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 613 records · Page 34Linked to original sources

PubMed2005

Oxidative stress and endometriosis.

BACKGROUND: Little is known about the aetiology of endometriosis; however, in the presence of oxidative stress, reactive oxygen species might increase growth and adhesion of endometrial cells in the peritoneal cavity, leading to endometriosis and infertility. Within a study investigating persistent organic compounds and endometriosis, the authors evaluated the association between oxidative stress and endometriosis. METHODS: Women aged 18-40 years who were undergoing laparoscopy were contacted to participate in the study (n = 100); 84 were eligible and agreed to be interviewed; 78 provided blood specimens. Four markers of oxidative stress and antioxidant status were measured in serum for 61 women. Multiple imputation of missing data was used to generate values for the missing oxidative stress data. RESULTS: Thirty-two women had visually confirmed endometriosis at laparoscopy while 52 did not, including 22 undergoing tubal ligation and 30 with idiopathic infertility. There was a weak association between thiobarbituric acid-reactive substances (nmol/ml) and endometriosis, after adjusting for age, body mass index, current smoking, hormone use in the past 12 months, gravidity, serum vitamin E, serum estradiol, and total serum lipids (beta = 1.18; 95% CI-0.04, 2.39). CONCLUSIONS: These results suggest that oxidative stress might play a role in the development and progression of endometriosis, which should be evaluated in larger studies.

Adolescent↗

PubMed2005

Glutathione-S-transferase P1 gene polymorphism and susceptibility to endometriosis.

BACKGROUND: Glutathione-S-tranferase (GST) is the part of the key phase II detoxifying enzyme system. Many studies have investigated the role of GSTM1 and GSTT1 gene polymorphisms in endometriosis. Although GSTP1 was found to be one of the most abundant types of GST in genital system, there are insufficient data about the importance of the role of GSTP1 gene polymorphism in endometriosis. METHODS: This case-control study involved 150 patients with endometriosis and 150 controls. The frequency of GSTP1 single nucleotide polymorphisms was evaluated using PCR and melting curve analysis. RESULTS: The proportion of GSTP1 ile/ile tended to be higher in patients with endometriosis than control group, although the difference was not significant [odds ratio (OR)=1.53; 95% confidence interval (CI)=0.95-2.46]. In contrast, GSTP1 val/val was significantly higher in control patients and seems protective for endometriosis (OR=0.10; 95% CI=0.02-0.42). CONCLUSION: The results of this study suggest that GSTP1 polymorphism might modulate the risk of endometriosis with significantly decreased risk for GSTP1 val/val and marginally increased risk for GSTP1 ile/ile. Further studies on not only the disease processes but also normal distribution of the enzyme in female genital tract may provide better understanding about the role of GST types and their polymorphs in endometriosis.

Adult↗

PubMed2005

The effect of endometriosis, cycle stage, lymphocyte suppression and pregnancy on CA-125 levels in peritoneal fluid and serum in baboons.

BACKGROUND: Serum CA-125 during the mid-follicular phase has been reported to be a clinically useful and reproducible marker in the diagnosis of advanced endometriosis in women. This study was undertaken to document the effect of the menstrual cycle, pregnancy and lymphocyte suppression on CA-125 levels in peritoneal fluid (PF) and serum in baboons with a normal pelvis and baboons with endometriosis. METHODS: CA-125 levels were measured in 264 serum samples that were serially obtained during one menstrual cycle from 10 animals with and without endometriosis. In addition, CA-125 levels were determined in 204 archived samples (serum, n = 112 and PF, n = 92) obtained from 32 female baboons with or without endometriosis. The CA-125 assays were performed by radioimmunoassay using kits from Centocor (Malvern, PA, USA). RESULTS: Serum CA-125 levels were at their highest during menstruation and decreased progressively during the follicular and luteal phase. PF CA-125 levels were increased during the follicular phase in baboons with a normal pelvis, but no cyclic changes were observed in animals with endometriosis. Serum CA-125 levels were unaffected by induction, lymphocyte suppression or pregnancy. Induction of endometriosis resulted in increased PF CA-125 levels, whereas lymphocyte suppression or pregnancy had no effect. CONCLUSION: In baboons, serum CA-125 originates mainly from eutopic endometrium whereas the main source of PF CA-125 seems to be the peritoneum or ectopic endometrium. The baboon appears to be a valid model to further study the relationship between endometriosis and CA-125.

Animals↗

PubMed2005

Serum adiponectin concentrations are decreased in women with endometriosis.

