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• W2023685569 abstract "A cross-sectional comparative study among women who underwent surgical treatment for endometriosis revealed that frequency of the Ala/Ala genotype at aryl hydrocarbon receptor repressor (AHRR) Pro185Ala polymorphism was three times higher (27.6% vs. 9.9%) in the younger group (≤30 years) than in the older group (>30 years). AHHR genotyping may help to identify a subpopulation of women who are susceptible to the earlier onset of endometriosis. A cross-sectional comparative study among women who underwent surgical treatment for endometriosis revealed that frequency of the Ala/Ala genotype at aryl hydrocarbon receptor repressor (AHRR) Pro185Ala polymorphism was three times higher (27.6% vs. 9.9%) in the younger group (≤30 years) than in the older group (>30 years). AHHR genotyping may help to identify a subpopulation of women who are susceptible to the earlier onset of endometriosis. Endometriosis is a condition in which functioning endometrial tissue is present outside of the uterine cavity (1Cramer D.W. Wilson E. Stillman R.J. Berger M.J. Belisle S. Schiff I. et al.The relation of endometriosis to menstrual characteristics, smoking, and exercise.JAMA. 1986; 255: 1904-1908Crossref PubMed Scopus (296) Google Scholar), and it occurs in approximately 10% of women during their reproductive period (2Wheeler J.M. Epidemiology of endometriosis-associated infertility.J Reprod Med. 1989; 34: 41-46PubMed Google Scholar). Both genetic and environmental factors likely contribute to the development of endometriosis (3Kennedy S. The genetics of endometriosis.Eur J Obstet Gynecol Reprod Biol. 1999; 82: 129-133Abstract Full Text Full Text PDF PubMed Scopus (72) Google Scholar). An increased risk of endometriosis among the relatives of individuals with endometriosis unambiguously supports the contribution of genetic factors (4Matalliotakis I.M. Arici A. Cakmak H. Goumenou A.G. Koumantakis G. Mahutte N.G. Familial aggregation of endometriosis in the Yale Series.Arch Gynecol Obstet. 2008; Crossref Scopus (43) Google Scholar, 5Moen M.H. Magnus P. The familial risk of endometriosis.Acta Obstet Gynecol Scand. 1993; 72: 560-564Crossref PubMed Scopus (184) Google Scholar, 6Kashima K. Ishimaru T. Okamura H. Suginami H. Ikuma K. Murakami T. et al.Familial risk among Japanese patients with endometriosis.Int J Gynaecol Obstet. 2004; 84: 61-64Crossref PubMed Scopus (30) Google Scholar, 7dos Reis R.M. de Sa M.F. de Moura M.D. Nogueira A.A. Ribeiro J.U. Ramos E.S. et al.Familial risk among patients with endometriosis.J Assist Reprod Genet. 1999; 16: 500-503Crossref PubMed Scopus (39) Google Scholar, 8Kennedy S. Mardon H. Barlow D. Familial endometriosis.J Assist Reprod Genet. 1995; 12: 32-34Crossref PubMed Scopus (153) Google Scholar). Experimental and epidemiologic studies also suggest exposure to dioxin as a possible environmental factor in the development of endometriosis: First, the exposure of rhesus monkeys to dioxin led to an increased incidence of endometriosis, the severity of which was dose dependent (9Giudice L.C. Kao L.C. Endometriosis.Lancet. 2004; 364: 1789-1799Abstract Full Text Full Text PDF PubMed Scopus (2432) Google Scholar, 10Rier S.E. Martin D.C. Bowman R.E. Dmowski W.P. Becker J.L. Endometriosis in rhesus monkeys (Macaca mulatta) following chronic exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin.Fundam Appl Toxicol. 1993; 21: 433-441Crossref PubMed Scopus (393) Google Scholar); second, Belgium, which has the highest environmental level of dioxin in the world, has the highest incidence of endometriosis as well as the highest prevalence of severe endometriosis (11Koninckx P.R. Braet P. Kennedy S.H. Barlow D.H. Dioxin pollution and endometriosis in Belgium.Hum Reprod. 1994; 9: 1001-1002Crossref PubMed Scopus (129) Google Scholar). Intriguingly, polymorphisms in genes encoding dioxin-related proteins are associated with endometriosis. Examples of such proteins include the detoxification enzymes glutathione S-transferases M1/T1 (12Guo S.W. Glutathione S-transferases M1/T1 gene polymorphisms and endometriosis: a meta-analysis of genetic association studies.Mol Hum Reprod. 2005; 11: 729-743Crossref PubMed Scopus (58) Google Scholar) and CYP1A1 (13Guo S.W. The association of endometriosis risk and genetic polymorphisms involving dioxin detoxification enzymes: a systematic review.Eur J Obstet Gynecol Reprod Biol. 2006; 124: 134-143Abstract Full Text Full Text PDF PubMed Scopus (48) Google Scholar). Apart from polymorphisms in detoxification enzymes, a Pro/Ala (CCC/GCC) polymorphism at codon 185 (14Fujita H. Kosaki R. Yoshihashi H. Ogata T. Tomita M. Hasegawa T. et al.Characterization of the aryl hydrocarbon receptor repressor gene and association of its Pro185Ala polymorphism with micropenis.Teratology. 