{"paper_id":"82fbf0be-197c-4c38-bbaa-bbaecee1f57c","body_text":"Clin. Exp. Obstet. Gynecol. 2025; 52(2): 26272\nhttps://doi.org/10.31083/CEOG26272\nCopyright: © 2025 The Author(s). Published by IMR Press.\nThis is an open access article under the CC BY 4.0 license .\nPublisher’s Note: IMR Press stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.\nOriginal Research\nDo Interventions on the Uterine Wall Increase the Risk of Developing\nAbdominal Wall Endometrioma?\nNevin Sakoglu1,*\n , Seymin Ayvaz2\n1General Surgery Department, Medipol University, 34196 Istanbul, Turkey\n2Obstetric and Gynecology Department, Medipol University, 34196 Istanbul, Turkey\n*Correspondence: nsakoglu@medipol.edu.tr (Nevin Sakoglu)\nAcademic Editor: Andrea Tinelli\nSubmitted: 26 August 2024 Revised: 12 December 2024 Accepted: 16 December 2024 Published: 5 February 2025\nAbstract\nBackground: Abdominal wall endometriosis, which can affect the rectus abdominis muscle, has been documented in association with\ncesarean section scars or along pathways formed by abdominopelvic surgeries. Our study aimed to assess the risk of developing abdominal\nwall endometriomas following surgical interventions (cesarean section, myomectomy) on the uterine wall. Methods: Between 2011 and\n2021, a total of 19,574 patients underwent cesarean section delivery through a Pfannenstiel incision. The average age of patients was\n36 (20–58) years. On average, 1.5 to 2.0 years after cesarean section, 204 patients developed abdominal wall endometrioma (Group\nI). The control group (Group II) comprised 204 patients who had undergone cesarean section by the same method but did not develop\nscar endometriosis. During the same period, 200 patients underwent myomectomy with a similar incision for intramural and submucosal\nmyomas (Group III). Postoperatively, these patients were also monitored for the development of endometrioma. One of the patients who\nunderwent myomectomy also had surgery for an ectopic pregnancy at the same time. The data analysis included descriptive statistical\nmethods, such as calculating the mean ± standard deviation, median (min–max), and frequencies (n (%)). The Shapiro-Wilk normality\ntest, Kruskal-Wallis test, Dunn’s multiple comparison test, Chi-Square test, and Fisher-Freeman-Halton exact test were applied. The\nresults were evaluated for statistical significance at a level of p < 0.05. Results: Abdominal wall endometriomas developed in 204\nof 19,574 patients who delivered by cesarean section (1.04%). Endometrioma development was significantly higher in Group I, where\nestrogen levels were elevated ( p < 0.001). The most common complaints among the patients were swelling and cyclical pain in the\nabdominal wall. 9 of the 204 patients who had previously developed abdominal wall endometriomas experienced recurrence (4.41%). An\nabdominal wall endometrioma developed in the patient who underwent myomectomy and surgery for ectopic pregnancy simultaneously\n(0.5%). Conclusions: Endometrioma is a multifactorial condition. High estrogen levels, surgical techniques, and an increased imbalance\nbetween estrogen and progesterone levels can trigger inflammation and lead to the development of endometriomas. We suggest that\nfurther detailed studies are needed to better understand these mechanisms.\nKeywords: abdominal wall endometrioma; section; intramural myoma; submucous myoma; recurrence\n1. Introduction\nEndometriosis is a medical condition in which tissue\nsimilar to the lining of the uterus, the endometrium, begins\nto grow outside the uterus. This can occur on the ovaries,\nfallopian tubes, the outer surface of the uterus, and other\norgans within the pelvic cavity. It can cause various symp-\ntoms such as pelvic pain, painful periods, and infertility.\nEndometriosis impacts around 15% to 40% of women in\ntheir childbearing years, typically occurring within the ab-\ndominal cavity, particularly in the pelvis, and sometimes\nin locations outside of the pelvis [ 1]. Previous surgical\nprocedures, such as cesarean sections or hysterectomies,\ncan lead to this condition. Abdominal wall endometrioma\n(AWE), also known as extrauterine endometriosis or scar\nendometriosis, is a rare condition where endometrial tissue\nis found in the subcutaneous fatty layer or muscles of the\nabdominal wall. AWE typically occurs due to the spread\nof endometrial tissue at the incision site during obstetri-\ncal or gynecological surgeries. This can occur as a result\nof previous surgical procedures, such as cesarean sections\nor hysterectomies, or from other abdominal surgeries [ 2,3].\nThe incidence of scar endometriosis following a cesarean\nsection is estimated to be around 0.03% to 1% [ 4–6]. The\ntypical symptoms of this condition may involve discomfort,\npuffiness, and the observation of a bump or growth near the\nscar area. This ailment commonly affects women aged be-\ntween 24 and 47 years [ 4].\nThere are 2 main theories proposed for the develop-\nment of scar endometriosis: the cellular transport theory\nand the coelomic metaplasia theory. The cellular transport\ntheory suggests that endometrial cells are transported to dif-\nferent areas of the body through various channels such as\nlymphatic vessels, blood vessels, or surgical procedures,\nwhere they implant and grow, leading to the development\nof scar endometriosis. The coelomic metaplasia theory sug-\ngests that cells resembling endometrial tissue can undergo\na transformation from the lining of the abdominal cavity\n(coelomic epithelium) in response to hormonal or inflam-\n\nmatory stimuli, leading to the formation of scar endometrio-\nsis. Both theories provide explanation for the occurrence of\nscar endometriosis [ 5]. Other causes thought to be related\nto the development of surgical scar endometriosis include\nhematogenous and lymphatic spread [ 6]. The precise pro-\ncess underlying the development of scar endometriosis is\nnot completely understood.