BACKGROUND: Adiponectin is a pleiotropic cytokine originally discovered as an adipocyte-specific gene product. Serum adiponectin concentrations have been reported to be low in women with endometrial cancer, breast cancer and uterine leiomyoma, suggesting possible involvement of adiponectin in these estrogen-related diseases. We thus addressed the relevance of adiponectin to endometriosis, an estrogen-dependent disease, in the present study. METHODS: Women with (n = 48) and without (n = 30) endometriosis undergoing laparoscopy were recruited in this study. Blood samples were collected, and serum adiponectin concentrations were measured using a specific enzyme-linked immunosorbent assay. The relationship between laparoscopic findings and serum adiponectin concentrations was analysed. RESULTS: The adiponectin concentrations in the serum of the women with endometriosis (median, 13.1 microg/ml; interquartile range, 10.2 - 16.7) were significantly lower than those of the women without endometriosis (15.9 microg/ml, 13.5 - 19.5; P = 0.008). A significant negative correlation was found between serum adiponectin concentrations and both endometriosis scores (R = - 0.307, P = 0.006) and adhesion scores (R = - 0.254, P = 0.026) of the revised American Society for Reproductive Medicine classification of endometriosis. CONCLUSIONS: The present findings suggest that adiponectin is implicated in the pathophysiology of endometriosis.

Adiponectin↗

PubMed2006

Endometriosis and the risk of cancer with special emphasis on ovarian cancer.

BACKGROUND: Several observations of the coexistence of endometriosis and cancer have been published. One study concerning endometriosis patients from 1969 to 1986 showed an overall relative cancer risk of 1.2 and relative risks for breast cancer, ovarian cancer and non-Hodgkin's lymphoma to be 1.3, 1.9 and 1.8, respectively. The aim of this study was to see whether these risk ratios stand in an extended study with longer follow-up. METHODS: Women discharged from a hospital, with a diagnosis of endometriosis from 1969 to 2000, were identified using the National Swedish Inpatient Register. Data were linked to the National Swedish Cancer Register to identify cases of cancer. Data on hysterectomies and oophorectomies were available. Standardized incidence ratios (SIR) were calculated. RESULTS: 64 492 women entered the study. First year of follow-up was excluded, leaving 3349 cases of cancer. There was no increased overall risk of cancer [SIR 1.04, 95% CI 1.00-1.07]. Elevated risks were found for ovarian cancer (SIR 1.43, 95% CI 1.19-1.71), endocrine tumours (SIR 1.36, 95% CI 1.15-1.61), non-Hodgkin's lymphoma (SIR 1.24, 95% CI 1.02-1.49) and brain tumours (SIR 1.22, 95% CI 1.04-1.41). Women with early diagnosed and long-standing endometriosis had a higher risk of ovarian cancer, with SIR of 2.01 and 2.23, respectively. The average age at endometriosis diagnosis was 39.4, indicating that there are the moderate/severe cases that are included in this study. Women who had a hysterectomy before or at the time of the endometriosis diagnosis did not show an increased risk of ovarian cancer. CONCLUSION: Women with endometriosis have an increased risk of some malignancies, particularly ovarian cancer, and the risk increases with early diagnosed or long-standing disease. Hysterectomy may have a preventive effect against ovarian cancer.

Adolescent↗

PubMed2006

Progesterone receptor polymorphism +331G/A is associated with a decreased risk of deep infiltrating endometriosis.

BACKGROUND: Alterations in the progesterone receptor (PR) are considered a risk factor for the development of endometriosis. In this study, the frequencies of the PROGINS and +331G/A polymorphisms of the PR gene were determined in deep infiltrating endometriosis and correlated with the expression of the PR protein. METHODS AND RESULTS: The frequencies of the PR polymorphisms were determined in women with deep infiltrating endometriosis (n = 72), women with adenomyosis in the uterine wall (n = 40), gynaecological patients without symptomatic endometriosis (n = 102) and healthy females (n = 93). Detection of +331G/A and PROGINS polymorphisms was performed using PCR-restriction fragment length polymorphism (RFLP) analysis. Expression of PR-A and PR-B protein was assessed with immunohistochemistry. The allelic frequency of the polymorphic allele +331A was lower in women with endometriosis (P < 0.01) and adenomyosis (P < 0.02) compared with healthy females. The frequency of the PROGINS polymorphism did not differ between the groups. The mean staining index (SI) for PR-B in endometriotic epithelium was higher in the presence of the +331A polymorphic allele (n = 2) (P < 0.001) compared with +331G/G individuals (n = 61). The PROGINS polymorphism did not affect the SI for PR-A and PR-B. CONCLUSIONS: The presence of the PR gene polymorphic allele +331A is associated with a reduced risk of deep infiltrating endometriosis and adenomyosis compared with healthy population controls. The PROGINS polymorphism does not seem to modify the risk of deep infiltrating endometriosis.

