{"paper_id":"140432b9-4487-4ed4-a92c-8c9510883d75","body_text":"Volume 1- Issue 6 : 2017 \n1647\n             Case Report                                                                                                                                   Open Access \nIdentical Ovarian and Deep Pelvic Endometriosis with \nColorectal Involvement in Monozygotic Twins: A Case \nReport and Review of the Literature\nAdel Shervin*1,Fariba Behnia-Willison2 and Joseph Miller3\n1FBW Gynaecology Plus, Flinders University Adelaide, Australia\n2Department of Obstetrics, Gynecology and MIS, Farmanieh Hospital, Tehran, Iran \n3Department of Obstetrics, Gynecology and Minimally invasive surgery (MIS), Farmanieh Hospital, Tehran, Iran\nReceived: October 30, 2017;  Published: November 08, 2017\n*Corresponding author: Adel Shervin, FBW Gynaecology Plus, Flinders University Adelaide, Australia; Email: \n ISSN: 2574-1241\nDOI: 10.26717/BJSTR.2017.01.000505\nJoseph Miller. Biomed J Sci & Tech Res\nIntroduction \nEndometriosis is a polygenic multi factorial disease. Incidence \nof deep infiltrating endometriosis (DIE) involving the GI tract is \nestimated at 8-12% [1,2] and commonly involves the rectosigmoid \ncolon. Endometriosis is one of the most common benign gynecologic \ndiseases. It causes pelvic pain and sub fertility, and is characterised \nby the presence of ectopic endometrial tissue outside the uterus \n[3]. Endometriosis is under-diagnosed and associated with a \nmean latency of 6.7 years from onset of symptoms to definitive \ndiagnosis [4]. Most estimates of prevalence are made on the basis \nof surgical cases or small samples, and are highly selective, ranging \nbetween 5% and 10% in women of reproductive age, and up to \n50% among infertile women [5-7]. Endometriosis has an important \nsocio-economic impact, because it greatly lowers quality of life \nfor a significant portion of the population, and is responsible for \nsubstantial health expenditure, diagnosis, treatment, and loss of \neconomic performance. The cost of endometriosis to the US health \ncare system was $69.4 billion in 2009 [8]. Despite 150 years of \nhypothesis-driven research, the cause of endometriosis remains \nuncertain. Therapeutic options are therefore limited, often lacking  \n \nunanimous consensus. However, there is mounting evidence \nthat endometriosis is a complex multifactorial disease, with both \ngenetic and environmental components contributing to disease \nsusceptibility [7]. In 1980, Simpson et al. published the first formal \ngenetic study of endometriosis [9]. Studying 123 probands with \nhistologically proven endometriosis, they found that 5.9% of female \nsiblings over the age of 18 years had endometriosis; the mothers \nwere affected in 8.1% of cases. \nHowever, only 1% of the patients’ husband’s first-degree \nrelatives (controls) had the disease. Women with an affected sibling \nor parent were more likely to have a severe form of endometriosis \n[10]. Severe endometriosis was present in 61% of probands who \nhad an affected first-degree relative, whereas it was only present \nin 23% of the affected probands with no affected first-degree \nrelatives. One recent meta-analysis combining results from a \ngenome-wide association study and replication studies showed \nthat of the nine loci found to be associated with endometriosis \nin at least one of the studies, six remained statistically significant \ngenome-wide, and two showed borderline statistically significant \nCite this article: Adel S, Fariba B W, Joseph M. Identical Ovarian and Deep Pelvic Endometriosis with Colorectal Involvement in Monozygotic    \n   Twins: A Case Report and Review of the Literature. Biomed J Sci  & Tech Res 1(6)-  2017.  BJSTR. MS.ID.000505.