\nEspecially during the postpartum period, estrogen lev-\nels can be elevated after a cesarean section. The heightened\npresence of estrogen can potentially affect the endometrium\nand promote the expansion of endometrial tissue outside the\nuterus. When it comes to estrogen exposure and the spread\nof endometrial cells, local growth factors may play a role in\nthe growth and sustenance of these cells beyond the uterus\n[7–9].\nThe goal of this study was to determine the frequency\nand causes of abdominal wall endometrioma developing in\nthe suprapubic transverse Pfannenstiel incision line and rec-\ntus abdominis muscle in 19,574 female patients who gave\nbirth by cesarean section between 2011 and 2021 in our\nhealth institution and 200 women operated for “intramural\nand submucous myoma” in the same period.\n2. Materials and Methods\nThe research protocol was approved by Istan-\nbul Medipol University Ethics Committee (E-10840098-\n772.02-7514). The aim of this study was to determine the\nfrequency and causes of abdominal wall endometrioma af-\nter surgical interventions such as cesarean section and my-\nomectomy in cases where the uterine wall was opened. All\nprocedures conducted in the study adhered to ethical prin-\nciples and followed the guidelines of the Declaration of\nHelsinki. This study was a single center study conducted\nretrospectively in 608 cases. Patients who gave birth by ce-\nsarean section with and without endometrioma and had my-\nomectomy were included in the group. We did not include\npatients who had normal births in the study.\nGroup I; Abdominal wall endometrioma (+) cesarean\nsection patients: 204, Group II; Cesarean section patients\nwithout abdominal wall endometrioma: 204 and, Group III;\nintramural & submucous myomectomy: 200 cases oper-\nated by the same general surgeon and gynecologist between\n2011 and 2021. After receiving ethics committee approval\nfor the study, symptoms of patients, laboratory tests, radio-\nlogic examinations, surgical procedure, intraoperative find-\nings and postoperative complications, and pathology results\nwere evaluated in terms of recurrence and recovery crite-\nria. The inclusion of the cases in the research was to de-\ntermine abdominal wall endometrioma (n = 204) and in-\ntramural + submucous myoma (n = 200) based on clinical\nfindings and radiological imaging (superficial & transvagi-\nnal ultrasound). As some of the patients were illiterate, we\nobtained written consent from their relatives.\nAll patients underwent thorough questioning and ex-\namination in the outpatient department before being indi-\nvidually admitted to the hospital on the day of surgery. The\npreanesthetic evaluation was conducted by the same anes-\nthesia team for each patient. After the anesthesia, and the\nsurgical area was cleaned of hair, we used an antiseptic\ncleansing agent, povidone iodine in the surgical field, and\n2 preoperative doses of antibiotic were used. All patients\nwere operated on with a transverse Pfannenstiel incision in\nsupine position.\nIn cases of abdominal wall endometrioma following a\ncesarean section, a wide excision with a 1-cm margin was\nperformed to minimize the risk of recurrence. The fascia\nwas sutured with 2/0 polydioxanone synthetic (PDS) loop.\nOut of the 204 patients who underwent surgery for abdom-\ninal wall endometrioma, 110 had the endometrioma local-\nized above the rectus abdominis muscle fascia, while 94 had\nit localized at the level of the rectus abdominis muscle facia.\nNo skin flap was needed to cover the tissue after resection\nor mesh to repair the fascia defect. After the surgery, the\npatients’ complaints decreased dramatically.\nFor adenomyotic lesions, the same transverse Pfan-\nnenstiel incision was used. Complete excision of intramu-\nral and submucous myomas from normal myometrium was\nperformed. Care was taken to avoid unwanted removal of\nnormal myometrial tissues.\nDuring the same period, a control group consisting\nof 204 patients who did not develop abdominal wall en-\ndometrioma clinically and radiologically during at least 1\nyear of follow-up after giving birth by cesarean section was\ncreated.\nStatistical Analysis\nStatistical analyses for this study were conducted us-\ning the NCSS (Number Cruncher Statistical System) 2007\nStatistical Software package program from Utah, USA. De-\nscriptive statistics for the variables are presented as mean\n± standard deviation, median (min–max), and frequencies\nn (%). The normality assumption was tested using the\nShapiro-Wilk tests. Group comparisons of continuous vari-\nables that did not show normal distribution were tested us-\ning the Mann-Whitney U, Kruskal-Wallis tests, and Dunn’s\nmultiple comparison test in subgroup comparisons. Cat-\negorical data analyses were performed using the Pearson\nChi-Square test and the Fisher-Freeman-Halton Exact test,\nconsidering the number of categories (rows x columns) and\nthe expected values in crosstab tables cells. The results\nwere evaluated at the significance level of p < 0.05.\n3. Results\nBetween 2011 and 2021, 19,574 patients delivered by\ncesarean section. The average age of patients who un-\nderwent cesarean section was 30 (16–52) years. Abdom-\ninal wall endometrioma developed in 204 of these patients\n(Group I) (1.04%), on average 12–18 months after birth.\nDuring the same period, 200 patients underwent myomec-\ntomy surgery due to intramural and submucous myoma\n2\n\n\nTable 1. Preoperative laboratory values of the patients.