2002; 65: 10-18Crossref PubMed Scopus (44) Google Scholar) in the aryl hydrocarbon receptor repressor (AHRR), which plays a critical negative regulatory role in the dioxin signaling pathway (15Mimura J. Ema M. Sogawa K. Fujii-Kuriyama Y. Identification of a novel mechanism of regulation of Ah (dioxin) receptor function.Genes Dev. 1999; 13: 20-25Crossref PubMed Scopus (429) Google Scholar), has been associated with the development of endometriosis by two independent groups (16Tsuchiya M. Katoh T. Motoyama H. Sasaki H. Tsugane S. Ikenoue T. Analysis of the AhR, ARNT, and AhRR gene polymorphisms: genetic contribution to endometriosis susceptibility and severity.Fertil Steril. 2005; 84: 454-458Abstract Full Text Full Text PDF PubMed Scopus (44) Google Scholar, 17Kim S.H. Choi Y.M. Lee G.H. Hong M.A. Lee K.S. Lee B.S. et al.Association between susceptibility to advanced stage endometriosis and the genetic polymorphisms of aryl hydrocarbon receptor repressor and glutathione-S-transferase T1 genes.Hum Reprod. 2007; 22: 1866-1870Crossref PubMed Scopus (32) Google Scholar). These molecular epidemiologic studies, lacking the direct evaluation of dioxin exposure levels in each subject, have not yet documented a synergy between genetic and environmental factors in a quantitative fashion. Yet the results of these studies collectively indicate that subpopulations with certain genetic backgrounds may be susceptible to endometriosis partly because of polymorphisms in dioxin-related proteins. Earlier cross-sectional studies have detected two general trends in the epidemiology of endometriosis: First, the prevalence of endometriosis has increased in industrialized countries over recent decades, and this increase may be ascribed to an increasing exposure to dioxins (11Koninckx P.R. Braet P. Kennedy S.H. Barlow D.H. Dioxin pollution and endometriosis in Belgium.Hum Reprod. 1994; 9: 1001-1002Crossref PubMed Scopus (129) Google Scholar, 18Koninckx P.R. The physiopathology of endometriosis: pollution and dioxin.Gynecol Obstet Invest. 1999; 47 (discussion 50): 47-49Crossref PubMed Scopus (51) Google Scholar); second, a decreasing age of onset was reported during the period between 1980 and 1998 (19Ballweg M.L. Impact of endometriosis on women's health: comparative historical data show that the earlier the onset, the more severe the disease.Best Pract Res Clin Obstet Gynaecol. 2004; 18: 201-218Crossref PubMed Scopus (143) Google Scholar). Whether these two trends share a common biologic basis is currently unknown. We hypothesized that the subpopulation that develops endometriosis at an earlier age may have a “susceptible” genetic background and is responding to increasing environmental dioxin levels at an earlier age than the remaining subpopulation with a “less susceptible” genetic background. The purpose of the present study was to test whether a particular AHRR genotype is associated with the earlier onset of endometriosis, using a cross-sectional comparative study between younger patients and older patients with endometriosis in a relatively genetically homogeneous population, Japanese women. From 2001 to 2006, 120 women were recruited at the Department of Obstetrics and Gynecology, Keio University School of Medicine Hospital. A diagnosis of endometriosis was established by visual or pathologic criteria during laparoscopy. The participants were patients between the ages of 21 and 47 years (median 35 years, interquartile range 31–38 years) who underwent laparoscopic treatment for endometriosis. Blood samples were obtained at the time of admission for surgical intervention. Genomic DNA was extracted from peripheral leukocytes. The AHRR polymorphisms were genotyped, as reported elsewhere (14Fujita H. Kosaki R. Yoshihashi H. Ogata T. Tomita M. Hasegawa T. et al.Characterization of the aryl hydrocarbon receptor repressor gene and association of its Pro185Ala polymorphism with micropenis.Teratology. 