\n   DOI : 10.26717/BJSTR.2017.01.000505\nAbstract\nEndometriosis is a common benign gynecologic disease characterised by the presence of ectopic endometrial tissue outside the uterus. We \npresent a brief review on the genetic factors underlying endometriosis, followed by a case report on concordant anatomical distribution of deep \ninfiltrating endometriosis (DIE) in a pair of monozygotic (MZ) twins. To our knowledge, this is one of the first reported cases of DIE in MZ twins. \nThe remarkable concordance and resemblance of deep disease involving the same anatomical sites, ovaries, pelvic floor and rectosigmoid colon \nin our MZ twins reiterates the role and impact of genetic factors in the pathogenesis of endometriosis.\nKeywords: Deep Infiltrating Endometriosis; Sigmoid Resection; Monozygotic Twins; Genetics\nAbbreviations: MZ: Mono Zygotic; DZ: Di Zygotic; DIE : Deep Infiltrating Endometriosis; IVP: Intravenous Pyelogram; TVS: Transvaginal \nUltrasound; RES: Rectal Endoscopic Sonography; SMM: Smooth Muscle Metaplasia\n\nSubmission Link: http://biomedres.us/submit-manuscript.php\nJoseph Miller. Biomed J Sci & Tech Res Volume 1- Issue 6 : 2017 1648\ngenome-wide association with moderate/severe disease [11]. In an \nAustralian twin-based study, a twofold increase in endometriosis \nrisk in monozygotic (MZ) compared with dizygotic (DZ) twin pairs \nwas reported [7], which suggests that the genetic component \ncontributing to phenotypic variability in endometriosis is about \n52%. These data imply that endometriosis is a complex genetic \ntrait, and indicate that a number of genes interact with each other \nto form disease susceptibility, with the phenotype emerging in \nthe presence of environmental risk factors which in themselves \naccount for 53% of disease liability. Environmental chemicals, as \nwell as food, have been discussed as possible contributing factors \n[12-14]. However, there is no existing evidence as to the nature of \nthis environmental contribution. Only one study to date has used \nquantitative analysis to examine the contribution of genetic and \nenvironmental factors to endometriosis, using a small twin sample \n[7]. A larger twin sample is expected to provide further clarification \non the role of genetic and environmental factors [12-14]. In this \nreport, we present a case of deep infiltrating endometriosis (DIE) \nin a pair of monozygotic (MZ) twins.\nMaterials and Methods\nA pair of monozygotic twins was referred to our office within the \nsame year, mainly due to severe chronic pelvic pain and infertility, \nwith the following pertinent clinical information.\na) Twin A : A 31-year-old nulliparous woman was admitted \nto Farmanieh Hospital (Tehran, Iran) complaining of heavy \nmenstrual blood loss, progressive chronic severe pelvic pain \nand dyspareunia for the past six years, painful defecation with \npassage of narrow, occasionally blood-tinged stool, and history \nof failed hormonal medical treatment on and off during the past \nsix years. The patient had been infertile for the past two years. \nShe had a history of hypothyroidism, thalassemia minor, cervical \nspinal cord tumour surgery, rhinoplasty and eye surgery. \nTransvaginal ultrasound detected a 25 x 22mm cyst in the right \novary and two heterogeneous hypoechoic foci (32 x 21mm and \n29 x 18mm respectively) in the left ovary; these observations \nwere compatible with endometrioma. Colonoscopy results \nwere negative. Hemoglobin level was 11.4g/dL, serum CA 125 \nlevel was 60.67U/mL, serum CA 19-9 level was 6.4 U/mL, and \nAMH level was 5.7ng/mL. Intravenous pyelogram (IVP) results \nwere negative.Magnetic Resonance Imaging (MRI) revealed \ntwo T1 foci in both ovaries (25 x 15mm and 20 x 10mm high \nrespectively), which was suggestive of a hemorrhagic cyst or, \nmore probably, a dermoid cyst. No other pathology was noted, \nincluding for the intestinal tract.