\nV ariables\nGroup I (n = 204) Group II (n = 204) Group III (n = 200)\npMean ± SD Mean ± SD Mean ± SD\nMedian (Min–Max) Median (Min–Max) Median (Min–Max)\nAge (year) 31.53 ± 5.92 33.64 ± 4.92 42.49 ± 4.74 <0.001&\n31.0 (20.0–43.0) 34.0 (23.0–44.0) 43.0 (31.0–58.0)\nE2 (pg/mL) 202.03 ± 104.37 131.39 ± 103.53 180.54 ± 86.75 <0.001&\n188.0 (37.0–396.0) 97.0 (30.0–398.0) 182.5 (28.0–387.0)\nPg (ng/mL) 2.77 ± 3.02 3.33 ± 5.23 5.79 ± 6.59 <0.001&\n2.0 (0.10–23.0) 1.32 (0.10–24.0) 3.0 (0.10–32.0)\nHTC (%) 33.85 ± 2.10 34.02 ± 1.88 33.05 ± 2.64 <0.001&\n34.0 (27.0–39.0) 34.0 (28.0–38.0) 33.0 (26.72–40.15)\nHGB (g/dL) 10.34 ± 0.84 10.45 ± 0.70 9.83 ± 1.14 <0.001&\n10.0 (8.0–12.30) 10.4 (8.5–12.0) 10.0 (7.0–12.60)\nWBC (103/mL) 7223.06 ± 1840.47 7278.62 ± 1911.86 7100.17 ± 1500.83 <0.001&\n7195.0 (9.0–10,960.0) 7320.0 (4485.0–19,885.0) 6830.0 (4718.0–10,740.0)\nPLT (103/mL) 264.46 ± 61.72 244.03 ± 31.00 197.44 ± 42.0 <0.001&\n260.0 (135.0–390.0) 243.0 (174.0–372.0) 197.0 (95.0–320.0)\nAPTT (sec) 29.37 ± 2.41 29.47 ± 2.91 31.13 ± 3.70 <0.001&\n30.0 (23.0–34.0) 29.0 (23.0–36.0) 32.0 (23.0–45.0)\nINR 0.93 ± 0.55 0.90 ± 0.05 0.91 ± 0.07 0.008&\n0.89 (0.76–8.86) 0.89 (0.80–1.0) 0.91 (0.68–1.23)\nSGPT (u/L) 29.52 ± 9.33 26.82 ± 8.52 32.04 ± 6.69 <0.001&\n34.0 (18.0–43.0) 27.0 (11.60–42.0) 34.0 (11.0–41.0)\nGlucose (mg/dL) 90.67 ± 8.01 90.15 ± 10.66 91.81 ± 9.97 0.173&\n90.0 (70.0–125.0) 90.0 (70.0–137.0) 90.0 (75.0–125.0)\nCreatinine (mg/dL) 0.75 ± 0.08 0.78 ± 0.12 0.76 ± 0.13 0.105&\n0.75 (0.56–1.0) 0.77 (0.55–1.30) 0.76 (0.45–1.20)\nTSH (mIU/L) 4.03 ± 0.78 2.91 ± 1.39 3.28 ± 1.74 <0.001&\n4.0 (2.45–6.40) 2.66 (0.35–6.45) 2.98 (0.29–23.60)\nDiameters (mm) 33.51 ± 4.01 – 60.51 ± 14.55 <0.001#\n34.0 (19.0–43.0) 60.0 (35.0–100.0)\n&, Kruskal-Wallis Test; #, Mann-Whitney U test; SD, standard deviation; E2, estrogen; Pg, progesterone; HTC, hematocrit;\nHGB, hemoglobin; WBC, white blood cell count; PLT, platelet; APTT, activated partial thromboplastin time; INR, inter-\nnational normalized ratio; SGPT, serum glutamate pyruvate transaminase; TSH, thyroid stimulating hormone.\n(Group III). The average age of patients who underwent\nmyomectomy and abdominal wall endometrioma was 43.0\n(31.0–58.0) years, and 31.0 (20.0–43.0) years respectively.\nA control group was created, including a similar number\nof patients who gave birth by cesarean section in the same\nperiod and did not develop abdominal wall endometrioma\n(Group II). We followed patients for approximately 1.5–2\nyears to determine the development of endometrioma after\ncesarean section and myomectomy surgeries. Preoperative\nlaboratory values were compared and are shown in Table 1.\nIn this table, we compared various laboratory parameters\nbetween the 3 different patient groups. There was a sig-\nnificant difference in age between the groups ( p < 0.001).\nGroup III was on average older [43.0 (31.0–58.0) years]\nwhile Group I had a lower average age [31.0 (20.0–43.0)\nyears]. There was a significant difference in estrogen (E2)\nlevels ( p < 0.001). Group I had the highest average E2\nlevel [188.0 (37.0–396.0) years]. There was also a signif-\nicant difference in progesterone (Pg) levels ( p < 0.001).\nGroup III had the highest average Pg level [3.0 (0.10–32.0)\nng/mL]. There were significant differences in hematocrit\n(HTC) and hemoglobin (HGB) values between all 3 groups\n(p < 0.001). There was a significant difference in platelet\n(PLT) counts (p < 0.001). It was noted that Group I had the\nhighest mean PLT count. The activated partial thrombo-\nplastin time (APTT) of the myomectomy group was longer\nthan the other groups ( p < 0.001). There was a significant\ndifference in the international normalized ratio (INR) lev-\nels (p = 0.008). There was a significant difference in serum\nglutamate pyruvate transaminase (SGPT) level (p < 0.001).\n3\n\nTable 2. Dunn’s multiple comparisons test.\nGroups Age Estrogen Pg HTC HGB PLT APTT INR SGPT TSH\nMyomectomy/Caserean with endometrıoma\n(Group III/Group I)\n<0.001 0.072 <0.001 0.002 <0.001 <0.001 <0.001 0.950 0.006 <0.001\nMyomectomy/Caserean (Group III/Group II) <0.001 <0.001 <0.001 <0.001 <0.001 <0.001 <0.001 0.026 <0.001 0.052\nCaserean with endometrıoma/Caserean (Group I/Group II) <0.001 <0.001 0.463 0.771 0.423 <0.001 0.973 0.714 0.007 <0.001\nThere was no significant difference between the groups in\nglucose levels ( p = 0.173). There was no significant dif-\nference in creatinine levels ( p = 0.105). It was noted that\nGroup II had the highest median 0.77 (0.55–1.30) mg/dL.\nThere were significant differences in thyroid stimulating\nhormone (TSH) values ( p < 0.001). TSH value was higher\nin Group I [4.0 (2.45–6.40) mIU/L]. There was also a sig-\nnificant difference in diameters levels between Group I and\nGroup III ( p < 0.001). The myomectomy group stands out\nwith the largest average diameter and this parameter was\nnot provided for group II.\nThe results of Dunn’s multiple comparisons Test are\npresented in Table 2. According to these results, the dif-\nferences in ages between all comparison groups were sta-\ntistically significant ( p < 0.001). There was no significant\ndifference in E2 levels between Group III and Group I ( p\n= 0.072). There was a statistically significant difference\nin E2 levels between Group III and Group II ( p < 0.001).\nThere was a statistically significant difference in E2 levels\nbetween Group I and Group II ( p < 0.001). Regarding Pg\nvalues, the differences between Group III and Group I, as\nwell as between Group III and Group II, were statistically\nsignificant ( p < 0.001). However, the difference between\nGroup I and Group II was not statistically significant ( p =\n0.463). For HTC values, the difference between Group III\nand Group I was statistically significant ( p = 0.002), as was\nthe difference between Group III and Group II ( p < 0.001).\nHowever, the difference in HTC values between Group I\nand Group II was not statistically significant ( p = 0.771).