzymes, such as GALT and GSTM, have been implicated in the pathogenesis of endometriosis and in the progression to carcinoma of the ovary. PTEN, a tumor suppressor commonly mutated (50%) in endometrial carcinoma, is found mutated in endometrioid carcinoma of the ovary, but not in other forms of ovarian cancer. A recent study has shown that somatic mutations in the PTEN gene were identified in 20% of endometrioid carcinomas and 20.6% of solitary endometrial cysts, suggesting that inactivation of the PTEN tumor suppressor gene is an early event in the development of ovarian endometrioid carcinoma. In addition to cancerous transformation at the site of endometriosis, there is recent evidence to indicate that having endometriosis itself may increase a woman's risk of developing non-Hodgkin's lymphoma, malignant melanoma, and breast cancer.

Breast Neoplasms↗

PubMed2002

Experimental endometriosis: the nude mouse as a xenographic host.

Endometriosis is a complex disease that can develop as a consequence of retrograde menstruation, occurring in association with the cyclic loss of endometrial tissue in primates and humans. In addition, progression of disease parallels a woman's exposure to ovarian steroids, rarely occurring prior to menarche and generally resolving following menopause. Because of the cost of developing primate models to study endometriosis, numerous small animal models have been established to approach various elements related to the pathophysiology of this disease. Our laboratory has developed an experimental endometriosis model using nude mice as a xenographic host for human tissues. Our goal is to approach the basic cellular mechanisms of estrogen and progesterone action that link these hormones to the development or prevention of endometriosis. In our initial studies, we have sought to understand steroid-associated regulation of matrix metalloproteinases (MMPs) with regard to the development of experimental endometriosis. Using both short-term organ cultures and nude mice as xenographic hosts of human tissue, we have demonstrated a critical role of progesterone and progesterone-associated cytokines in preventing the initial establishment of experimental disease. Women with endometriosis appear to lack normal endometrial responsiveness to progesterone, resulting in altered expression of several MMPs and an enhanced ability of these tissues to establish ectopic lesions in nude mice. Developing a better understanding of the impairments in the normal endometrial physiology of women with endometriosis should aid in the development of better treatment or diagnostic strategies.

Animals↗

PubMed2002

Complete removal of endometriosis improves fecundity.

Endometriosis is one of the causative factors of impaired fecundity. Whatever the mechanisms are of this impairment, surgical removal of endometriosis appears to increase postoperative fecundity. Our strategy in laparoscopic surgery for symptomatic endometriosis is to completely remove endometriosis. However, despite this strategy, laparoscopic surgery nonetheless creates two categories of patients; complete and incomplete surgery groups. We found by comparing the two groups that both were comparable in terms of fecundity during the early postoperative phase, whereas unlike the complete surgery group, fecundity in the incomplete surgery group stayed low during the late postoperative phase. Deep rectal endometriosis and deeply invading pelvic endometriosis are conditions wherein complete removal of endometriosis is difficult. We have developed laparoscopic surgeries for these conditions: laparoscopic anterior rectum slicing (LARS) and laparoscopic pelvic wall slicing (LPWS) operations, respectively. Both operations are effective in alleviating disease-related symptoms with minimal surgical invasiveness.

Adult↗

PubMed1999

Role of cytokines in progression of endometriosis.

Peritoneal fluid in women with endometriosis contains an increased number of activated macrophages that secrete a variety of cytokines, including interleukin (IL)-6, IL-8, vascular endothelial growth factor, and tumor necrosis factor-alpha (TNF-alpha). Cytokines may be involved in the control of implantation and the growth of endometrial cells outside the uterus. In addition, several cytokines have been implicated in or directly associated with angiogenic activity in endometriosis. There could be a relationship between the levels of cytokines in the peritoneal fluid of patients with endometriosis and the status of the lesions in such patients. Peritoneal endometriosis can be classified as having red, black, or white lesions. Red lesions are known to be an active form of early endometriosis, because vascularization and mitotic activity are shown to be most prominent in these lesions. We found that the peritoneal fluid levels of TNF-alpha and IL-8 were significantly higher in patients with endometriosis, and correlated with the size and number of active lesions. In addition, TNF-alpha and IL-8 stimulated the growth of ectopic endometrial stromal cells. These cytokines with angiogenic activity may therefore have significant roles in the pathogenesis of endometriosis.

Cell Division↗

PubMed2003

Obstetric outcome in women with endometriosis--a matched case-control study.

BACKGROUND: Immunological deficiencies, altered angiogenic activity, infiltrative potential and growth factors are plausible factors behind endometriosis. The aim of this study was to determine whether endometriosis interferes with the course or outcome of pregnancy. STUDY DESIGN: In this matched case-control study, we analyzed obstetric outcome among 137 women with endometriosis and 137 controls matched as regards IVF procedures and parity who gave singleton births at Kuopio University Hospital between January 1994 and December 2000. In affected women, the diagnosis was histologically verified, whereas the controls were eligible for the study only if they had undergone laparoscopy/tomy in connection with tubal sterilization, or infertility unrelated to endometriosis. RESULTS: No statistically significant differences were detected in reproductive risk factors in women with endometriosis, with the exception of mean maternal age (31.2 years in the cases vs. 34 years in the controls). The mean birth weight (+/-SD) among those delivering at term (>37 completed weeks) was 3,600 (+/-542) g in the control group and 3,547 (+/-456) g in the study group. Placental weight was comparable in both groups. Overall pregnancy characteristics and pregnancy outcome measures were similar in women affected by endometriosis when compared with the control group. CONCLUSIONS: Any potential negative effect of endometriosis on obstetric outcome was undetectable.

Adult↗

PubMed2004

The link between exposure to dioxin and endometriosis: a critical reappraisal of primate data.

Endometriosis is a common and enigmatic disease affecting women of reproductive age. In 1993, Dr. Sherry Rier and her colleagues reported a serendipitous finding that quickly sent a shock wave through the endometriosis research community. They found that rhesus monkeys exposed daily for 4 years to dioxin developed endometriosis, with incidence and severity related to dose. The study prompted more animal and epidemiologic studies regarding the link between dioxin exposure and endometriosis. Yet, 10 years after the first piece of evidence was reported, the primate data are still equivocal, and the human data supporting the dioxin-endometriosis association are scanty and conflicting. While many reviewers of the subject recognize the need for more data, other reviewers tend to discount negative studies when reviewing positive studies. In this paper, a critical reappraisal of all evidence from human and primate data is presented. While there is evidence suggesting that exposure to dioxin may facilitate the short-term survival of endometrial implants in non-human primates, this evidence is not supported by both human and non-human primate studies evaluating the relationship between dioxin exposure and the development of spontaneous endometriosis. Weighing all converging evidence, it seems that there are no solid, credible data available at this moment to support the hypothesis that dioxin exposure may lead to the development of endometriosis.

Animals↗