{"paper_id":"7ab9d632-86a9-4288-8f93-bf02f8fe751c","body_text":"Kulvinder Kochar Kaur1*, Gautam Allahbadia1 and Mandeep Singh2\n1Scientific Director, India\n2Consultant Neurologist, India\n*Corresponding author:  Kulvinder Kochar Kaur, Scientific Director, India\nSubmission: \n  December 26, 2018; Published: \n  January 09, 2019\nDissecting the Reduced Ovarian Reserve Seen with \nOvarian Enometriomas with That Caused by  \nSurgical Excision of Ovarian Enometriomas- \nWhat Comes First\nOpinion\nThere have been concerns raised regarding the possibility \nof surgical excision of the endometrioma causing damage to \nthe ovarian reserve. Three recent systematic reviews reported \na decrease in serum anti mullerian hormone (AMH) levels as \ncompared to preoperative levels after endometrioma excision [1-\n3]. But very recently Muzli et al. [4], gave a meta-analysis on the \nperipheral levels of AMH in women having ovarian endometriomas. \nIn contrast to earlier met-analyses they reported lower levels \nof AMH as compared to controls and in women having any other \novarian cysts which suggests that what is reported following \nsurgery, the damage to the ovarian reserve ,may at least in part \nbe present before any intervention. Although these results might \nanswer a lot of unresolved questions, they need to be interpreted \nusing some caution.\nThis study by Muzli et al. [4] shows that there is a lower serum \nAMH in women having endometriomas. But they do not show that \novarian reserve is injured in women having endometriomas. Thus, \none might hypothesize that the presence of these endometriomas \nmay not directly damage the ovarian reserve but might disturb \nthe physiology of the ovary which =>temporary derangement \nof the complex and yet unknown mechanisms that regulate \nAMH production. Further one needs to consider the importance \nof changes in local vascularization that is induced by large \nendometriomas. It may be that AMH is normally produced in the \novaries carrying these endometriomas but may have difficulties \nin reaching the peripheral circulation. Since AMH is a paracrine \nfactor and not a typical hormone, hence if there are any impaired \nsecretion processes of AMH they do not get compensated by \nfeedback mechanisms, like other hormones. Hence till date there \nis not enough evidence to say that the decreased serum AMH in \nwomen carrying endometriomas actually portray any definitive \ndamage to the ovarian reserve but only a temporary and potentially \nreversible interruption of ovarian physiology. As highlighted by  \n \nMuzli et al. [4] role of timing is important i.e. the comparison of \nage of endometriomas on the effect on levels of serum AMH, \nalthough they could not resolve this problem. Clinically doing \nthis will support causality, but unfortunately the possible role \nof time related damage induced by endometriomas has not got \nmuch attention and when done occasionally contrasting data has \nbeen published by Benaglia et al. [5] & Kasapoglu et al. [6] in a \nvery recent study [5,6]. Another important aspect of this study by \nMuezli et al. [4] is the size of endometriomas considered. In their \nmeta-analysis the mean diameter of endometriomas considered \nis large [which exceeds 5cm in the majority]. As said by Muzli et \nal. [4] this has not got enough attention earlier, but might play a \nsignificant role. It is important to understand that how volumes \nvary with the increasing size of endometriomas, e.g. once size is \n6cm then volume of endometriomas is 27-fold greater to that in \ncomparison of volume of endometriomas of 2cm (about 113ml \nand 4ml respectively). Also, importantly these cysts develop within \nan organ namely ovary whose basal volume is 4ml. Hence this \nmight explain the differences seen in metanalyses by Muzli [4] and \nHumaidan in previous evidence obtained in in vitro fertilization \nshowing minimum impact by ovarian endometriomas. Most studies \nfocused on ovarian endometriomas of 2cm in IVF studies. In a rare \nstudy where large ovarian