\nRegarding HGB values, the differences between Group III\nand Group I, as well as between Group III and Group II,\nwas statistically significant (p < 0.001). The difference be-\ntween Group I and Group II was not statistically significant\n(p = 0.423).\nThe differences in PLT between all comparison groups\nwere statistically significant ( p < 0.001).\nRegarding APTT values, the differences between\nGroup III and Group I, as well as between Group III and\nGroup II, were statistically significant ( p < 0.001). How-\never, the difference between Group I and Group II was not\nstatistically significant (p = 0.973).\nRegarding INR values, the difference between Group\nIII and Group I was not statistically significant ( p = 0.950).\nThe difference between Group III and Group II was sta-\ntistically significant ( p = 0.026). The difference between\nGroup I and Group II was not statistically significant ( p =\n0.714). For SGPT values, the difference between Group III\nand Group I was statistically significant ( p = 0.006). The\ndifference between Group III and Group II was statistically\nsignificant ( p < 0.001). The difference between Group I\nand Group II was statistically significant ( p = 0.007). Re-\ngarding TSH values, the difference between Group III and\nGroup I was statistically significant ( p < 0.001). The dif-\nference between Group III and Group II was not statistically\nsignificant (p = 0.052). The difference between Group I and\nGroup II was statistically significant ( p < 0.001).\nMyoma patients presented to the gynecology clinic\ndue to complaints of prolonged menstrual bleeding and dys-\nmenorrhea. During the transvaginal ultrasound (TVUS) ex-\namination, an intramural myoma was detected in 105 pa-\ntients, submucous myoma in 35 patients, and intramural\nand submucous myoma detected in 60 patients (Figs. 1,2).\nOvarian endometriosis was present in 105 of these patients.\nThese patients were operated on by gynecologists. Pathol-\nogy results were compatible with leiomyoma uteri (Fig. 3).\nThe hospital stay was for 2 days. In the postoperative\nperiod, surgical site infection developed in 6 patients and\nhematoma at the incision line in 3 patients. Hematoma\ndrainage was performed in only 1 patient. Surgical site\ninfection resolved with antibiotic treatment. During the\nfollow-up period, abdominal wall endometrioma developed\nonly in the patient who underwent intervention due to my-\nomectomy + ectopic pregnancy at the same time (0.5%).\nCharacteristics of the 3 groups are shown in Tables 3,4.\nFig. 1. Transvaginal ultrasonography of intramural myoma.\n4\n\n\nTable 3. Characteristics of patients.\nGroup I (n = 204) Group II (n = 204) Group III (n = 200) p\nPain\nY es (cyclic/non-cyclic) 202 (182/20) (99.0%) 0 (0.0%) 174 (87.0%) <0.001&\nNo 2 (1.0%) 204 (100.0%) 26 (13.0%)\nBleeding\nY es 0 (0.0%) 0 (0.0%) 120 (60.0%) <0.001&\nNo 204 (100.0%) 204 (100.0%) 80 (40.0%)\nMass in the abdominal/uterine wall\nAbdominal wall 204 (100.0%) 0 (0.0%) 1 (0.5%) <0.001&\nUterine wall 0 (0.0%) 0 (0.0%) 199 (99.5%)\nFrequent urination\nY es 0 (0.0%) 0 (0.0%) 16 (8.0%) <0.001&\nNo 204 (100.0%) 204 (100.0%) 184 (92.0%)\nRadiologic examination (Ultrasound-US)\nSuperficial US 204 (100.0%) 0 (0.0%) 0 (0.0%)\n<0.001&\nSuperficial implant 110 (53.9%) 0 (0.0%) 0 (0.0%)\nIntermediate implant 94 (46.1%) 0 (0.0%) 0 (0.0%)\nTransvaginal US 0 (0.0%) 0 (0.0%) 200 (100.0%)\nIntramural 0 (0.0%) 0 (0.0%) 105 (52.5%)\nSubmucous 0 (0.0%) 0 (0.0%) 35 (17.5%)\nIntramural + submucous 0 (0.0%) 0 (0.0%) 60 (30.0%)\nIntraabdominal endometriosis\nY es 11 (5.4%) 16 (7.8%) 28 (14.0%) 0.008&\nNo 193 (94.6%) 188 (92.2%) 172 (86.0%)\nLocation\nPosterior 0 (0.0%) 0 (0.0%) 168 (84.0%)\n<0.001&Other 0 (0.0%) 0 (0.0%) 32 (16.0%)\nRight 160 (78.4%) 0 (0.0%) 0 (0.0%)\nLeft 44 (21.6%) 0 (0.0%) 0 (0.0%)\nPathology\nLeiomyoma uteri 0 (0.0%) 0 (0.0%) 199 (99.5%)\n<0.001#Endometriosis 203 (99.5%) 0 (0.0%) 1 (0.5%)\nOthers (desmoid tumor) 1 (0.5%) 0 (0.0%) 0 (0.0%)\nComplication\nY es 1 (0.5%) 6 (2.9%) 9 (4.5%) 0.040&\nNo 203 (99.5%) 198 (97.1%) 191 (95.5%)\nRecurrence\nY es 9 (4.4%) 0 (0.0%) 0 (0.0%) <0.001#\nNo 195 (95.6%) 204 (100.0%) 200 (100.0%)\n&, Pearson Chi-Square test; #, Fisher-Freeman-Halton Exact Test.\nAbdominal wall endometrioma was detected in the\nphysical and radiological examination (superficial ultra-\nsound) (Fig. 4) of 204 patients who presented to our gen-\neral surgery clinic due to complaints of swelling and pain\nin the abdominal wall. Masses were on the right side of the\nincision line in 160 (78.4%) patients. In the superficial ul-\ntrasound of the patients, AWE was above the rectus fascia\nin 110 patients and at the level of the rectus abdominis fas-\ncia in 94 patients. In only 1 patient, the mass was localized\noutside the cesarean scar site. Wide excision was performed\nunder general anesthesia in 204 patients. The pathology of\n203 patients was evaluated as compatible with endometri-\noma (Fig. 5). The pathology result of the remaining 1 pa-\ntient was compatible with desmoid tumor. Postoperatively,\nonly 1 patient had a hematoma. She recovered with con-\nservative treatment. Repeat pregnancy was planned in 204\npatients after an average of 2.5 years. AWE recurred in 9 of\nthe patients in Group I during the follow-up period (4.4%).\nThese patients underwent repeat total excision.\nAbdominal wall endometrioma did not develop dur-\ning the follow-up period in our 204 patients (Group II)\nwho gave birth via cesarean section, although 16 of them\nhad ovarian and peritoneal endometriosis. No pathologi-\ncal findings were found in the subsequent follow-up of our\npatients in this group, who had an average of 3 births.\nTable 3: while 174 (87.0%) of the patients in Group\nIII had pain in the preoperative period, this rate was 202\n(99.0%) in patients who developed endometrioma after ce-\n5\n\nFig. 2. Transvaginal ultrasonography of submucous myoma.