{"paper_id":"79020ded-c8a7-4b2d-8ffc-34f9e0328bd3","body_text":"Manuscript accepted for publication\n1 \nProvisionally accepted for publication \nORIGINAL ARTICLE \nAssociation between anti Mullerian hormone levels with size and bilaterality of \novarian endometrioma : a cross-sectional study \nAssociation AMH with size of endometrioma \nA\nndi Muldiani Dwi Rachmayana 1,*, Nusratuddin Abdullah 1, Eddy Hartono 1, Fatmawati\nMadya 1, Sriwijaya Sriwijaya 1, Firdaus Hamid 2\n1 Department of Obstetrics and Gynecology, Faculty of Medicine, Hasanuddin University, \nMakassar, Indonesia \n2 Department of Public Health, Faculty of Medicine, Hasanuddin University, Makassar,\nIndonesia\nC\norrespondence to: Andi Muldiani Dwi Rachmayana, M.D. Departement of Obstetrics and \nGynecology, Faculty of Medicine, Hasanuddin University, Jl. Perintis kemerdekaan,\nMakassar, South Sulawesi, Indonesia, 90242, email address: muldianiandi@gmail.com,\nPhone number: +62 812-6800-7842 ORCID 0009-0006-6671-2571\nDo\ni: 10.36129/jog.2024.181 \nABS\nTRACT \nObjective. This study aims to analyze the association between anti-Mullerian hormone \nlevels and the size and bilaterality of ovarian endometriomas.\nMaterials and Methods. The study was conducted from January to October 2023  at\nWahidin Sudirohusodo Hospital in Makassar using a cross-sectional design through \nconsecutive sampling of ovarium endometrioma patient confirmed by histopathological\nexamination. AMH levels were measured by ELISA technique, size and bilaterality were \ndetermined based on abdominal ultrasound examination.\nResults. A total of 50 women, with a mean age 32.24 ± 0.75 years, were enrolled in the\nstudy. There was no difference in the effect of age, menarche age, education, parity, BMI,\nendometrioma bilaterality, or tumor size on AMH levels(p > 0.05). In the correlation test, age \n(r = -0.248) and tumor size (r = -0.276) were negatively correlated with AMH levels, while \nmenarche age (r = 0.067) was positively correlated with AMH levels, but all three variables\nwere statistically insignificant (p > 0.05).\nConclusions. There was no association anti mullerian hormone level with the size and\nbilaterality of ovarium endometrioma. Further research is needed with a larger sample size \nto confirm it.\nK\neywords: Endometrioma, Anti-Mullerian Hormone, Unilateral, Bilateral, Tumor Size \n\nManuscript accepted for publication\n2 \n \nIntroduction \nEndometriosis is an estrogen-dependent condition characterized by the presence of ectopic \nendometrial-like tissue [1]. The most common sites of endometriosis are the ovaries, \nfollowed by the Douglas pouch, the posterior leafs of the broad ligaments, and the \nsacrouterine ligaments [2]. Ovarian endometriomas occur in 17–44% of patients with \nendometriosis and account for 35% of all benign ovarian tumors [3]. Several studies have \nindicated a correlation between endometriosis and a higher prevalence of obstetric \ncomplications, including preterm births, placental disorder, gestational diabetes, cesarean \nsection (CS), and postpartum hemorrhage (PPH) [4]. Additionally, there is a correlation \nbetween endometriomas and infertility, and it is now widely accepted that endometriomas \naffect fertility. Although the mechanism is unclear, research suggests that it can negatively \naffect spontaneous ovulation rates and reduce the number and activity of follicles in adjacent \novarian tissue [5]. \nAnti-Mullerian Hormone (AMH) is a glycoprotein hormone with a molecular weight of 140 \nkDa linked by a disulfide chain [6]. It is produced by granulosa cells of non-growing follicles, \nsuch