DNA Transposable Elements↗

PubMedDate not supplied

Angiogenesis: a new theory for endometriosis.

Excessive endometrial angiogenesis is proposed as an important mechanism in the pathogenesis of endometriosis. Evidence is reviewed for the hypothesis that the endometrium of women with endometriosis has an increased capacity to proliferate, implant and grow in the peritoneal cavity. Data is summarized indicating that the endometrium of patients with endometriosis shows enhanced endothelial cell proliferation. Results are also reviewed indicating that the cell adhesion molecule integrin alphavbeta3 is expressed in more blood vessels in the endometrium of women with endometriosis when compared with normal women. Taken together, these results provide evidence for increased endometrial angiogenesis in women with endometriosis when compared with normal subjects. Endometriosis is one of the family of angiogenic diseases. Other angiogenic diseases include solid tumours, rheumatoid arthritis, psoriasis and diabetic retanopathy. Excessive endometrial angiogenesis suggests novel new medical treatments for endometriosis aimed at the inhibition of angiogenesis.

Cell Division↗

PubMedDate not supplied

Apoptosis in human endometrium and endometriosis.

Apoptosis plays a critical role in maintaining tissue homeostasis and represents a normal function to eliminate excess or dysfunctional cells. Accumulated evidence suggests that apoptosis helps to maintain cellular homeostasis during the menstrual cycle by eliminating senescent cells from the functional layer of the uterine endometrium during the late secretory and menstrual phase of the cycle. The BCL-2 family and Fas/FasL system have been extensively studied in human endometrium and endometriotic tissues. Eutopic endometrium from women with endometriosis reportedly has some fundamental differences compared with normal endometrium of women without endometriosis. The differences could contribute to the survival of regurgitating endometrial cells into the peritoneal cavity and the development of endometriosis. One mechanism that recently gained a lot of interest is the finding that apoptosis appeared in eutopic and ectopic endometrium of patients with endometriosis. This study is a current review of the literature focused on the physiological role of apoptosis in normal endometrium and the alterations in regulation of apoptosis in eutopic and ectopic endometrium from women with endometriosis. Similarities in characteristics of endometriosis at a molecular level with gynaecological tumours are also discussed. Finally, the role of apoptosis in the treatment of endometriosis is reviewed to link the basic research findings into clinical applications.

Apoptosis↗

PubMed2005

Endometriosis and pelvic pain: epidemiological evidence of the relationship and implications.

The relationship between chronic pelvic pain symptoms and endometriosis is unclear because painful symptoms are frequent in women without this pathology, and because asymptomatic forms of endometriosis exist. Our comprehensive review attempts to clarify the links between the characteristics of lesions and the semiology of chronic pelvic pain symptoms. Based on randomized trials against placebo, endometriosis appears to be responsible for chronic pelvic pain symptoms in more than half of confirmed cases. A causal association between severe dysmenorrhoea and endometriosis is very probable. This association is independent of the macroscopic type of the lesions or their anatomical locations and may be related to recurrent cyclic micro-bleeding in the implants. Endometriosis-related adhesions may also cause severe dysmenorrhoea. There are histological and physiopathological arguments for the responsibility of deeply infiltrating endometriosis (DIE) in severe chronic pelvic pain symptoms. DIE-related pain may be in relation with compression or infiltration of nerves in the sub-peritoneal pelvic space by the implants. The painful symptoms caused by DIE present particular characteristics, being specific to involvement of precise anatomical locations (severe deep dyspareunia, painful defecation) or organs (functional urinary tract signs, bowel signs). They can thus be described as location indicating pain. A precise semiological analysis of the chronic pelvic pain symptoms characteristics is useful for the diagnosis and therapeutic management of endometriosis in a context of pain.

Bias↗

PubMed2006

Animal models in endometriosis research.