\nFig. 3. Microscopic appearance of intramural myoma. The\nwhite line marked with a white arrow in the image delineates the\nborder between the leiomyoma and the adjacent myometrium. En-\ndometrioma tissue is visible on the left side. The myometrium in\nthe lower right corner appears distorted due to pressure, while an\nintramural myoma is observed in the upper left corner. Scale bar:\n100 μm (H&E, hematoxylin and eosin, ×10).\nsarean section ( p < 0.001). There was no reported pain in\ncesarean section patients who did not develop endometri-\noma. In Table 3, 120 (60.0%) patients undergoing myomec-\ntomy reported bleeding, but there was no bleeding in any of\nthe other 2 procedures ( p < 0.001). A mass on the abdom-\ninal wall was detected in cases who developed endometri-\nTable 4. Prior surgeries.\nGroup I (n =\n204)\nGroup II (n =\n204)\nGroup III (n\n= 200)\nYES\nAppendectomy 11 (5.39%) 10 (4.90%) 7 (3.50%)\nCaserean 29 (14.21%) 35 (17.1%) 6 (3.0%)\nCholecystectomy 4 (1.96%) 3 (1.47%) 2 (1.0%)\nCystocele 3 (1.47%) 1 (0.49%) 2 (1.0%)\nRectocele 0 (0.0%) 1 (0.49%) 3 (1.5%)\nHemorrhoidectomy 7 (3.43%) 9 (4.41%) 3 (1.5%)\nThyroidectomy 2 (0.98%) 2 (0.98%) 3 (1.5%)\nInguinal hernia 0 (0.0%) 0 (0.0%) 5 (2.5%)\nOvarian abscess 0 (0.0%) 0 (0.0%) 1 (0.5%)\nOvarian cyst rupture 0 (0.0%) 1 (0.49%) 1 (0.5%)\nPeptic ulcus perforation 0 (0.0%) 0 (0.0%) 1 (0.5%)\nNO 148 (72.5%) 142 (69.6%) 166 (83.0%)\nFig. 4. Superficial ultrasonography of abdominal wall en-\ndometrioma.\noma after cesarean section and in 1 patient in Group III. Fre-\nquent urination was a complaint seen only in patients with\nmyoma. Frequent urination was observed in 16 (8.0%) of\npatients in Group III, while this problem was not reported\nin the other 2 groups ( p < 0.001) in Table 3. Transvaginal\nultrasound was used as a radiological diagnosis method in\npatients with myoma and abdominal ultrasound was used in\npatients with endometrioma. Intra-abdominal endometrio-\nsis was seen in 28 (14.0%) patients with myoma, 11 (5.4%)\nin cesarean section patients with endometrioma, and 16\n(7.8%) in normal cesarean section patients (Table 3). Al-\nthough there was more intra-abdominal endometriosis in\nmyomectomy patients, more endometriomas were detected\nin Group I (p < 0.001). In the cesarean section patients with\nendometrioma, 160 (78.43%) endometriomas were found to\nbe localized to the right of the cesarean section incision and\n44 (21.56%) to the left. Myomas were found to be located\n6\n\n\nFig. 5. Microscopic appearance of abdominal wall endometri-\noma. Arrows indicate ectopic endometrial tissue with preserved\ngland and stroma integrity within striated muscle and connective\ntissue. The rectus muscle is located in the upper right corner, while\nthe abdominal wall endometrioma is visible in the lower left cor-\nner. Scale bar: 100 μm (H&E, hemtoxylin and eosin, ×10).\nin the posterior part of the uterus in 168 (84.0%) patients\nand in other regions in 32 (16.0%) patients. Endometriosis\npathology was detected in 203 (99.5%) patients in Group I\nand only 1 (0.5%) patient in Group III ( p < 0.001). Com-\nplications such as wound infection and hematoma were re-\nported at a rate of 9 (4.5%) in myomectomy patients, 1\n(0.5%) in cesarean section cases with endometrioma, and\n6 (2.9%) in normal cesarean section cases ( p = 0.040). A\nrecurrence rate of 9 (4.4%) was detected only in Group I\nafter the operation ( p < 0.001).\nTable 4 shows the past surgical operations of the pa-\ntients for the 3 groups. No previous surgical interventions\nrelated to endometriosis were detected in any of the groups.\n4. Discussion\nEndometriosis is a gynecological disease marked by\nthe presence of endometrial tissue outside the uterus. This\ngrowth can be categorized based on location as either\npelvic, involving the uterosacral ligaments, ovaries, fallop-\nian tubes, and pouch of Douglas, or extra pelvic, affect-\ning areas such as surgical scars, groin, diaphragm, kidneys,\nliver, lungs, and pleura [10,11]. Sometimes endometrial tis-\nsue starts to grow on the skin [12]. There are 2 main types of\ncutaneous endometriosis: Primary (spontaneous) cutaneous\nendometriosis occurs when endometrial tissue implants into\nthe skin without any prior surgery or trauma in that area.\nIts etiology is not clear [ 13]. Secondary (scar) cutaneous\nendometriosis occurs when endometrial tissue is inadver-\ntently implanted into the skin during a surgical procedure,\nsuch as a cesarean section or episiotomy [ 12,13]. The most\ncommon symptoms of both types are cyclic pain, swelling,\nand the formation of nodules or lumps in the skin. Scar en-\ndometriosis occurs most commonly after cesarean section,\nat the corners of the Pfannenstiel incision line [ 14]. In their\nstudy, Ping Zhang et al . [ 14] found Pfannenstiel incision\nin 80% of their patients presenting with cesarean scar en-\ndometriosis. In our study, scar endometriosis was in the\nPfannenstiel incision line in 203 patients. It was localized\noutside the incision line in only 1 patient. The mean age of\naffected women varied from 20–43 years with an average\nof 31.0 years [ 4].\nThe prevalence of endometriosis worldwide is esti-\nmated to be between 10% and 15% [ 15]. Structural dif-\nferences of endometrioma cells arise from abnormalities in\ntheir location.