as primary, secondary, preantral, and early antral follicles. It can predict the state of \novarian reserve and follicular growth, which are critical to fertility [7]. AMH is commonly used \nas a primary fertility marker, particularly in conditions or diseases that affect ovarian reserve, \nsuch as polycystic ovarian syndrome [8]. \nThe decline in AMH levels was found to be more rapid in women with endometriomas \ncompared to healthy women and women with other benign ovarian cysts [9]. The correlation \nbetween AMH levels and endometrioma volume is not well known due to conflicting study \nresults. A study by Suardi et al. found a negative correlation between AMH levels and \novarian endometrioma volume, but it was not statistically significant (r = -0.332; p=0.066). \nThe study also found significantly lower AMH levels in the endometrioma group compared to \ncontrols, but this was not affected by laterality [10].  Another study which compared AMH \nlevels tested one month pre-surgery in the ovarian endometrioma group with controls, found \nAMH levels were not significantly different between the two groups and serum AMH levels \nwere significantly positively correlated with ovarian endometrioma cyst volume (r\n2=0.23; 95% \nCI: 0.007-0.1; p=0.02) [11]. In addition, a meta-analysis also showed postoperative AMH \nlevels were affected by the bilaterality of the endometrioma but not preoperative AMH levels \n[12].  \nExisting research about association between anti mullerian hormone levels  with the size \nand bilaterality of ovarium endometrioma is still controversial. Therefore, this study aims to \nanalyze the association between anti-Mullerian hormone levels and the size and bilaterality \nof ovarian endometriomas through abdominal ultrasound examination especially in the \nlimited health facilities so the ovarian reserves can be predicted with a simple modality. \nMaterials and Methods \nThis study was conducted at Wahidin Sudirohusodo Hospital, Makassar  Indonesia, between \nJanuary until October 2023. The study received approval from the Health Research Ethics \nCommittee of the Faculty of Medicine, Hasanuddin University \n(No.20/UN4.6.4.5.31/PP36/2023). Informed consent was obtained from all participants. The \nparticipants were enrolled into the study by consecutive sampling technique. The inclusion \ncriteria were: 1) Diagnosed as endometrioma based on ultrasound examination, 2) >20 \nyears old and not yet menopause. The exclusion criteria were: 1) Using hormonal \ncontraception in the last 1 year, 2) Taking vitamin D supplements, 3) History of previous \nendometrioma surgery, pelvic inflamatory disease or polycystic ovarian syndrome, 4) \n\nManuscript accepted for publication\n3 \n \nHistopathological examination results not endometrioma. We excluded patients using \nhormonal contraception and vitamin D supplements because contraception can reduce AMH \nlevels, while vitamin D can increase AMH levels [13,14]. \nAll participants underwent transabdominal USG to assess the size and characteristics of \novarian endometrioma. The ultrasonographic criteria for diagnosing endometrioma included \nthe presence of a cystic structure with uniform low-level internal echoes lacking papillary \nproliferations and exhibiting poor vascularization, or a cystic structure with uniform low-level \ninternal echoes containing an echogenic portion devoid of detectable blood flow. The \nendometrioma was measured in two dimensions, \nThe levels of AMH measured at the Clinical Pathology Laboratory of Hasanuddin University \nHospital using an enzyme-linked immunosorbent assay (ELISA) kit (AMH ELISA kit, \nBioassay Technology lab,Shanghai) according to the manufacturer’s instructions. The kit has \na sensitivity of  0.024 ng/mL and a detection range between 0.05 - 30ng/ml.  