{"paper_id":"3a75cbe8-433f-4b03-be7d-01fa7865597d","body_text":"Int. J. Med. Sci. 2020, Vol. 17 \n \n \nhttp://www.medsci.org \n536 \nInternational Journal of Medical Sciences\n \n2020; 17(4): 536-542. doi: 10.7150/ijms.38679 \nReview \nAbdominal wall endometriosis (a narrative review) \nMara Carsote1, Dana Cristiana Terzea2, Ana Valea3, Ancuta-Augustina Gheorghisan-Galateanu4 \n1. Department of Endocrinology, “Carol Davila” University of Medicine and Pharmacy, 050474, Bucharest, Romania; “C.I. Parhon” National Institute of \nEndocrinology, 011863, Bucharest, Romania \n2. Department of Pathology, “C.I. Parhon” National Institute of Endocrinology, 011863, Bucharest, Romania \n3. Department of Endocrinology, “Iuliu Hatieganu” University of Medicine and Pharmacy, 400012, Cluj-Napoca, Romania \n4. Department of Cellular and Molecular Biology and Histology, “Carol Davila” University of Medicine and Pharmacy, 050474, Bucharest, Romania; “C.I. \nParhon” National Institute of Endocrinology, 011863, Bucharest, Romania  \n Corresponding author: Ancuta-Augustina Gheorghisan-Galateanu, agheorghisan.a@gmail.com \n© The author(s). This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). \nSee http://ivyspring.com/terms for full terms and conditions. \nReceived: 2019.07.23; Accepted: 2020.01.27; Published: 2020.02.10 \nAbstract \nOne of the rarest forms of endometriosis is abdominal wall endometriosis (AWE), which includes \ncaesarean scar endometriosis. AWE remains a challenging condition because some issues related to \nthis topic are still under debate. The increasing number of caesarean sections and laparotomies will \nexpect to increase the rate of AWE. The current incidence in obstetrical and gynaecological \nprocedures is still unknown. The disease is probably underestimated. The pathogenic mechanism \ninvolves local environment at the implant site including local inflammation and metalloproteinases \nactivation due to local growth factors, estrogen stimulation through estrogen receptors and \npotential epigenetic changes. However, the underlying mechanisms are not fully explained, and we \nneed more experimental models to understand them. The clinical presentation is heterogeneous; \nthe patient may be seen by a gynaecologist, an endocrinologist, a general surgeon, an imaging \nspecialist, or even an oncologist. No particular constellation of clinical risk factors has been \nidentified, and the histological report is the major diagnostic tool for confirmation. Surgery is the \nfirst line of therapy. Further on we need protocols for multidisciplinary investigations and \napproaches. \nKey words: endometriosis, abdominal wall endometriosis, caesarean scar endometriosis \n1. Introduction \nEndometriosis, a classic topic of gynaecological \nendocrinology and a condition that is challenging, is \ncharacterized by the presence of endometrial \nepithelial and stromal cells in non-uterine locations. \nEndometriosis is typically associated with chronic \npain and infertility and affects one in ten women of \nreproductive age, with different frequencies \ndepending on the site of endometriotic implant [1]. \nFor instance, the most common pelvic locations of \nendometriotic tissue are the ovary and pelvic \nperitoneum. Sites of extra-pelvic localization include \nthe gastrointestinal tract, the urinary tract, and the \nrespiratory system [2,3,4]. Among these, one of the \nrarest forms of endometriosis is abdominal wall \nendometriosis (AWE) or parietal endometriosis, \nincluding caesarean scar endometriosis (CSE). \nPost-surgical subgroups of endometriosis have \nincreased due to the higher use of caesarean sections \nworldwide. To date, this particular type of implant is \nonly partially understood, and the diagnosis is often \nmissed and delayed [5,6,7]. The effects of oestrogen \nexposure after caesarean section and concomitant \nendometrial seeding during the surgery are enhanced \nby chronic inflammation, altered immunity, and local \ngrowth factors [1,5,6]. No particular constellation of \nclinical risk factors has been identified, and the \nhistological report is the major tool for confirmation, \nsince the preoperative diagnostic rate is low [7,8]. \n2. Materials and Methods \nThis is a narrative review of the literature based \non research using the keywords “endometriosis”, \n \nIvyspring  \nInternational Publisher \n\nInt. J. Med. Sci. 2020, Vol. 17 \n \nhttp://www.medsci.org \n537 \n“abdominal wall endometriosis”, and “caesarean scar \nendometriosis”. We mainly included articles \npublished between 2014 and 2019. Due to the rarity of \nthe condition, the highest level of