Endometriosis is a common gynaecological disease, defined as the presence of endometrial tissue outside the uterus, causing pelvic pain and subfertility in approximately 10% of women of reproductive age. Current therapies lead to pain relief, however, do not address the causes and entail severe side effects. Still little is known about the pathogenic processes leading to the development and maintenance of endometriosis. Because endometriosis occurs spontaneously only in humans and some non-human primates, animal models of induced endometriosis have been developed and are of high value for the evaluation of pathophysiological mechanisms underlying the development of this disease. These experimental models include the autotransplantation of uterine fragments into the peritoneal cavity of rodents and non-human primates or the heterotransplantation of human endometrial or endometriotic tissue to immunodeficient mice or onto the chicken chorioallantoic membrane (CAM). This review describes the animal models for endometriosis and assesses their different potentials and limitations in regard to endometriosis research, with the aim of developing novel non-invasive diagnostic tools and improved strategies for the treatment of endometriosis in women.

Animals↗

PubMed1996

Interleukin-8 concentration in peritoneal fluid of patients with endometriosis and modulation of interleukin-8 expression in human mesothelial cells.

Interleukin-8 (IL-8) is a chemoattractant and activating factor for human neutrophlls and a potent angiogenic agent. The peritoneal fluid of women with endometriosis has been shown to have increased neutrophil chemotactic activity. We postulate that IL-8 may be an important modulator in the pathogenesis of endometriosis and adhesion formation. We first investigated IL-8 concentrations in the peritoneal fluid of women with or without endometriosis, then assessed peritoneal mesothelial cells as a potential source of peritoneal fluid IL-8. Northern blot analysis and enzyme-linked immunosorbent assay (ELISA) were used to investigate IL-8 mRNA and protein modulation. The mean concentration of IL-8 in samples obtained from control patients (n = 28) was 4.8 +/- 0.5 pg/ml; from patients with minimal-mild endometriosis (n = 24) was 27.5 +/- 2.6 pg/ml; and from patients with moderate-severe endometriosis (n = 21) was 530.2 +/- 65.1 pg/ml. Confluent mesothelial cells were incubated with human recombinant IL-1 alpha (0.01-100 IU/ml) or tumour necrosis factor (TNF)-alpha (0.01 to 100 ng/ml) for 2-24 h. IL-8 mRNA was detectable in non-treated cells, however both IL-1 alpha and TNF-alpha induced higher amounts of IL-8 mRNA in a dose- and time-dependent manner. Non-treated mesothelial cells in culture also produced and secreted IL-8 protein quantified by ELISA, but again higher concentrations were induced by IL-1 alpha and TNF-alpha treatment. In conclusion, we found that IL-8 concentrations were elevated in peritoneal fluids from women with endometriosis. Cultured mesothelial cells expressed cytokine-inducible IL-8 mRNA and secreted IL-8 protein. The regulated expression of this angiogenic factor may play a role in pathogenesis of endometriosis.

Ascitic Fluid↗

PubMed2002

Distinct mechanisms regulate cyclooxygenase-1 and -2 in peritoneal macrophages of women with and without endometriosis.

Prostaglandin (PG) E2 has been shown to stimulate steroidogenesis in ectopic endometriotic stromal cells and may be involved in the development of endometriosis since this disorder is highly estrogen dependent. The biosynthesis of PGE2 is controlled by the rate-limiting enzyme termed cyclooxygenase (COX). The objective of the current study was to investigate the expression of COX in peritoneal macrophages isolated from women with and without endometriosis, and to explore the effects of pro-inflammatory agents on COX expression in peritoneal macrophages. Using quantitative RT-PCR and Western blot analyses, we found that expression of COX-2 was markedly increased (P < 0.05) in peritoneal macrophages isolated from women with early or severe endometriosis, whereas expression of COX-1 was elevated only in the severe stage (P < 0.05). On the contrary, monocytes/macrophages purified from peripheral blood of patients with endometriosis had minimal or undetectable levels of COX-2, and this was not different from disease-free women. Treatment with interleukin-1beta, tumour necrosis factor-alpha or PGE2 caused a significant increase in COX-2 (P < 0.05) but not COX-1 expression in peritoneal macrophages isolated from disease-free women. In contrast, these agents had no substantial effect on COX-1 and COX-2 expression in peritoneal macrophages from women with endometriosis. In summary, expression of COX in peritoneal macrophages was associated with the severity of endometriosis. Elevated expression of both COX-1 and COX-2 in peritoneal macrophages may contribute to the increased peritoneal fluid PGE2 concentrations and may thus play an important role in the development of endometriosis.

Cyclooxygenase 1↗

PubMed2002

Pleiotrophin (PTN) and midkine (MK) mRNA expression in eutopic and ectopic endometrium in advanced stage endometriosis.