\nb) Twin B: A 31-year-old nulliparous woman was \nadmitted to Farmanieh Hospital (Tehran, Iran) complaining \nof menorrhagia, progressive severe pelvic pain with rectal \nradiation for six years, painful defecation with occasional \nblood-tinged stool, severe dyspareunia for the past two years \nand failed hormonal medical treatment for the past six years. \nShe had a history of hypothyroidism, thalassemia minor, mitral \nvalve prolapse rhinoplasty and eye surgery. Two transvaginal \npelvic ultrasounds revealed a small anterior wall myoma; \nthere were no other findings. Hemoglobin level was 10.8g/dL, \nserum CA 125 level was 21U/mL, serum CA 19-9 level was 9.4 \nU/mL, and AMG level was 7.4ng/mL. IVP results were within \nnormal limits. MRI of the pelvis detected three small myomas \n(10-15mm) at the anterior uterine wall and a 20 mm follicle \nin the left ovary. There were no other findings, including for \nthe bowel. Colonoscopy results were within normal limits. A \ndouble-contrast barium enema detected segmental luminal \nnarrowing with upward displacement of the sigmoid area, with \nmucosal thinning. These findings suggested extrinsic pressure, \nmostly due to endometriosis, which seemed to have involved \nthe posterior wall of the sigmoid colon.\nResults\nTwin A\nA laparoscopic segmental sigmoid resection was performed, \nwith staple re-anastomosis, resection of pelvic floor DIE, and \nresection of a bilateral endometrioma. The procedure took 152 \nminutes. The patient was discharged after four days shown in \nbelow Figure 1.\nFigure 1: Laparoscopic images for Twin A. \n(A) Anterior uterine myoma,\n (B) Attached left adnexa to stenotic RS colon,\n(C) Left adnexal colonic adhesion,\n(D) Left ovarian endometrioma, \n(E) Right ovarian endometrioma, \n(F) Segmental resection of RS colon,\n(G) Resected bowel with deep endometriosis, \n(H) DIE pelvic floor,and \n(I) DIE at peritoneal site of invagination.\nTwin B \nTwin B’s initial procedure was performed in the same \nmonth as Twin A’s procedure. Laparoscopic adhesiolysis was \nperformed, with resection of pelvic floor DIE, resection of ovarian \nendometrioma, and shaving of rectal deep endometriosis. Bowel \nresection was deferred because of inadequate bowel preparation, \nand laparoscopic sigmoid resection with staple anastomosis was \nperformed 8 weeks after the initial procedure (Figure 2).\nDiscussion\nAnatomical involvement of the relevant pelvic organ in \nthis pair of identical twins was nearly identical. The twins had \ngrown up in the same environment all their lives, both worked as \nsecretaries at the same institution, and both were experiencing \n\nSubmission Link: http://biomedres.us/submit-manuscript.php\nJoseph Miller. Biomed J Sci & Tech Res \nVolume 1- Issue 6 : 2017 \n1649\nnot only the symptoms of DIE, but also signs and symptoms of \nintestinal involvement. The ultrasound and MRI for both patients \nwas reported negative, which clearly indicates the importance of \nexperienced radiologists for the detection of deep endometriosis \n[15], and reiterates the importance of bimanual exam by clinicians, \nparticularly at the time of menstruation, to achieve an accurate \ndiagnosis,. In fact, available data clearly indicates that the accuracy \nof good physical examination (PE) is not much different from that \nof transvaginal ultrasound (TVS), rectal endoscopic sonography \n(RES) and MRI, all within the 80% range [16]. Twin A was managed \nby laparoscopic segmental sigmoid resection and staple re-\nanastomosis, along with global resection of DIE from the pelvic floor \nand endometriomas. We were intending to do the same for Twin B, \nbut in OR the lack of adequate bowel preparation was noted; thus \nbowel resection was postponed and was performed 8 weeks later \nunder adequate bowel preparation. \nFigure 2: Laparoscopic images for Twin B. \n(A) Myoma at anterior uterine wall, \n(B) Left ovarian endometrioma severely attached to \nsigmoid colon,\n(C) Ovarian attachment to sigmoid colon, \n(D) Left ovarian endometriosis, \n(E) Right ovarian endometriosis, \n(F) Shaving DIE off rectal surface, \n(G) Defect at rectal surface, \n(H) DIE pelvic floor with rectal involvement, \n(I) DIE peritoneal site on invagination, right side, \n(J) Segmental resection of RS colon,\n(K) Resected bowel with undivided DIE nodule and \n(L) Resected bowel with divided DIE nodule. \nHowever, after resection of endometriomas and pelvic floor \ndeep lesions, larger DIE at the posterior cervix with extension to \nthe rectum was managed by laparoscopic shaving, and the defect \nwas closed in two layers. No intraoperative or postoperative \ncomplications were encountered in either twin. In many instances, \nthe culprit for DIE is endometrioma, which starts from its peritoneal \nsite of invagination (Figure 3). By extension medially, it involves \nthe parametrium, rectum, recto-vaginal space, and, by deeper \nextension, the ureter and hypogastric nerve may also be involved. \nThus, timely and proper surgical management of endometrioma \nand excision of its dependent peritoneal site could serve not only to \nmanage patients’ pain, but also to conceivably prevent a significant \npercentage of DIE. In one study focusing exclusively on patients with \nrectosigmoid lesions, 48% and 84% had ovarian endometriosis and \nretrocervical lesions, respectively [17] (Figure 3).\nFigure 3: Endometrioma and the peritoneal site of\ninvagination.\nBoth superficial peritoneal and ovarian endometriomas may \nbe found in association with DIE in variable percentages, thus \ncontributing to the intensity of painful stimuli, as well as to infertility \n[18]. Thisraises the question of whether DIE is an independent \nform of the disease, or whether it represents its most severe clinical \nrepresentation [19]. Nisolle and Donnez have argued that peritoneal \nendometriosis, ovarian endometriosis and adenomyotic nodules \nof the rectovaginal septum are three different entities [20]. In a \nretrospective observational study by Kamergorodsky [21]. Involving \n176 patients and 271 biopsies, the histologic differentiation in \nsuperficial endometriosis, DIE and ovarian endometriomas was \nevaluated. Results showed a predominance of the undifferentiated \nglandular pattern (33.5%) and mixed glandular pattern (46.9%) \nin deeply infiltrating endometriosis lesions, whereas the well-\ndifferentiated glandular pattern (41.8%) was most frequently seen \nin superficial endometriosis lesions, and in ovarian endometriomas \na predominance of both the undifferentiated (40.5%) and mixed \npatterns (37.8%) was observed. There was no significant histologic \ndifference between infiltrative endometriosis of the uteroscacral \nligaments, recto-vaginal endometriosis, or bowel endometriosis. \nThere was a predominance of the well-differentiated pattern in \nmore superficial lesions and the undifferentiated pattern in deeper \nlesions, suggesting a similar mechanism to explain the invasive \npotential of endometriosis.\nRecently, Sapkota [22] analysed genetic risk scores derived \nfrom two large European genome-wide association (GWA) datasets \nfrom a previous multi-ethnic GWA meta-analysis of endometriosis. \nThey found that genetic factors contributing to minimal disease \nmight differ from those contributing to more severe endometriosis, \nand that more severe endometriosis cases exhibit greater genetic \nloading than minimal or mild disease. The genetic burden generally \nincreased from less severe (minimal) to more severe disease, \nconsistent with disease progression. Considering the fact that \nendometriotic lesions undergo repeated cyclic bleeding (injury) \nand repair like other organs leading to fibrosis [23], it has been \nsuggested that endometriotic lesions are fundamentally wounds \nwith repeated tissue injury resulting in smooth muscle metaplasia \n\nSubmission Link: http://biomedres.us/submit-manuscript.php\nJoseph Miller. Biomed J Sci & Tech Res Volume 1- Issue 6 : 2017 1650\n(SMM) and ultimately fibrosis, which somehow do not heal like an \nordinary wound [24]. This points to the complex microenvironment \nand cross-reaction of endometrioc lesions with other cells, i.e. \nplatelets and macrophages, their gradual but progressive evolution \nto SMM and fibrosis and, on occasion, to malignancy and the new \ntraits/phenotypes they may acquire while losing old ones. This \ndynamic feature of endometriotic lesions may explain the reason \nfor some conflicting results in this area of research, including the \nfact that development of biomarkers for the diagnosis or prognosis \nof endometriosis has posed a challenge, at least until now.