clinical evidence \nfrom included papers are observational studies, case \nseries, one case-control study, one prospective cohort \nstudy, and some molecular biology-based experi-\nmental studies. The aim of this article is to provide an \nupdate on AWE from a multimodal and multidisci-\nplinary perspective. \n3. Prevalence \nAWE follows a variety of obstetrical and \ngynaecological surgeries that are mostly represented \nby caesarean sections (approximately 85% by some \nauthors) but also comprise hysterotomy, hysterec-\ntomy, and laparoscopic procedures that are \nperformed for non-surgical endometriosis [3,9,10]. \nSumathy et al. reported concurrent endometriosis in \n18.9% of cases, while others reported no synchronous \npelvic lesions [10,11]. The mean age at diagnosis is 35 \nyears, and the time from surgery to endometriosis \nrecognition varies from 3 months to 2 decades [11,12]. \nThe reported incidence of CSE is 0.03-0.45%; \nhowever, many authors suggest that this low number \nis due to the rarity of the condition and that the \ncurrent incidence of AWE (including CSE) cannot be \naccurately evaluated since consistent epidemiological \ndata are non-existent [13,14]. Subcutaneous endome-\ntriosis near caesarean scars has been described in only \na few isolated cases, including a case of cutaneous \nendometrial cancer [15]. Recently, a case of scar \nendometriosis at the level of the uterine cavity was \nreported [16]. Additionally, 18 cases of trocar port site \nendometriosis has been reported in the literature [17]. \n4. Pathogenic context \nEven though AWE is described by some as the \n\"iatrogenic\" subtype of endometriosis, the clear \nexplanation for why some people develop this \ncondition after caesarean section is unclear. In \naddition to the technical details and precautions \nthemselves, it seems that the pathogenic mechanism is \nmore complex, and endocrine, immune and \ninflammatory pathways have been considered. While \nthe mechanism is still an enigma, some mechanisms \nsuch as metaplasia and cell migration in association \nwith direct seeding have been proposed [18]. \nIntra-operative implantation is certainly not relevant \nto non-surgical endometriosis (or “endogenous” \nendometriosis), and retrograde menstruation (or the \nSampson hypothesis) is not involved in post- \ncaesarean section endometriosis, in contrast to pelvic \nendometriosis [19,20,21]. Only a few studies have \nidentified pre-existent pelvic endometriosis [10,11]. \nThe local environment that allows the growth of \nendometrial cells and stroma includes oestrogen \nexposure and chronic inflammation [6,19]. \nAngiogenic growth factor anomalies may be \nassociated with this condition [22]. \nGenetic and epigenetic changes in endometrial \ncells are also observed in endometriosis. Genome- \nwide association studies have identified 12 single \nnucleotide polymorphisms at 10 independent genetic \nloci that are associated with endometriosis. Two \nchromosomal areas of significant linkage were \nobserved on 10q26 and 7p13‐15 (harbouring genes \nsuch as CYP2C19, INHBA, SFRP4 and HOXA10). The \nidentified epigenetic changes comprise methylation \nand demethylation of DNA and modifications of the \nhistone code [23,24]. The genetic/epigenetic theory \nmight explain the heterogeneity of this disease with a \nhereditary profile, but further studies are needed. \nRecently, high expression of PPAR-γ, a nuclear \nreceptor with anti-inflammatory and neuroprotective \nroles, has been shown in post-operative lesions, and it \nhas been suggested that PPAR-γ could be a \npathogenic mechanism of associated pain [25]. In a \nstudy focused on “iatrogenic” or “incisional” \nendometriosis, Lac et al. found that one in four women \nwith this condition had a somatic cancer mutation \nthat may involve two signal transduction pathways, \nMAPK/RAS or PI3K-Akt-mTor [20]. \nNon-uterine endometrial cells require \nmetalloproteinases for local remodeling and \ninteraction. These enzymes are activated by local \nfactors, such as TGFβ.  