Endometriosis is characterized by the ectopic implantation of endometrium on peritoneal surfaces. Angiogenic and growth factors may play a significant role in the pathogenesis of endometriosis. Midkine (MK) and pleiotrophin (PTN) are two related peptides associated with carcinogenesis and angiogenesis. To test the hypothesis that a higher expression of MK and PTN in ectopic and eutopic endometrium from women with endometriosis might favour increased angiogenesis and growth with subsequent ectopic implantation, we investigated PTN and MK expression by quantitative competitive PCR (QC-PCR) in endometrium from 30 women with severe, stages III and IV endometriosis and from 30 women without endometriosis. Total RNA was extracted and reverse transcribed into cDNA, and QC-PCR was performed to evaluate PTN and MK mRNA expression. Results were analysed by analysis of variance. Eutopic endometrium from endometriosis patients showed increased expression of MK and PTN mRNA compared with endometrium from normal women in the luteal phase (P < 0.05). MK and PTN mRNA expression in ectopic endometrium was significantly lower than that in eutopic endometrium from women with and without endometriosis (P < 0.05). Our results suggest increased MK and PTN expression may be related to the initiation of ectopic endometrial implants and peritoneal invasion.

Adult↗

PubMed2002

Increased leptin expression in endometriosis cells is associated with endometrial stromal cell proliferation and leptin gene up-regulation.

Endometriosis is a polygenic disease with complex, multifactorial aetiologies affecting approximately 10% of women of reproductive age. Leptin is the product of the ob gene, which is related to reproductive function and immunological alteration. The angiogenic and mitogenic action of leptin may influence the formation of endometriosis. This study was aimed at determining whether leptin and leptin receptor expression differs in eutopic and ectopic endometria collected from laparoscopy and at investigating the pathophysiological role of leptin in the development of endometriosis. Leptin mRNA was undetectable in seven out of 14 eutopic endometria and only a minute amount was detected in the remaining samples. In contrast, there was a marked increase in leptin mRNA and protein expression in ectopic endometriotic lesions of patients with endometriosis (P < 0.05). Receptors for leptin were immunologically stained in eutopic endometrium as well as in ectopic endometriotic implants. However, the levels of mRNA for the long and total forms of leptin receptors were suppressed in association with the severity of endometriosis (P < 0.05). Administration of leptin stimulated its own mRNA expression in ectopic endometriotic stromal cells but decreased steady-state concentrations of mRNA encoding for leptin receptor (n = 6). In addition, leptin significantly enhanced both eutopic and ectopic endometrial stromal cell proliferation (P < 0.05). In conclusion, the differential distribution of mRNA for leptin and its receptor suggests an important autocrine and paracrine role for leptin in human endometriosis. The mitogenic and auto-augmentation effects of leptin may further contribute to the pathogenesis of endometriosis.

Adult↗

PubMed2004

Polymorphisms of the genes encoding the GSTM1, GSTT1 and GSTP1 in Korean women: no association with endometriosis.

Endometriosis, one of the most common gynaecologic disorders, shows significantly elevated prevalence in industrial areas and there is also a possible genetic predisposition. Glutathione-S-transferases (GSTs) are enzymes involved in the metabolism of many disease-causing carcinogens and mutagens that are present in human environments. An association between the incidence of endometriosis and the GST genotypes of patients has been suggested. The objective of the present study was to investigate whether the polymorphisms of GSTM1, GSTT1 and GSTP1 are related to endometriosis. Blood samples were available from 259 controls and 194 patients with advanced endometriosis diagnosed by both pathology and laparoscopic findings. The proportion of the GSTM1, GSTT1 and GSTP1 genotypes of the control group were comparable to other populations. There was no significant evidence that the distribution of the GSTM1 and GSTT1 genotype differed between the patients and the controls, with an allelic odds ratio (OR)=1.074 [95% confidence interval (CI)=0.737-1.564] and 1.239 (95% CI = 0.853-1.799), respectively. Also, there was no significant difference in the proportion of GSTP1 genotypes between the women with endometriosis and the control group with the OR = 0.823 (95% CI = 0.536-1.264). The higher risk alleles were contended as GSTM1, GSTT1 null mutation and GSTP1 Ile105Ile polymorphism. There was no significant increase in the risk of endometriosis as the number of higher risk alleles of the GST family increased. In conclusion, our findings suggest that the GSTM1, GSTT1 and GSTP1 genetic polymorphisms are not associated with the development of endometriosis in Korean women.