\nIf endometrial cells settle outside the uterus, there is\nthe potential for them to lose their normal functions. These\ncells normally grow and shed in a cyclical manner within\nthe uterus. However, if they are located outside the uterus,\nthis cyclical change may be disrupted and lead to abnor-\nmal tissue growth. Factors affecting the development of\nendometriosis include conditions such as genetic predispo-\nsition, immune system disorders, hormonal imbalances (es-\npecially estrogen hormone), inflammation and infections\ndeveloping in the incision line [ 16]. Patients with en-\ndometriosis may have alterations in iron metabolism (serum\niron level, ferritin, transferrin saturation, total iron binding\ncapacity) due to chronic inflammation and menstrual blood\nloss [ 17]. Monitoring these markers of iron metabolism\ncan help healthcare providers assess iron status and make\nappropriate recommendations for supplementation or treat-\nment in patients with endometriosis. These factors lead\nto the formation of a pro-inflammatory environment that\nsupports the continued presence of endometriosis, which is\nclosely associated with the two primary symptoms of the\ndisease: pain and infertility. So far, no specific marker for\nendometriosis has been detected in peripheral blood or en-\ndometrium [18]. The markers used were analyzed together\nwith the patient’s clinical and radiological findings. Intra-\nabdominal endometriosis was present in 5.4% of our pa-\ntients who developed scar endometriosis (Group I), 7.8% of\nour patients who did not develop scar endometriosis (Group\nII), and 14% of our patients who underwent surgery for my-\noma (Group III). There was no significant difference in the\nperipheral blood picture of all 3 groups. Rather than spe-\ncific markers, the clinical and radiological findings of the\npatients were more significant during diagnosis.\nThe development of endometrioma in the abdominal\nwall can often be under the influence of estrogen as in our\nstudy. Group I has the highest average estrogen level 188.0\n(37.0–396.0) pg/mL (p < 0.001) as shown in Table 1. Also,\nit is known that platelets play an important role in the devel-\n7\n\nopment of endometriosis. Some substances released from\nthese cells prepare the environment for the development of\nendometriosis. In our study, PLT levels were found to be\nsignificantly higher in our Group I patients, as seen in Ta-\nble 1. As a result of these factors coming together, it is pos-\nsible for endometrial cells to proliferate outside the uterus\nand form an endometrioma.\nDue to the recent increase in cesarean deliveries, it\nhas been determined that there is an increase in the preva-\nlence of abdominal wall endometriomas. It has been shown\nthat the indication for cesarean section and surgical tech-\nnique are not factors contributing to the development of\nendometriomas, as they are not seen after every cesarean\nsection, although the risk of implantation is equal [ 4]. Our\nstudy also supports this situation. Only 204 of our 19,574\ncesarean section patients developed scar endometriosis.\nTherefore, other factors such as genetics, endocrine factors,\nor wound environment may be contributory. Therefore, the\nfactors determining the spread of endometrial cells and the\nformation of an endometrioma may differ among patients.\nThe incidence of abdominal wall endometrioma af-\nter cesarean section is very rare (0.03–1%) [ 19]. In our\nstudy it was 1.04%. Surgical technique, handling of tis-\nsue, the method of closing incisions, as well as the materi-\nals and sutures used, might affect implantation risk. Pa-\ntient demographics: some populations may have genetic\npredispositions that increase the likelihood of endometrio-\nsis, including abdominal wall endometriomas, due to dif-\nferences in hormonal receptor sensitivity or immune re-\nsponses [20]. V ariability in menstrual cycle characteristics,\nsuch as shorter cycles or heavier flows, could contribute to\nincreased incidences due to more aggressive endometrial\ngrowth and potential seeding during surgical interventions\n[20]. Abdominal wall endometriomas and intra-abdominal\nendometriomas are not usually seen together. However, in\nrare cases, both types of endometriomas can be found in the\nsame person. The probability of this situation occurring is\nvery low. In our study, 11 patients in Group I had scar en-\ndometriosis and intra-abdominal endometriosis at the same\ntime (5.4%).\nHowever, there is no clear explanation as to exactly\nwhy endometrioma occurs, and it is thought that it may be\nunder the influence of many factors. In a study by Ozel\net al. [ 19], it was recommended that specific cesarean de-\nlivery practices, including effective bleeding control, thor-\nough washing of the abdominal cavity prior to closure, and\nminimizing subcutaneous dead space by carefully bringing\ntogether wound edges, could potentially diminish the oc-\ncurrence of AWE. The average duration between the initial\nsurgery and the onset of AWE symptoms was found to be\n14.1 months (range 1 to 72 months). In our study, AWE\ndeveloped on average within 12–18 months after cesarean\nsection.\nAbdominal wall endometriosis typically presents with\na noticeable lump under the skin near a previous surgical\nscar, accompanied by increased pain and swelling during\nmenstruation. This condition is commonly characterized by\nmenstrual pain, especially in individuals who have under-\ngone cesarean section. If a palpable mass is found in the\narea of a surgical scar in conjunction with a history of ce-\nsarean section and menstrual pain, the diagnosis of abdom-\ninal wall endometriosis should be strongly considered [ 8].\nPing Zhang and colleagues [ 14] found that the most com-\nmon reason for admission of their patients was an abdomi-\nnal mass (98.5%) and accompanying cyclic pain in 87%. In\nour study, pain was cyclic in 182 of our patients (89.2%).\nTwenty of our patients described pain only with touch. Two\npatients with a scar endometriosis diameter of ≤2 cm did\nnot describe pain. Pain was more pronounced in our pa-\ntients with a larger scar endometriosis diameter.