Itoh H et al. showed that \nstromal endometrial cells of AWE have an abnormal \nresponse to TGFβ1. This may be prevented by \nprogesterone, which does not allow the implant to \nattach to the local matrix, but it seems that in AWE, \nthere is resistance to progesterone action [26]. \nEpithelial endometrial glands and stromal cells \nare positive for oestrogen receptor (ER) expression \n(Figure 1). \nMolecular biology studies of endometriosis have \nshown the importance of ER as a hallmark of local \nchanges. Endometriotic foci have oestrogen and \nprogesterone receptors that mediate their responsi-\nveness during the menstrual cycle. Methylation \ndefects of genes encoding transcription factors \n(GATA6, steroidogenic factor-1) and ERβ cause \nincreased production of oestrogens in the lesion, with \nsecondary inhibition of progesterone receptor. \nSubsequently, retinol uptake and further metaboli-\nzation are decreased, causing defects in the endome-\ntriotic tissue, with a high level of inflammation and \nanomalies of prostaglandin production [27]. \nMoreover, Gou Yet al. showed that the activation of \nERβ in stromal cells is linked to local inflammation \n\nInt. J. Med. Sci. 2020, Vol. 17 \n \nhttp://www.medsci.org \n538 \nbecause ER induces local CCL2 production through \nthe NF-kB pathway, which triggers local macro-\nphages [28]. Colón-Caraballo et al. demonstrated that \nthe stroma has a tendency for low expression of ERα \nand progesterone and high expression of ERβ in the \nstroma, but the ERβ: ERα ratio varies with the site of \nthe endometriotic lesion [29]. \nOverall AWE is developed after surgery only by \nsome females. The mechanisms involve local \nenvironment at the implant site including local \ninflammation and metalloproteinases activation due \nto local growth factors, estrogen stimulation through \nestrogen receptors and potential epigenetic changes. \n5. Clinical onset \nSpecific symptoms are absent in many cases. \nLocal pain at the caesarean scar/incision site of the \nabdominal wall during menstruation has been \nreported to be the most common complaint. \nAdditionally, chronic pain that is unrelated to the \nmenstrual cycle may involve not only the abdominal \nwall but also the pelvic and lumbar regions [30]. \nSometimes, the onset is an acute abdominal emer-\ngency [31]. On rare occasions, a patient presents with \nskin changes; for instance, the patient shows \necchymosis at the level of the abdominal wall during \nmenstruation or hyperpigmentation of a scar (with/ \nwithout small local nodules) [13]. A lump may be \npalpable at the abdominal wall, including on the \npost-operative scar, with a volume that may vary \naccording to the menstrual cycle [30,32]. Sometimes \nthe lesion is not palpable, and the pain is atypical; \nthus, the patient is admitted in the general surgery \ndepartment. Clinical diagnosis is established in \n20-50% of cases, and if additional imaging methods \nare used, this frequency increases to 70% [11,31,32]. \nThe clinical triangle includes cyclical pain, a lump at \nor near the level of the scar/abdominal wall and a \nhistory of caesarean section or similar gynaecological \nprocedures [3,11]. A study by Zhang et al. showed that \nthe main reason patients present with this condition is \nabdominal tumour identification (98.5%), followed by \ncyclic pain (86.9%). Almost 95% of subjects had only \none lump [33]. Regarding the risk factors for AWE, \nthere is not a specific profile. A case-control study by \nKhan et al. from the Mayo Clinic, in which 2539 \nfemales who underwent surgery for endometriosis \nwere enrolled, showed that 1.34% of the patients had \nAWE, most frequently (59%) of CSE type. The \naccuracy of the diagnosis is increased when \nindependent risk factors, such as the presence of \ncyclical abdominal pain without dysmenorrhoea and \na prior laparotomy, are evident [34]. A study \nconducted by Andolf et al. showed that the risk for \ndeveloping endometriosis after caesarean section is \n1.8%. [35]. \n6. Preoperative investigations \nIf AWE is suspected, the most useful assessment \ntools are ultrasound, computed tomography (CT) and \nmagnetic resonance imaging (MRI) of the abdomen, \nincluding the abdominal wall (Figure 2). \nMRI is better used in cases with small lesions, \nwhile CT provides better results in cases with muscle \nand subcutaneous layer involvement [36]. Ultrasound \nremains the best screening method [37]. The mean \ndiameter of the AWE was 4.7 ± 1.53 cm in one \nretrospective observational cohort study [38]. The \nlesions of AWE have an isoechoic or hyperechoic \npattern (46.7%), with peripheral vascularization \n(61.5%) on ultrasound and are homogenous and \nhypervascular on CT scan [39]. MRI is the most \ncommonly used method for evaluating pelvic \nendometriosis. It is also used for preoperative disease \nstaging [40]. \n \nFigure 1. Abdominal wall endometriosis. Immunohistochemistry report. A. High oestrogen receptor positivity in the epithelium of the endometrial glands (arrow heads) and in \nstroma (arrow). Cell nuclei are stained intensely for estrogen receptors (10x). B. CD10 positivity in the endometrial stroma (arrow) (10x). \n \n\n\nInt. J. Med. Sci. 