It were \nexamined from vein blood specimens using the ELISA method and reported in ng/ml. The \nsamples were collected from venous blood in EDTA tubes from presurgical endometrioma \npatients. After mix 10-20 minutes, sample was centrifuged  for 20 minutes at 2000-3000 \nRPM then supernatant without sediment was collected. Samples were stored at 80°C, \nwaiting for histopathological examination. Serum AMH levels for fertile women range from \n1.0 ng/ml to 4.0 ng/ml [15]; AMH levels below 1.0 ng/ml are considered low and indicate a \ndecrease in ovarian reserve [16]. The endometrioma was confirmed through \nhistopathological examination using hematoxylin-eosin staining. \nStatistical analysis was conducted using the SPSS 24.0 for Windows software (IBM, USA). \nBaseline characteristics were reported as frequencies and percentages. For normally \ndistributed data, the results were reported as Mean ± SD and analyzed with an independent \nt-test. While in non-normally distributed data were reported as Median ± Interquartile Range \n(IQR) and analyzed using the Mann-Whitney test. The differences in baseline characteristics \nbetween the two groups will be analyzed using a chi-square test. A p-value of <0.05 was \nconsidered significant. \nResults \nA total of 67 presurgical participants were enrolled; however, 7 samples were lysed, and 10 \nhistopathological examinations did not show endometrioma. All groups were similar with \nrespect to age, menarche age, and BMI. The demographic data of the groups are shown in \nTable 1. The median (±IQR) OMA size was 53.85 ± 31.03 mm2 in the low AMH group and \n37.71 ± 55.17 mm2 in the normal AMH group, but the difference was not significant (P > \n0.05). Bilaterality also was found not to significantly affect the AMH level (P > 0.05). Age and \ntumor size were negatively correlated with AMH levels, while age at menarche was positively \ncorrelated with AMH levels. However, none of these variables were statistically significant \n(Table 2). The correlation between endometrioma size and serum AMH levels is shown in \nFigure 1. \n \nDiscussion \nOne of several method to assess the ovarian reserve is by measuring serum AMH levels, \nwhich are produced by granulosa cells in small to medium-sized follicles. These follicles, \nranging from 4 to 8 mm in diameter, account for approximately 60% of circulating AMH [17]. \nAMH plays a crucial role in controlling ovarian function in the initial stages of follicle growth \nby preventing the excessive activation of primordial follicles and slowing down their \n\nManuscript accepted for publication\n4 \n \nprogression to the primary stage, thereby preserving the follicle pool[17,18]. Unlike FSH, \nAMH levels stay consistent throughout the menstrual cycle [19]. Serum AMH levels are lower \nin women with endometriomas, suggesting a decreased ovarian reserve in these women  \n[10].   . \nIn this study, an AMH value of <1 ng/mL was used as a benchmark for low AMH levels. For \nthe characteristic data, the variables of age, menarche age, education, parity, BMI, \nendometrioma location, and tumor size were not found to be significantly different in the two \ngroups. AMH levels decrease with age, resulting in lower pregnancy rates in infertile \npatients. Age is considered one of the factors that affect AMH levels [20]. Khan et al. found \nthat AMH levels decrease by about 6% per year, suggesting a direct relationship between \nincreasing age and decreasing follicular reserve [21]. However, in this study, age levels were \nnot found to be different in groups with low and normal AMH. Multivariate testing and \ncorrelation tests were carried out, but no association was found with AMH. Feferkorn et al.'s \nstudy found that AMH levels had a significant effect on endometriosis only in the age group > \n35 years, but not in the age group under 35 years. According to this study, this is because at \nthe age of under 35 years, there are still many follicular reserves, so the increase in age \ndoes not have a significant effect [22]. In Lie Fong's study, AMH concentration was positively \ncorrelated with age until it peaked at 15.8 years, then remained stable, and inversely \ncorrelated after the age of 25 years [23]. Normal AMH values vary by age group, which could \nbe a confounding factor when categorizing the low AMH group [24].  \nMenarche age, which also seems to play a role in follicular reserve, was found to be \nunrelated to AMH levels in this study. Weghover's study found that the age at menarche is \nassociated with follicular reserve. The younger the patient is at menarche, the higher the risk \nof having low AMH levels. This can be caused by several factors, such as the amount of \novarian follicular reserve, the rate of follicular depletion, or a combination of both [25]. \nThis study also found no significant difference between parity and AMH levels. Moini found \nthat women with higher parity had higher AMH levels compared to nulliparous women [26]. \nDifferent results were also found in a study of Filipino women, primiparous and multiparous \nsamples had significantly lower AMH levels than nulliparous [27]. \nIn this study, there was no effect of BMI on AMH levels. This differs from Albu's study, which \nreported a positive relationship between BMI and serum AMH levels in infertile patients. The \npresence of overweight and obesity is associated with higher AMH levels compared to \npatients with normal or lean BMI. Circulating androgens, insulin, and insulin resistance \nincrease with BMI. These parameters have also been shown to be positively associated with \nserum AMH levels [28]. However, some other studies found that AMH levels are negatively \ncorrelated in patients with older age (>35 years) or severe obesity (BMI ≥ 40 kg/m²) \n[29,30].In addition, several previous studies have also found no relationship between BMI \nand AMH levels [31–33]. \nThere was no significant difference between tumor size and unilateral/bilateral tumor location \nin this study. This is consistent with a study conducted at Hasan Sadikin Hospital, which \nfound a weak correlation between AMH levels and ovarian endometrioma volume but was \nnot statistically significant (r = -0.332, p = 0.066). However, the group with endometriosis \nexhibited lower AMH levels compared to the non-endometriosis control group [10]. Another \nstudy also found that patients with endometriomas had lower AMH levels compared to \npatients with other benign ovarian cysts, especially in the 30-39 age group (3.77 ± 2.28 vs \n6.58 ± 2.63, p < 0.05). This study also categorized endometriomas into four groups: single \nunilateral, single bilateral, multiple unilateral, and multiple bilateral. However, there was no \nsignificant difference in AMH levels among the four groups (p = 0.173). Total cyst diameter \n\nManuscript accepted for publication\n5 \n \nand the number of cysts were found to be negatively correlated with AMH, although the \ncorrelation was not significant, which is consistent with the findings of this study[34]. The \nstudy