\nUltrasonography is the first-line diagnostic imaging\nmethod in the evaluation of abdominal wall abnormalities\n[21]. Three positions for abdominal wall endometrioma\n(AWE) have been identified based on its location relative to\nthe rectus abdominis muscle: superficial placement (above\nthe fascia of the rectus muscle), intermediate placement\n(at the level of the fascia of the rectus muscle), and deep\nplacement (below the fascia of the rectus muscle) [ 22]. In\nour study, AWE localized under the muscle was not de-\ntected. On ultrasound, AWE appears as a heterogeneous hy-\npoechoic mass with hemorrhagic and fibrous components\npresent.\nFine needle aspiration (FNA) cytology was deemed\nunnecessary due to clear clinical and radiological imaging\nfindings, along with the history of previous cesarean sec-\ntion, making the diagnosis of abdominal wall endometrio-\nsis well-documented. Confirmation of the diagnosis was\nachieved through histopathological examination of the sur-\ngical specimen. In 203 of our patients, the pathology re-\nsult was consistent with endometriosis. Desmoid tumor was\ndetected in only 1 patient. The standard treatment method\nis wide surgical excision [ 23]. Pharmacological treatment\nis palliative, and not effective in treating the disease com-\npletely.\nPing Zhang et al . [ 14], Rohit Nepali et al . [ 24],\nand Fatimah Alnafisah et al. [ 25], similarly managed their\ncases by performing surgical excision of the mass. The re-\nported risk of recurrence following surgery ranges from 5–\n9% [23]. Consequently, during the excision of the mass, it\nis essential to ensure at least 1 cm of surrounding tissue is\nremoved to reduce the likelihood of recurrence [ 26]. Re-\ncurrence was detected in 9 of our 204 patients with AWE\nafter the next caesarean section (4.41%). We re-operated on\nthese patients with clean surgical margins. In our patients,\nthe AWE diameter was between 1.87 and 4.3 cm. During\noperation, mesh placement was not deemed necessary to re-\npair the fascial defect. We did not have any patients who\ndeveloped a hernia.\n8\n\n\nThe malignancy risk of endometriosis in any re-\ngion is 1%. Malignant transformations of atypical well-\ndifferentiated endometriosis are indeed rare, with clear cell\ncarcinoma and adenocarcinomas being documented in the\nliterature [ 27,28]. No cases of cancer were identified in\nour study. In cases where malignancy does occur, around\n80% of them are associated with endometriosis in the ovary,\nwhile the remaining 20% are found in extra-gonadal sites,\nsuch as the abdominal wall [ 28].\nAnother reason for intervention in the uterine wall\nis the benign masses of the uterine wall called adeno-\nmyosis. Adenomyosis is the cause of 20–30% of hysterec-\ntomy surgery. Adenomyosis can arise directly from the\nextension of the basal layer of the endometrium into the\nmyometrium. Adenomyosis occurs when the endometrial\nglands extend into the myometrium, resulting in an ectopic\nlocation due to disruptions in the tissue barrier between the\nendometrial basal layer and the myometrium [ 29].\nEctopic localization can manifest as diffuse (adeno-\nmyosis) or focal (adenomyoma), impacting various areas\nof the uterus, with the posterior uterine wall frequently af-\nfected [29]. This occurrence may follow surgical curettage\nor placental invasion, potentially leading to additional dis-\nruptions and invasion of the endometrium. It is recognized\nas a type of endometriosis variant, with both conditions\nco-occurring in around 20% of individuals affected [ 16].\nThe most common symptoms of the disease are uterine ten-\nderness and enlargement, dysmenorrhea, menorrhagia and\ndyspareunia. In 168 of our 200 patients who underwent\nmyomectomy, the myoma was localized on the posterior\nwall. The incidence of the disease is higher in multiparous\nwomen as in our study [ 16].\nIn recent years, magnetic resonance imaging (MRI)\nand ultrasound have emerged as the preferred imaging tech-\nniques for diagnosing adenomyosis. Transvaginal ultra-\nsonography (TVUS) is particularly favored in gynecolog-\nical examinations because it enables a dynamic assess-\nment of organ mobility and position. Through both two-\ndimensional (2D) and two-dimensional (3D) configura-\ntions, as well as color flow Doppler technology, TVUS\nprovides a detailed view of the uterus and any associated\npathologies [ 16]. Additionally, it is more accessible and\ncost-effective compared to MRI.\nIn transvaginal ultrasound (TVUS), adenomyosis may\npresent as heterogeneous myometrium, cysts within the my-\nometrium, linear patterns within the myometrium, areas\nwith indistinct borders, unclear connection between the en-\ndometrium and myometrium, and thickening of the my-\nometrium [30,31]. V arious studies have reported sensitivity\nand specificity values for TVUS in diagnosing adenomyosis\nranging from 87.1% to 57.4% and 97.5% to 60.1%, respec-\ntively [16].\nAdenomyosis can be treated with uterus-sparing exci-\nsional techniques, which include complete excision of ade-\nnomyosis, known as adenomyomectomy, for cases of fo-\ncal adenomyosis (adenomyoma), and partial excision or cy-\ntoreductive surgery for more extensive cases, referred to as\ndiffuse adenomyosis.\nDuring surgery of adenomyotic lesions, they should\nbe carefully separated from the normal myometrium tissue\nto avoid damaging the normal myometrial tissues. There\nwas no widespread adenomyosis in our patients. There-\nfore, only total excision of myomas was performed through\ntransverse Pfannenstiel incision.\n5. Conclusions\nEndometriosis is a complex and often debilitating con-\ndition that affects a significant number of individuals world-\nwide, causing pain, infertility, and various quality-of-life\nissues. Despite significant research efforts, there remain\nsignificant gaps in our understanding of its etiology, pro-\ngression, and treatment outcomes. Although patients in\nGroups I and II (control group) underwent caesarean sec-\ntion, abdominal wall endometrioma developed in all pa-\ntients in Group I, but it was not detected in Group II. In\nGroup III, where myomectomy was performed, abdominal\nwall endometriomas developed only in a patient with an ec-\ntopic pregnancy.