Asian People↗

PubMed2004

Angiotensin I-converting enzyme ACE 2350G and ACE-240T-related genotypes and alleles are associated with higher susceptibility to endometriosis.

Endometriosis displays features similar to malignancy, ranging from neovascularization to local invasion and aggressive spread to distant organs. The altered vascular-related genes might be related to the development of endometriosis. This study investigates whether angiotensin I-converting enzyme (ACE) *A2350G and A-240T gene polymorphisms could be used as markers of susceptibility in endometriosis. Women were divided into two groups: (1) endometriosis group (n=150) and (2) non-endometriosis group (n=159). Genomic DNA was obtained from peripheral leukocytes. ACE A2350G and A-240T gene polymorphisms were amplified by PCR and detected after restriction enzyme digestion with BstUI and XbaI. Genotypes and allelic frequencies in both groups were compared. We observed that genotype distribution and allele frequency of ACE 2350 and ACE-240 gene polymorphisms in both groups were significantly different. Proportions of ACE 2350*A homozygote/heterozygote/G homozygote in both groups were: (1) 66.7/29.3/4% and (2) 96.2/3.1/0.7%. Proportions of ACE-240*A homozygote/heterozygote/T homozygote in both groups were: (1) 43.3/46/10.7% and (2) 62.9/35.8/1.3%. We concluded that ACE 2350*G and ACE-240*T-related genotypes and alleles are associated with higher susceptibility to endometriosis. ACE A2350G and A-240T gene polymorphisms might be associated with endometriosis development.

Adult↗

PubMed2005

The function of the SNP in the MMP1 and MMP3 promoter in susceptibility to endometriosis in China.

Matrix metalloproteinases (MMPs) may contribute to the development of endometriosis. Genetic variations in several MMP promoters may influence the transcription and expression of MMPs. The purpose of the present study was to assess how gene polymorphisms in the MMP1 and MMP3 promoters affect the risk of development of endometriosis. We genotyped 100 women with endometriosis and 150 control subjects in North China. There was a significant difference in frequency of the MMP1 genotype between cases and controls (P=0.03). The 2G homozygote in endometriosis and controls was significantly different (P=0.02). The frequency of the 2G allele among affected women (79%) was significantly higher than among the healthy controls (66.9%; P=0.003). However, the overall genotype and allelotype distribution of the MMP3 single nucleotide polymorphism (SNP) in patients was not different from that of controls (P> or =0.05). MMP1 and MMP3 polymorphisms were in linkage disequilibrium in cases and controls (D'=0.47; P=0.00). The haplotype frequency distribution derived from these two polymorphisms was significantly different between cases and controls (P=0.00). The haplotype analysis suggested an implication of both MMP1 and MMP3 polymorphisms in the susceptibility to endometriosis. We conclude that the MMP1 promoter SNP and MMP 2G/6A haplotype may modify susceptibility to endometriosis, but that the MMP3 promoter SNP is unlikely to be associated with endometriosis in the population of North China.

Adult↗

PubMed2006

Polymorphisms in the promoter regions of the matrix metalloproteinases-7, -9 and the risk of endometriosis and adenomyosis in China.

Matrix metalloproteinases (MMPs) may contribute to the development of endometriosis. The aim of this study was to assess the effects of the polymorphisms in the promoters of MMP-7 (181A/G) and MMP-9 (1562C/T) on the risk of occurrence of endometriosis and adenomyosis. We genotyped 219 patients (143 women with endometriosis, 76 women with adenomyosis) and 160 control women in North China. There was a significant difference in frequency of the MMP-7 genotype between endometriosis and controls (P = 0.01) and also between adenomyosis and controls (P = 0.01). The frequency of the G allele in two groups of patients (7.3 and 7.9%) was significantly higher than in the controls (2.8%) (P = 0.01 and 0.01, respectively). Compared to the A/A genotype, the genotype with the -181G allele showed a significantly increased susceptibility to both diseases, with adjusted odds ratio of 2.62 [95% confidence interval (CI) = 1.17-5.87] for endometriosis and 3.14 (95% CI = 1.26-7.81) for adenomyosis. However, the overall genotype and allelotype distribution of the MMP-9 in the two case groups were not different from that of controls. We conclude that MMP-7-181A/G polymorphism has a potential to be a susceptibility factor for endometriosis and adenomyosis while MMP-9-1562C/T polymorphism may not provide a useful marker to predict susceptibility to endometriosis and adenomyosis, at least in women from North China.

Adult↗