of Niewegloska et al. demonstrated that only bilateral tumor (p=0.003) and patient age \n(p < 0.001) were significant factors. However, cyst volume was found to have a negative \ncorrelation with AMH serum concentration, although it was not significant [35]. \nSerum AMH levels in women with endometriomas tend to be low due to chronic \ninflammatory processes and massive reactive oxygen species (ROS) found in the ovaries. \nToxic factors, such as proteolytic enzymes, iron, and ROS can penetrate the tissue around \nendometrioma cysts, causing fibrosis, smooth muscle metaplasia, and reduced follicles in \novarian tissue [36]. The mechanisms underlying low serum AMH levels and decreased \novarian reserve are inflammatory processes and immunomodulation abnormalities \nassociated with toxic endometriomas [37,38]. The inflammatory process causes follicular \ndamage and dysfunction so that follicular quality and quantity are also reduced [10].  As in \nprevious studies, AMH levels are not affected by endometrioma size, but AMH levels can \ndescribe the severity/degree of endometrioma in patients and the extent to which \nendometriomas cause damage and inflammation [39]. \nLimitation \nThe cross-sectional nature of this study was a limitation. This study also used tumor area as \na measure of tumor size insteasd of volume as a benchmark for tumor size. Tumor size was \nmeasured using abdominal ultrasound, which has lower accuracy compared to transvaginal \nultrasound. However, the study can be used as a reference in health facilities, especially in \ndeveloping countries that do not have transvaginal ultrasound modalities. \n \nConclusion \nBased on the study, it was found that there is no association between anti-Mullerian \nhormone levels and the size and bilaterality of ovarian endometriomas. This finding indicates \nthat transabdominal ultrasound cannot predict ovarian reserve accurately. Therefore, it is \nrecommended to consider using transvaginal ultrasound or other biomarkers like AMH and \nFSH. Further research with a larger sample size to confirm it. \n \nCOMPLIANCE WITH ETHICAL STANDARDS \nAuthors contribution \nA.M.D.R: Conceptualization, data curation, investigation, formal analysis, validation, \nvisualization. N.A.: Data curation, supervision. E.H.:Data curation, supervision. F.H.: formal \nanalysis,supervision. S.S.: Writing – review & editing. F.M: Writing – review & editing. \n \nFunding: The authors declared that this study received no financial support. \nStudy registration : N/A. \nDisclosure of Interest : None of the authors have any conflict of interests  related to this \nwork. \nEthical approval: This study was approved by the Ethics Committee of Hasanuddin \nUniversity of Medical Sciences (No.20/UN4.6.4.5.31/PP36/2023, date: 9.1.2023). \n\nManuscript accepted for publication\n6 \n \nInformed Consent: Informed consent was obtained from all participants.  \nData sharing: The data that support the findings of this study are available from the \ncorresponding author upon reasonable request. \n \nReferences \n1.  Chaggar P, Tellum T, Thanatsis N, De Braud L V., Setty T, Jurkovic D. Prevalence of \ndeep and ovarian endometriosis in women attending a general gynecology clinic: \nprospective cohort study. Ultrasound Obstet Gynecol. 2023;61(5):632–41. doi: \n10.1002/uog.26175 PMID: 36776112 \n2.  Gordts S, Koninckx P, Brosens I. Pathogenesis of deep endometriosis. Fertil Steril. \n2017;108(6):872-885.e1. doi: 10.1016/j.fertnstert.2017.08.036 PMID: 29100623 \n3.  