\nEndometriosis appears to be a progressive disease, as evidenced \nby longitudinal laparoscopies in female baboons [25]. There are at \nleast eight studies reported (with a total of 162 patients) on repeat \nlaparoscopy in women assigned to placebo treatment. The results \nindicate nearly equal distribution among women whose disease \nstage deteriorated (31%), was unchanged (32%), or improved \n(38%). In fact, all but one study noted that 23% of placebo patients \nhad complete regression of the disease over intervals of 4 to 39 \nmonths, meaning that in over two thirds of women the disease \nwill either persist or progress [26-33]. The clinical presentation of \nthe disease followed a similar trend and evolution in both of our \ncases. Each twin had undergone a long history of slowly progressive \npelvic pain from the point of intensity, developing bowel symptoms \nand dyschesia as time passed, with dyspareunia and change in stool \ndiameter to the point of bowel stenosis and impending obstruction. \nAll of this is consistent with the progressive nature of the disease \nreported in the existing literature.\nDeep infiltrating endometriosis, contrary to being an estrogen-\ndependent disease, usually does not respond well to hormonal \nsuppressive therapy. Adequate surgical excision of the lesions \nprovides the best long-term results and symptomatic relief [31-\n34] but surgical treatment of colorectal endometriosis has been \nquite controversial, and there is no consensus on whether the \ntreatment should be conservative (shaving or discoid resection) \nor radical (segmental bowel resection and anastomosis) [35]. \nLately, there has been a great deal of effort to advocate shaving \nas the treatment of choice, mainly because of higher early and \nlate complications in segmental colorectal resection [36]. The \nefficacy of segmental colorectal resection is very debatable; data in \nthis regard is controversial and, to a great deal, dependent upon \nthe surgeon’s experience [37,38]. Findings from histopathologic \nanalysis of specimens from segmental bowel resection indicates \nthat in 50% of cases there is a satellite lesion independent of \nthe primary deep nodule.The deepest layer of the bowel wall \ncontaining endometrioticfoci at the primary lesion is in the \nsubmucosal layer in 70% of cases and the internal circular muscle \nlayer in 30%. Furthermore, persistent lesions are present in 50% of \npatients treated with discoid or shaving resection [39]. The latest \nsystematic review of different surgical approaches to bowel and \nrectovaginal endometriosis showed that the complication rate is \nvariable for conservative and radical treatment. Recurrence rate for \nshaving was reported at 22.2%, for discoid resection 5.17%, and in \nsegmental resection 2.19%; these rates were significantly different \n[37]. Positive bowel resection margins as well as age <31 years and \nbody mass index ≥23kg/m2 appear to be important independent \npredictors of disease recurrence [40].\nOur patients were managed according to the extent of their \npathology, intensity of pelvic pain, and future fertility, thus \nminimising the chance of recurrence. Most importantly, patients’ \nwishes and decisions regarding the type of clinical management \nto be pursued were incorporated, following proper counselling \nand explanation. It is crucial to keep in mind that there is currently \nno scientifically proven best treatment technique for bowel \nendometriosis, and comparison of different currently practised \ntechniques is not possible. According to our current knowledge \nregarding the nature of disease pathology and its progression, \nrecurrence should