endometriomas >5cm were considered, \na decreased responsiveness was seen in the affected ovaries by \nFerrero et al. [7]. \n Still there are lacunae in Muzli et al. [4]. There are \nmethodological errors which doesn’t allow one to believe the \nestimation of magnitude of this reduction of AMH seen with ovarian \nendometriomas. High heterogeneity of the meta-analysis used, use \nof parametric statistics as serum AMH gets positively skewed, along \nwith unilaterality of the lesion are not all helpful in being able to \nreliably conclude that this effect on AMH is being caused by ovarian \nendometriomas per sec. One needs to disentangle the effect ovarian \nendometriomas vis a vis that of surgery on reduced ovarian reserve.\nOpinion \nSurgical Medicine Open \nAccess JournalC CRIMSON PUBLISHERS\nWings to the Research\n1/2Copyright © All rights are reserved by Kulvinder Kochar Kaur.\nVolume 2 - Issue - 3\nISSN 2578-0379\n\nSurg Med Open Acc J\n          \n  Copyright ©  Kulvinder Kochar Kaur\n2/2How to cite this article: Kulvinder K K, Gautam A, Mandeep S. Dissecting the Reduced Ovarian Reserve Seen with Ovarian Enometriomas with That Caused \nby Surgical Excision of Ovarian Enometriomas-What Comes First. Surg Med Open Acc J. 2(3). SMOAJ.000536.2019. DOI: 10.31031/SMOAJ.2019.02.000536\nVolume 2 - Issue - 3\nConclusion\nIn conclusion although this study by Muzli et al. [4] tries to move \nfurther by showing that probably ovarian endometriomas might be \nthe culprits in reducing ovarian reserve directly, but one should \nnot jump to the conclusions that surgery per se does not have a \ndetrimental effect. There is a need to keep working on to dissect the \nroles of each and the relationship of ovarian endometriomas, surgery \nand ovarian reserve. Further the role of time on deterioration of \nAMH with coexisting ovarian endometriomas and whether the \neffect of reduced ovarian reserve is permanent or temporary with \neither ovarian endometriomas itself or surgery per se and other \nfactors associated with surgery with ovarian endometriomas like \ninvolvement of mesosalpinx in this reduction [8], and how one can \nprevent the decreased in ovarian reserve either by conservative \nmethods or preventing surgery induced reduction in ovarian \nreserve.\nReferences \n1. Raffi F, Metwally M, Amer S (2012) The impact of excision of ovarian \nendometrioma on ovarian reserve: A systematic review and meta-\nanalyses. J Clin Endocrol Metab 97(9): 3146-3154.\n2. Somigliana E, Berlanda N, Benaglia L, Vigano P , Vercellani P , et al. (2012) \nSurgical excision of endometriomas and ovarian reserve. A systematic \nreview on serum anti mullerian hormone level modifications. Fertil \nSteril 98(6): 1531-1538.\n3. Hamdan M, Dunselman G, Li TC, Cheng Y (2015) The impact of \nendometrioma on IVF/ICSI outcomes: A systematic review and meta-\nanalyses. Hum Reprod Update 21(6): 809-825.\n4. Muzli L, Di Tucci C, Di Feliciantonio M, Galali G, Di Donato V, et al. \n(2018) Antimullerian hormone is reduced in the presence of ovarian \nendometriomas: A systematic review and meta-analyses. Fertil Steril \n110(5): 932-940.\n5. Benaglia L, Castiglioni M, Paffoni A, Sarais V, Vercellini P , et al. (2017) \nIs endometrioma-associated damage to ovarian reserve progressive? \nInsights from IVF cycles. Eur J Obstet Gynecol Reprod Biol 217: 101-105.\n6. Kasapoglu I, Ata B, Uyanklar O, Seyhan A, Orhan A, et al. (2018) \nEndometrioma-related reduction in ovarian reserve (ERROR): A \nprogressive longitudinal study. Fertil Steril 110(1): 122-127.\n7. Ferrrero S, Scala C, Tafi E, Racca A, Venturini PL, et al. (2017) Impact \nof large ovarian endometriomas on the response to superovulation for \nin vitro fertilization: A retrospective study. Eur J Obstet Gynecol Reprod \nBiol 213: 17-21.\n8. Saito A, Iwase A, Nakamura T , Osuka S, Murase T , et al. (2016) Involvement \nof mesosalpinx in endometrioma is a possible risk factor for decrease of \novarian reserve after cystectomy: A retrospective cohort study. 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