Gałczyński K, Jóźwik M, Lewkowicz D, Semczuk-Sikora A, Semczuk A. Ovarian \nendometrioma - A possible finding in adolescent girls and young women: A mini-review. J \nOvarian Res. 2019;12(1):4–11. doi: 10.1186/s13048-019-0582-5 PMID: 31699129 \n4.  Vannuccini S, La Torre F, Gallucci E, Toscano F, Ruotolo A, Capezzuoli T, et al. \nPrevious surgery for endometriosis: a further risk for obstetric complications? Ital J Gynaecol \nObstet. 2023 Jan;35(Supplement 01):81. doi: 10.36129/jog.2022.S80 \n5.  Karadağ C, Yoldemir T, Demircan Karadağ S, Turgut A. The effects of endometrioma \nsize and bilaterality on ovarian reserve. J Obstet Gynaecol. 2020;40(4):531–6. doi: \n10.1080/01443615.2019.1633518 PMID: 31460808 \n6.  Lehmann P, Vélez MP, Saumet J, Lapensée L, Jamal W, Bissonnette F, et al. Anti-\nMüllerian hormone (AMH): A reliable biomarker of oocyte quality in IVF. J Assist Reprod \nGenet. 2014;31(4):493–8. doi: 10.1007/s10815-014-0193-4 PMID: 24573377 \n7.  Dumont A, Robin G, Catteau-Jonard S, Dewailly D. Role of Anti-Müllerian Hormone in \npathophysiology, diagnosis and treatment of Polycystic Ovary Syndrome: A review. Reprod \nBiol Endocrinol. 2015;13(1):8–10. doi: 10.1186/s12958-015-0134-9 PMID: 26691645 \n8.  Dewailly D, Laven J. AMH as the primary marker for fertility. Eur J Endocrinol. 2019 \nDec;181(6):D45–51. doi: 10.1530/EJE-19-0373 \n9.  Muzii L, Di Tucci C, Di Feliciantonio M, Galati G, Di Donato V, Musella A, et al. \nAntimüllerian hormone is reduced in the presence of ovarian endometriomas: a systematic \nreview and meta-analysis. Fertil Steril. 2018;110(5):932-940.e1. doi: \n10.1016/j.fertnstert.2018.06.025 PMID: 30316440 \n10.  Suardi D, Permadi W, Djuwantono T, Hidayat YM, Bayuaji H, Gautama GPE. \nCorrelation of serum anti-mullerian hormone (AMH) level on ovarian volume in women with \nendometrioma. Int J Gen Med. 2021;14:1–8. doi: 10.2147/IJGM.S272071 \n11.  Marcellin L, Santulli P , Bourdon M, Comte C, Maignien C, Just PA, et al. Serum \nantimüllerian hormone concentration increases with ovarian endometrioma size. Fertil Steril. \n2019;111(5):944-952.e1. doi: 10.1016/j.fertnstert.2019.01.013 PMID: 30878253 \n12.  Younis JS, Shapso N, Fleming R, Ben-Shlomo I, Izhaki I. Impact of unilateral versus \nbilateral ovarian endometriotic cystectomy on ovarian reserve: A systematic review and \nmeta-analysis. Hum Reprod Update. 2019;25(3):375–91. doi: 10.1093/humupd/dmy049 \nPMID: 30715359 \n\nManuscript accepted for publication\n7 \n \n13.  Bacanakgil BH, İlhan G, Ohanoğlu K. Effects of vitamin D supplementation on \novarian reserve markers in infertile women with diminished ovarian reserve. Medicine \n(Baltimore). 2022 Feb 11;101(6):e28796. doi: 10.1097/MD.0000000000028796 \n14.  Nelson SM, Ewing BJ, Gromski PS, Briggs SF. Contraceptive-specific antimüllerian \nhormone values in reproductive-age women: a population study of 42,684 women. Fertil \nSteril. 2023 Jun;119(6):1069–77. doi: 10.1016/j.fertnstert.2023.02.019 \n15.  Iwase A, Asada Y , Sugishita Y , Osuka S, Kitajima M, Kawamura K. Anti-Müllerian \nhormone for screening, diagnosis, evaluation, and prediction: A systematic review and expert \nopinions. J Obstet Gynaecol Res. 2023;(October 2023):15–39. doi: 10.1111/jog.15818 \n16.  Romanski PA, Bortoletto P, Malmsten JE, Tan KS, Spandorfer SD. Pregnancy \noutcomes after oral and injectable ovulation induction in women with infertility with a low \nantimüllerian hormone level compared with those with a normal antimüllerian hormone level. \nFertil Steril. 2022;118(6):1048–56. doi: 10.1016/j.fertnstert.2022.09.010 PMID: 36379757 \n17.  Vicomandi V, Nacci I, Piccione E, Casadei L. Anti-Müllerian hormone: clinical \nimplications in Gynecological Endocrinology. An update review. Ital J Gynaecol Obstet. 