be as much a source of concern as complications \nfor any given surgical technique. Resection of DIE should be \nglobal, not local, and limited to the bowel. Operations should be \nperformed by an experienced surgeon and a well-organised team, \nin a multidisciplinary fashion. In summary, we present a case of \nadvanced DIE in monozygotic twins; one of the first such cases to \nour knowledge. Our findings reiterate the importance of genetic \nfactors in the aetiology of endometriosis. These cases also reinforce \nthe importance of the following considerations for surgeons \nconsidering conservative treatment for colorectal endometriosis:\na) The extent of lesions cannot be assessed macroscopically \nwith certainty.\nb) Assessment of the depth of infiltration of endometriosis \nfoci in the bowel requires an expert radiologist.\nc) In the majority of rectal endometriosis nodules, the \nfibrosis which is the landmark for shaving does not surround, \nbut follows behind the glandular epithelium and stroma. \nd) More than 2cm of bowel tissue must be removed from the \nmain lesion to obtain clear margins in two thirds of patients. \ne) Low rectal lesions (<5–8cm from the anal verge) are \nassociated with a higher risk of complications.\nf) A great majority of patients have been through previous \nsurgeries and have a good chance of recovering and becoming \npain-free.\nReferences\n1. 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Overton CE , Lindsay PC , Johal B , Collins SA , Siddle NC , et al. (1994) \nA randomized, double-blind, placebo-controlled study of luteal \nphase dydrogesterone (Duphaston) in women with minimal to mild \nendometriosis. Fertil Steril 62(4): 701-777.\n31. Sutton CJ, Pooley AS, Ewen SP , Haines P (1997) Follow-up report on a \nrandomized controlled trial of laser laparoscopy in the treatment of \npelvic pain associated with minimal to moderate endometriosis. Fertil \nSteril 68(6): 1070-1074.\n32. Harrison RF, Barry-Kinsella C (2000) Efficacy of medroxyprogesterone \ntreatment in infertile women with endometriosis: a prospective, \nrandomized, placebo-controlled study. Fertil Steril 74(1): 24-30.\n33. Abbott J, Hawe J, Hunter D, Holmes M, Finn P , et al. (2004) Laparoscopic \nexcision of endometriosis: a randomized, placebo-controlled trial. Fertil \nSteril 82(4): 878-884.\n34. Koninckx PR, Ussia A, Adamyan L, Wattiez A, Donnez J (2012) Deep \nendometriosis: definition, diagnosis, and treatment. Fertil Steril 98(3): \n564-571.\n35. Abrão MS, Petraglia F, Falcone T , Keckstein J, Osuga Y, et al. (2015) Deep \nendometriosis infiltrating the recto-sigmoid: critical factors to consider \nbefore management. Hum Reprod Update 21(3): 329-339. \n36. Roman H, Bridoux V, Tuech JJ, Marpeau L, da Costa C, et al. (2013) Bowel \ndysfunction before and after surgery for endometriosis. Am J Obstet \nGynecol 209(6): 524-530.\n37. Moustafa MM, Elnasharty MAA (2014) Systematic review of the \noutcome associated with the different surgical treatment of bowel and \nrectovaginal endometriosis. Gynecol Surg 11(1): 37-52.\n38. Keckstein J, Wiesinger H (2005) Deep endometriosis, including \nintestinal involvement--the interdisciplinary approach. Minim Invasive \nTher Allied Technol 14(3): 160-166.\n39. Jinushi M, Arakawa A, Matsumoto T , Kumakiri J, Kitade M, et al. (2011) \nHistopathologic. J Minim Invasive Gynecol 18(1): 48-53.\n40. Nirgianakis K, McKinnon B, Imboden S, Knabben L, Gloor B, et al. (2014) \nLaparoscopic management of bowel endometriosis: resection margins \nas a predictor of recurrence. Acta Obstet Gynecol Scand 93(12): 1262-\n1267.\n\nSubmission Link: http://biomedres.us/submit-manuscript.php\nJoseph Miller. Biomed J Sci & Tech Res Volume 1- Issue 6 : 2017 1652\nAssets of Publishing with us\n• Global archiving of articles\n• Immediate, unrestricted online access\n• Rigorous Peer Review Process\n• Authors Retain Copyrights\n• Unique DOI for all articles\nhttp://biomedres.us/","source_license":"CC0","license_restricted":false}