2002; 65: 10-18Crossref PubMed Scopus (44) Google Scholar). The study was approved by the Institutional Review Board of the Keio University School of Medicine; the participants provided their written informed consent. The patients were stratified according to age into two groups. Patients younger than the first interquartile (≤30 years) were classified as the younger group, and those that were older (>30 years) were classified as the older group. We arbitrarily selected a cutoff value of 30 years because 30 years corresponded to the quartile value. An age of 30 years may be a biologically significant cutoff, because the incidence of endometriosis exhibits an age-dependent biphasic pattern, with a younger peak occurring before the age of 30 years followed by a plateau in the early 30s and then another peak in the 40s (20Houston D.E. Evidence for the risk of pelvic endometriosis by age, race and socioeconomic status.Epidemiol Rev. 1984; 6: 167-191Crossref PubMed Scopus (149) Google Scholar). A chi-squared analysis was used to evaluate differences in the proportions of the genotypes and the clinical stage of endometriosis between the two age groups. The allele frequencies of each polymorphism are shown in Table 1. The frequency of Ala/Ala homozygosity at codon 185 of AHRR showed a statistically significant difference between the two age groups (younger group vs. older group: 27.6% vs. 9.9%; χ2 = 5.66; P=.012). Two of the six patients aged ≤26 years (33.3%) were homozygous for 185 Ala, and two of the 26 patients aged >38 years (7.6%) were homozygous for this genotype. However, no statistically significant difference in the frequency of the Ala/Ala + Pro/Ala genotypes was observed between the two age groups (55.1% vs. 63.7%; χ2 = 0.682; P=.409). In addition, no statistically significant difference in the proportion of severe clinical stage (rAFS III or IV) was observed between the two age groups (72.4% vs. 63.7%; χ2 = 0.736; P=.391).Table 1Distribution of codon 185 polymorphism in the AHRR gene.Younger groupaYounger group: patients with endometriosis aged ≤30 years. (n = 29)Older groupbOlder group: the patients with endometriosis aged >30 years. (n = 91)AHRR genotypesPro/Pro + Pro/Ala21 (72.4 %)82 (90.1 %)Ala/Ala8 (27.6 %)cChi-squared test: P=.012.9 (9.9 %)cChi-squared test: P=.012.a Younger group: patients with endometriosis aged ≤30 years.b Older group: the patients with endometriosis aged >30 years.c Chi-squared test: P=.012. Open table in a new tab Among the patients who underwent surgical treatment for endometriosis, the frequency of the Ala/Ala genotype at AHRR codon 185 was three times higher in the younger group (≤30 years) than in the older group (>30 years). Therefore, a particular AHRR genotype, Ala/Ala, was more prevalent among the younger patients with endometriosis. In previous studies comparing patients with endometriosis and a control population, the Ala/Ala genotype was also more prevalent among patients with endometriosis (16Tsuchiya M. Katoh T. Motoyama H. Sasaki H. Tsugane S. Ikenoue T. Analysis of the AhR, ARNT, and AhRR gene polymorphisms: genetic contribution to endometriosis susceptibility and severity.Fertil Steril. 2005; 84: 454-458Abstract Full Text Full Text PDF PubMed Scopus (44) Google Scholar, 17Kim S.H. Choi Y.M. Lee G.H. Hong M.A. Lee K.S. Lee B.S. et al.Association between susceptibility to advanced stage endometriosis and the genetic polymorphisms of aryl hydrocarbon receptor repressor and glutathione-S-transferase T1 genes.Hum Reprod. 2007; 22: 1866-1870Crossref PubMed Scopus (32) Google Scholar). We therefore suggest that the Ala/Ala genotype may be primarily associated with the development of endometriosis at an earlier age of onset. Our rationale is as follows: The frequency of the Ala/Ala genotype in a historical control of general east Asian women is estimated to be 12.5% (8.4%–18.5%), based on the sum of control subjects in previously published epidemiologic studies (16Tsuchiya M. Katoh T. Motoyama H. Sasaki H. Tsugane S. Ikenoue T. Analysis of the AhR, ARNT, and AhRR gene polymorphisms: genetic contribution to endometriosis susceptibility and severity.Fertil Steril. 2005; 84: 454-458Abstract Full Text Full Text PDF PubMed Scopus (44) Google Scholar, 17Kim S.H. Choi Y.M. Lee G.H. Hong M.A. Lee K.S. Lee B.S. et al.Association between susceptibility to advanced stage endometriosis and the genetic polymorphisms of aryl hydrocarbon receptor repressor and glutathione-S-transferase T1 genes.Hum Reprod. 2007; 22: 1866-1870Crossref PubMed Scopus (32) Google Scholar, 21Watanabe T. Imoto I. Kosugi Y. Fukuda Y. Mimura J. Fujii Y. et al.Human arylhydrocarbon receptor repressor (AHRR) gene: genomic structure and analysis of polymorphism in endometriosis.J Hum Genet. 