2020 \nJan;32(01):20. doi: 10.36129/jog.32.01.02 \n18.  Tan Z, Gong X, Wang CC, Zhang T, Huang J. Diminished Ovarian Reserve in \nEndometriosis: Insights from In Vitro, In Vivo, and Human Studies—A Systematic Review. Int \nJ Mol Sci. 2023 Nov 4;24(21):15967. doi: 10.3390/ijms242115967 \n19.  Van Disseldorp J, Lambalk CB, Kwee J, Looman CWN, Eijkemans MJC, Fauser BC, \net al. Comparison of inter- and intra-cycle variability of anti-Mullerian hormone and antral \nfollicle counts. Hum Reprod. 2010 Jan 1;25(1):221–7. doi: 10.1093/humrep/dep366 \n20.  Kozlowski IF, Carneiro MC, da Rosa VB, Schuffner A. Correlation between anti-\nMüllerian hormone, age, and number of oocytes: A retrospective study in a Brazilian in vitro \nfertilization center. J Bras Reprod Assist. 2022;26(2):214–21. doi: 10.5935/1518-\n0557.20210083 PMID: 34812600 \n21.  Khan HL, Bhatti S, Suhail S, Gul R, Awais A, Hamayun H, et al. Antral follicle count \n(AFC) and serum anti-Müllerian hormone (AMH) are the predictors of natural fecundability \nhave similar trends irrespective of fertility status and menstrual characteristics among fertile \nand infertile women below the age of 40 years. Reprod Biol Endocrinol. 2019;17(1):1–12. \ndoi: 10.1186/s12958-019-0464-0 PMID: 30744650 \n22.  Feferkorn I, Suarthana E, Kigloo HN, Abow-Mohamed I, Golyari Y , Tulandi T. \nCombined effects of age and endometriosis on ovarian reserve in women with infertility. Int J \nGynecol Obstet. 2023;161(1):129–36. doi: 10.1002/ijgo.14519 PMID: 36263878 \n23.  Lie Fong S, Visser JA, Welt CK, De Rijke YB, Eijkemans MJC, Broekmans FJ, et al. \nSerum anti-müllerian hormone levels in healthy females: A nomogram ranging from infancy \nto adulthood. J Clin Endocrinol Metab. 2012;97(12):4650–5. doi: 10.1210/jc.2012-1440 \nPMID: 22993032 \n24.  Shebl O, Ebner T, Sir A, Schreier-Lechner E, Mayer RB, Tews G, et al. Age-related \ndistribution of basal serum AMH level in women of reproductive age and a presumably \nhealthy cohort. Fertil Steril. 2011;95(2):832–4. doi: 10.1016/j.fertnstert.2010.09.012 PMID: \n20970126 \n\nManuscript accepted for publication\n8 \n \n25.  Weghofer A, Kim A, Barad DH, Gleicher N. Age at menarche: A predictor of \ndiminished ovarian function? Fertil Steril. 2013;100(4):1039–43. doi: \n10.1016/j.fertnstert.2013.05.042 PMID: 23809497 \n26.  Moini A, Hedayatshodeh M, Hosseini R, Rastad H. Association between parity and \novarian reserve in reproductive age women. Eur J Obstet Gynecol Reprod Biol. \n2016;207:184–7. doi: 10.1016/j.ejogrb.2016.10.024 PMID: 27865943 \n27.  Bragg JM, Kuzawa CW, Agustin SS, Banerjee MN, McDade TW. Age at menarche \nand parity are independently associated with Anti-Müllerian hormone, a marker of ovarian \nreserve, in filipino young adult women. Am J Hum Biol. 2012;24(6):739–45. doi: \n10.1002/ajhb.22309 PMID: 22915230 \n28.  Albu D, Albu A. The relationship between anti-Müllerian hormone serum level and \nbody mass index in a large cohort of infertile patients. Endocrine. 2019;63(1):157–63. doi: \n10.1007/s12020-018-1756-4 PMID: 30238328 \n29.  Buyuk E, Seifer DB, Illions E, Grazi R V., Lieman H. Elevated body mass index is \nassociated with lower serum anti-mullerian hormone levels in infertile women with \ndiminished ovarian reserve but not with normal ovarian reserve. Fertil Steril. \n2011;95(7):2364–8. doi: 10.1016/j.fertnstert.2011.03.081 PMID: 21529798 \n30.  Bernardi. LA, Mercedes R. Carnethon, Chavez PJ de, Ikhena DE, Neff LM, Baird DD, \net al. Relationship between obesity and anti-Müllerian hormone in reproductive-aged African \nAmerican women. Obes Silver Spring Md. 2017;25(1):229–35. doi: doi:10.1002/oby.21681 \n31.  