2020, Vol. 17 \n \n \nhttp://www.medsci.org \n539 \n \nFigure 2. A case of a 44-year-old female diagnosed with abdominal wall endometriosis 14 years after a caesarean section. She had chronic pain unrelated to the menstrual cycle. \nA. Preoperative aspect: computed tomography showing a poorly defined tumour of 3.9 cm at the abdominal wall, with a heterogeneous aspect. B. Post-operative aspect by \ncomputed tomography. \n \nFigure 3. A. Abdominal wall endometriosis. Endometrial glands (arrow heads) and stroma (arrows) in the abdominal wall; HE stain, 4x (A), 10x (B). \n \nSome studies have shown the enhancement of \nultrasound accuracy by elastography in the context of \nabdominal wall infiltration in subjects without \nexcessive fat mass [41]. Transabdominal sonoelasto-\ngraphy appears to be particularly useful in lesions of \nthe endometrioma type (but not in patients with a \nhigh body mass index) [42]. Positron emission \ntomography - computed tomography (PET-CT) is less \nuseful because of the low metabolic rate of the cells \n[38]. Some cases of subcutaneous endometriosis have \nbeen evaluated using dermoscopy techniques [43]. \nAdditionally, for superficial lesions, ultrasound- \nguided fine-needle aspiration has been used \ndepending on the anatomical profile of the lump \n[44,45]. Fine-needle aspiration (FNA) is a simple, \nnon-invasive, easy-to-perform procedure. For \ninstance, in a series of 33 cases, Lopez-Soto et al. used \nFNA in 72% of cases [32]. The association between cell \nblock analysis and the cytological report has been \nshown, and the results of the cytological report have \nbeen improved by adding the immunohistochemistry \nprofile based on cell block analysis [46]. FNA is useful \nfor positive diagnosis and for differential diagnosis so \nit may be the general case’ management with a \nminimal risk of secondary dissemination because the \nprocedure is minimally invasive.  \nGenerally the screening tool remains ultrasound \nand as a next step MRI or CT is useful. \n7. Pathological report \nTypically, the diagnosis is made after surgery, \nbased on the histological report (Figure 3). \nSome tumours are well defined and manifest as \nendometriomas [36,47,48]. \nIn AWE, endometrial cells are implanted in the \nrectus abdominis muscle and into the dermis during \nsurgery. Three AWE positions have been described in \nrelation to the rectus abdominis: the superficial \nimplant (above the muscle fascia), intermediate (at the \nlevel of the rectus muscle fascia), and the deep \nposition (below the fascia) [49]. \nThe differential diagnosis of AWE includes \nhernia (inguinal or incisional), abdominal wall \ntumours of other causes, lipomas, haematomas, \ngranulomas, metastases from distant tumours, and \ndesmoid tumours, among others [3,11,50,51]. \n8. Therapy \nAWE requires a multidisciplinary approach. \nTraditionally, endometriosis is treated by hormonal \ntherapy in addition to pain control drugs and/or \nsurgery, depending on the purpose, namely, pain \nmanagement and/or achieving fertility [1]. For AWE \nand CSE cases, surgery is the only curative therapy, \nand the removal of the lump also causes chronic pain \nto disappear [12,48]. Preoperative radioisotope \n\n\nInt. J. Med. Sci. 2020, Vol. 17 \n \nhttp://www.medsci.org \n540 \ninjection has recently been used to clearly identify \nsmall lesions during resection but there are limited \ndata [52]. A wide incision for endometriotic nodules is \nrecommended due to the risk of recurrence described \nin 5-9% of cases [16,32]. Sclerotherapy with ultra-\nsound guided ethanol injection into the lesion of scar \nendometriosis has been reported to be effective in \nisolated cases to prevent abdominal wall defects after \nwide excision [53]. Recently, as an alternative to \nsurgery, some authors have suggested, high-intensity \nfocused ultrasound ablation (HIFUA), which has a \nrecurrence rate of 3.9% [54,55]. Lee JS et al. showed \nthat the rate of side effects, such as blood loss and \nparietal defects, is lower when HIFUA is used against \nAWE [56]. Combined oral contraceptives, progesto-\ngens and hormone suppression therapy with \ngonadotropin-releasing hormone (GnRH) analogues \nare useful for patients who refuse surgery or for \npost-operative management to reduce the risk of \nrecurrence and delay new growth. Additionally, \nprevious hormonal treatment may be an option for \nlarger tumours and may reduce their sizes before \nsurgery. However, the clinical improvement observed \nfor endometriotic implants at other sites has not been \nobserved for AWE [57]. The main therapeutically \napproach is the