2001; 46: 342-346Crossref PubMed Scopus (86) Google Scholar). The frequency of the Ala/Ala genotype among patients aged ≤30 years in the present study was significant higher than this historical control figure (27.6% vs. 12.5%; χ2 = 5.27; P=.02), whereas the frequency of the Ala/Ala genotype among patients >30 years in the present study did not differ significantly from the historical control figure (9.9% vs. 12.5%; χ2 = 0.492; P=.48). Additionally, a higher percentage of Ala/Ala was seen in a younger age group (≤26 years, 33.3%) and a lower percentage was seen in an older age group (>38 years, 7.6%). This trend suggests that this particular genotype may be more strongly associated with the development of endometriosis at younger ages. The following limitations need to be appreciated when interpreting the results of the present study. First, we were unable to evaluate the dosage and period of the exposure to dioxins in the study subjects. This limitation applies to other previously reported molecular epidemiologic studies. Recent advances in the detection and quantification of dioxins in biological samples (22Pauwels A. Schepens P.J. D'Hooghe T. Delbeke L. Dhont M. Brouwer A. et al.The risk of endometriosis and exposure to dioxins and polychlorinated biphenyls: a case-control study of infertile women.Hum Reprod. 2001; 16: 2050-2055Crossref PubMed Scopus (151) Google Scholar) may alleviate this problem so that the direct association between the levels of exposure to dioxins and the risk of endometriosis in individuals with risk-conferring genotypes could be evaluated in future long-term prospective studies. Second, instead of evaluating the onset age of endometriosis, we examined the age at which a diagnosis of endometriosis was established using visual criteria obtained during laparoscopy for treatment. Previous studies have revealed that the elapsed time from the onset of symptoms until the diagnosis of endometriosis is about 7.0 years (23Arruda M.S. Petta C.A. Abrao M.S. Benetti-Pinto C.L. Time elapsed from onset of symptoms to diagnosis of endometriosis in a cohort study of Brazilian women.Hum Reprod. 2003; 18: 756-759Crossref PubMed Scopus (236) Google Scholar). Therefore, it is theoretically possible that some of the patients classified in the older group may have had asymptomatic endometriosis at a much earlier age. This limitation, inherent to any cross-sectional study such as this one, could be overcome using a cohort study in which the case and control subjects are strictly defined using a noninvasive examination, such as magnetic resonance imaging, or by the development of a sensitive biomarker for endometriosis. The present study does not prove but indicates that the AHHR genotype may help to identify a subpopulation of women who are susceptible to the earlier onset of endometriosis. The ability to screen for subpopulations at risk for the earlier onset of endometriosis has clinical relevance. Because some epidemiologic studies have indicated the effectiveness of oral contraceptive use for preventing the development or recurrence of endometriosis (24Vessey M.P. Villard-Mackintosh L. Painter R. Epidemiology of endometriosis in women attending family planning clinics.Bmj. 1993; 306: 182-184Crossref PubMed Scopus (177) Google Scholar, 25Vercellini P. Somigliana E. Daguati R. Vigano P. Meroni F. Crosignani P.G. Postoperative oral contraceptive exposure and risk of endometrioma recurrence.Am J Obstet Gynecol. 2008; 198: 504-505Abstract Full Text Full Text PDF PubMed Scopus (149) Google Scholar), the use of oral contraceptives may be helpful to women with an increased genetic risk of endometriosis if they do not plan to bear children. Because women with increasing numbers of live births are less likely to develop endometriosis (26Sangi-Haghpeykar H. Poindexter third, A.N. Epidemiology of endometriosis among parous women.Obstet Gynecol. 1995; 85: 983-992Crossref PubMed Scopus (230) Google Scholar), early pregnancy may have a preventive effect on the development of endometriosis. Furthermore, because endometriosis can lead to fertility problems, women who are genetically at a higher risk for endometriosis may be advised to become pregnant earlier during their reproductive period if they plan to bear children. Further genomic studies are warranted to better delineate the genetic risk factor(s) for endometriosis. We thank Hada Tomonori, M.D., and Masaaki Andou, M.D., from Kurashiki Medical Center for technical advices in endoscopic surgery for endometriosis." @default.
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• W2023685569 title "Association between patient age at the time of surgical treatment for endometriosis and aryl hydrocarbon receptor repressor polymorphism" @default.
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