Jung S, Allen N, Arslan AA, Baglietto L, Brinton LA, Egleston BL, et al. Demographic, \nlifestyle, and other factors in relation to antimüllerian hormone levels in mostly late \npremenopausal women. Fertil Steril. 2017;107(4). doi: 10.1016/j.fertnstert.2017.02.105 \n32.  La Marca A, Spada E, Grisendi V, Argento C, Papaleo E, Milani S, et al. Normal \nserum anti-Müllerian hormone levels in the general female population and the relationship \nwith reproductive history. Eur J Obstet Gynecol Reprod Biol. 2012;163(2). doi: \n10.1016/j.ejogrb.2012.04.013 \n33.  Simões-Pereira J, Nunes J, Aguiar A, Sousa S, Rodrigues C, Sampaio Matias J, et \nal. Influence of body mass index in anti-Müllerian hormone levels in 951 non-polycystic \novarian syndrome women followed at a reproductive medicine unit. Endocrine. 2018;61(1). \ndoi: 10.1007/s12020-018-1555-y \n34.  Jeon JH, Park SY , Lee SR, Jeong K, Chung HW. Serum Anti-Müllerian Hormone \nLevels before Surgery in Patients with Ovarian Endometriomas Compared to Other Benign \nOvarian Cysts. J Menopausal Med. 2015;21(3):142. doi: 10.6118/jmm.2015.21.3.142 \n35.  Nieweglowska D, Hajdyla-Banas I, Pitynski K, Banas T, Grabowska O, Juszczyk G, \net al. Age-related trends in anti-Mullerian hormone serum level in women with unilateral and \nbilateral ovarian endometriomas prior to surgery. Reprod Biol Endocrinol. 2015;13(1):1–9. \ndoi: 10.1186/s12958-015-0125-x PMID: 26596960 \n36.  Sanchez AM, Viganò P, Somigliana E, Panina-Bordignon P , Vercellini P, Candiani M. \nThe distinguishing cellular and molecular features of the endometriotic ovarian cyst: from \npathophysiology to the potential endometrioma-mediated damage to the ovary. Hum Reprod \nUpdate. 2014 Mar 1;20(2):217–30. doi: 10.1093/humupd/dmt053 \n\nManuscript accepted for publication\n9 \n \n37.  Carrillo L, Seidman DS, Cittadini E, Meirow D. The role of fertility preservation in \npatients with endometriosis. J Assist Reprod Genet. 2016 Mar;33(3):317–23. doi: \n10.1007/s10815-016-0646-z \n38.  Romanski PA, Brady PC, Farland LV, Thomas AM, Hornstein MD. The effect of \nendometriosis on the antimüllerian hormone level in the infertile population. J Assist Reprod \nGenet. 2019 Jun;36(6):1179–84. doi: 10.1007/s10815-019-01450-9 \n39.  Safdarian L, Ghalandarpoor Attar SN, Aleyasin A, Aghahosseini M, Sarfjoo FS, \nHosseinimousa S. Investigation of anti-mullerian hormone (AMH) level and ovarian response \nin infertile women with endometriosis in IVF cycles. Int J Reprod Biomed. 2018 \nNov;16(11):719–22. PMID: 30775688 \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\nManuscript accepted for publication\n10 \n \nTable 1. Demographic data of participant \n \nAMH level P \nValue Low ( n= 16) Normal ( n= 34) \nAge ( Mean±SD; years) 33.81±4.02 31.64±5.8 0.186# \nMenarch age(Median±IQR; years) 12(±11) 12(±0.25) 0.614+ \nEducation [n (%)]   \n    Senior High School 13 (26.0) 27 (54.0) \n1.0* \n    Diploma 3 (6.0) 7 (14.0) \nParity [n (%)]    \nNulipara 6 (12.0) 21 (42.0) \n0.132* Primipara 3 (6.0) 7 (14.0) \nMultipara 7 (14.0) 6 (12.0) \nBilaterality [n (%)]    \nUnilateral 12 (24.0) 22 (44.0) \n0.687* \nBilateral 4 (8.0) 12 (24.0) \nBody Mass Index [n (%)]    \nNormal 14 (28.0) 23 (46.0) \n0.251* \nOverweight 2 (4.0) 11 (22.0) \nTable 2 Correlation test of variables to AMH levels \nVariable Rho value P-value \nAge \nMenarch age \nEndometrioma size  \n-0.248 \n0.067 \n-0.276 \n0.082 \n0.643 \n0.052 \n*Spearman Correlation \n \n\n11 \n \n \nManuscript accepted for publication","source_license":"CC0","license_restricted":false}