surgical remove. \n9. Malignancy risk \nEndometriosis of any site has an associated \nmalignancy risk of 1%. Eighty percent of malignancy \ncases are related to endometriosis located at the ovary, \nand 20% of these cases are related to extra-gonadal \nlocations (including the abdominal wall) [58]. Genetic \nanomalies, such as loss of heterozygosity or PTEN, \nARID1A or p53 mutations, have been implicated [59]. \nLocal production of reactive oxygen species and \nprolonged oestrogen exposure may increase the risk \nof malignant transformation [60]. \nMalignant evolution is suspected in AWE cases \nwith rapid growth of the endometriotic implant [18]. \nIn 2017, a PRISMA systematic review was published \nin relation to the malignancy risk of endometriosis \nfollowing obstetrical surgery. This systematic review \nbased on prior reviews and case reports included 47 \ncases diagnosed with AWE-related cancer between \n1980 and 2016. A total of 87% of patients had a \nprevious caesarean section, while 13% had other types \nof gynaecological procedures. The median period of \ntime from surgery to cancer diagnosis was 19 years \n[9]. Previous data suggested an interval of up to 39 \nyears [61,62]. The median survival time was 42 \nmonths, with a poor prognosis for clear cell \nadenocarcinoma followed by endometrioid \nadenocarcinoma [63,64]. A prior review indicated a \npercentage of 44% mortality within the first few \nmonths after diagnosis [61]. The treatment for \nendometriosis-associated malignant transformation in \nan abdominal surgical scar is extensive surgery and \nadjuvant chemotherapy and/or radiotherapy. \n10. Conclusion \nAWE represents a dynamic, yet incompletely \nknown, multidisciplinary topic. The incidence is \nincreasing due to the increasing number of obstetrical \nand gynaecological procedures. The clinical aspects \nrange from a lump to local pain at the abdominal wall \nor caesarean scar. Imaging techniques like ultrasound \nand magnetic resonance may help but the definitive \ndiagnosis is based on a post-operative histological \nreport. Surgical removal of the implant currently \nrepresents the best management. The questions that \nstill do not have a clear answer are: the true \nprevalence in the female population; the risk of \nrecurrence after an initial surgical approach; the rate \nof malignant transformation; the underlying seeding \nmechanisms and pathways of cancer related. \nMoreover, standard protocols are needed. \nAbbreviations \nAWE: abdominal wall endometriosis; ARI1A: \nAT-rich interactive domain-containing protein 1A; \nCCL2: chemokine (C-C motif) ligand 2; CYP2C19: \ncytochrome P450 2C19; CSE: caesarean scar \nendometriosis; CT: computed tomography; DNA: \ndeoxyribonucleic acid; ER: oestrogen receptor; FNA: \nfine-needle aspiration; GABA6: gamma-aminobutyric \nacid 6; GnRH: gonadotropin-releasing hormone; \nHIFUA: high-intensity focused ultrasound ablation; \nHOXA10: homeobox protein Hox-A10; INHBA: \ninhibin, beta A; MRI: magnetic resonance imaging; \nMAPK: mitogen-activated protein kinases; NF-kB: \nnuclear factor kappa-light-chain-enhancer of \nactivated B cells; PET-CT: positron emission \ntomography - computed tomography; PPAR-γ: \nperoxisome proliferator-activated receptor gamma; \nPI3K-Akt-mTor: phosphatidylinositol-3-kinase (PI3K) \n/Akt and the mammalian target of rapamycin \n(mTOR); PTEN: phosphatase and tensin homolog; \nP53: tumor protein p53; SFRP4: secreted \nfrizzled-related protein 4; TGFβ: transforming growth \nfactor β. \nAcknowledgements \nAuthorship \nMC was involved in the design of the study, data \ncollection, literature review, and manuscript concep-\ntion. DCT was involved in performing histological \nand immunohistochemical staining and examinations, \nperforming pathology-based diagnoses and obtaining \n\nInt. J. Med. Sci. 2020, Vol. 17 \n \nhttp://www.medsci.org \n541 \nmicroscopy photos. AV was involved in the \nacquisition and analysis of data, the literature search \nand the drafting of the manuscript. AAGG was \ninvolved in the manuscript’s conception, microscopic \nimage analysis, microscopic image processing into the \nfinal form for publication, and critical revision of the \nmanuscript for important intellectual content. All \nauthors have read and approved the final manuscript. \nEthics approval and consent to participate \nThis study adhered to the tenets of the 1964 \nDeclaration of Helsinki. \nCompeting Interests \nThe authors have declared that no competing \ninterest exists. \nReferences \n Zondervan KT, Becker CM, Koga K, et al. Endometriosis. 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