\nIt should be considered that conditions such as en-\ndometriosis and endometrioma are multifactorial and that\niatrogenic factors may play a role. During menstruation, en-\ndometrial cells migrate backwards from the fallopian tubes\nand leak into the pelvic cavity where they implant. Ge-\nnetic factors, especially the growth of these tissues sec-\nondary to excessive production of hormones such as estro-\ngen, immune system disorders allowing endometrial tissue\nto survive and grow outside the uterus, and incorrect surgi-\ncal techniques are important to understand the cause and ef-\nfect relationship. In our patients’ hematological tests, some\nvaluessuch as E2 and PLT count are high, as well as an in-\ncrease in insulin-like growth factor 1 (IGF-1) and a decrease\nin Caspase 3, supporting endometrioma formation. We are\ncontinuing our prospective study to determine the effect of\nIGF-1 on endometrioma formation.\nMore detailed prospective studies are needed to under-\nstand the pathophysiology of the disease and to identify risk\nfactors. Prospective studies are vital to assessing the long-\nterm effectiveness and safety of current and new treatments.\nThese studies can help determine which treatments work\nbest for specific patient groups, leading to more personal-\nized and effective care. The main limitation of our study\nwas that it was retrospective in nature and our resources\nwere limited.\nAvailability of Data and Materials\nThe datasets used and analyzed during the current\nstudy are available from the corresponding author on rea-\nsonable request.\n9\n\nAuthor Contributions\nNS: conception, formal analysis, investigation,\nmethodology, writing original draft in English, re-writing\nafter review and final edition, operations on patients, and\nobtaining Ethics Committee approval. SA: operations\non patients, data curation, interpretation of data and\nreview. Both authors contributed to editorial changes in\nthe manuscript. Both authors read and approved the final\nversion of manuscript. Both authors have participated\nsufficiently in the work and agreed to be accountable for\nall aspects of the work.\nEthics Approval and Consent to Participate\nThe study was carried out in accordance with the\nguidelines of the Declaration of Helsinki. Approval of\nthe present study was obtained from the institutional re-\nview board of University of Medipol, Medical Faculty\n(29.11.2023/E-10840098-772.02-7514). As some of the\npatients were illiterate, we obtained written consent from\ntheir relatives with the permission of the Ethics Review\nBoard. Thus, all subjects gave their informed consent for\ninclusion before they participated in the study.\nAcknowledgment\nWe would like to express our gratitude to the referees\nfor their suggestions and contributions. We would also like\nto thank Prof. Dr. Ozkan GORGULU, Head of the Depart-\nment of Biostatistics at Kırsehir Ahi Evran University, who\nmade the statistical calculations in this study.\nFunding\nThis research received no external funding.\nConflict of Interest\nThe authors declare no conflict of interest.\nReferences\n[1] Gentile JKDA, Migliore R, Kistenmacker FJN, Oliveira MMD,\nGarcia RB, Bin FC, et al. Malignant transformation of abdomi-\nnal wall endometriosis to clear cell carcinoma: case report. Sao\nPaulo Medical Journal. 2018; 136: 586–590. https://doi.org/10.\n1590/1516-3180.2017.0103300417.\n[2] Rindos NB, Mansuria S. Diagnosis and management of abdom-\ninal wall endometriosis: A systematic review and clinical rec-\nommendations. Obstetrical & Gynecological Survey. 2017; 72:\n116–122. https://doi.org/10.1097/OGX.0000000000000399.\n[3] Blanco RG, Parithivel VS, Shah AK, Gumbs MA, Schein M,\nGerst PH. Abdominal wall endometriomas. American Jour-\nnal of Surgery. 2003; 185: 596–598. https://doi.org/10.1016/\ns0002-9610(03)00072-2 .\n[4] Zhang J, Liu X. Clinicopathological features of endometriosis\nin abdominal wall–clinical analysis of 151 cases. Clinical and\nExperimental Obstetrics & Gynecology. 2016; 43: 379–383. ht\ntps://doi.org/10.12891/ceog2126.2016.\n[5] Masereka R, Kiyaka SM, Sikakulya FK. Endometriosis arising\nin a cesarean section scar: A case report. International Journal\nof Surgery Case Reports. 2022; 92: 106862. https://doi.org/10.\n1016/j.ijscr.2022.106862.\n[6] Nominato NS, Prates LFVS, Lauar I, Morais J, Maia L, Geber\nS. Caesarean section greatly increases risk of scar endometrio-\nsis. European Journal of Obstetrics, Gynecology, and Reproduc-\ntive Biology. 2010; 152: 83–85. https://doi.org/10.1016/j.ejogrb\n.2010.05.001.\n[7] Zondervan KT, Becker CM, Koga K, Missmer SA, Taylor RN,\nViganò P . Endometriosis. Nature Reviews. Disease Primers.\n2018; 4: 9. https://doi.org/10.1038/s41572-018-0008-5 .\n[8] Grigore M, Socolov D, Pavaleanu I, Scripcariu I, Grigore AM,\nMicu R. Abdominal wall endometriosis: An update in clini-\ncal, imagistic features, and management options. Medical Ul-\ntrasonography. 2017; 19: 430–437. https://doi.org/10.11152/mu\n-1248.\n[9] Morales Martínez C, Tejuca Somoano S. Abdominal wall en-\ndometriosis. American Journal of Obstetrics and Gynecology.\n2017; 217: 701–702. https://doi.org/10.1016/j.ajog.2017.07.\n033.\n[10] Audebert A, Petousis S, Margioula-Siarkou C, Ravanos K, Pra-\npas N, Prapas Y . Anatomic distribution of endometriosis: A\nreappraisal based on series of 1101 patients. European Journal of\nObstetrics, Gynecology, and Reproductive Biology. 2018; 230:\n36–40. https://doi.org/10.1016/j.ejogrb.2018.09.001.\n[11] Andres MP , Arcoverde FVL, Souza CCC, Fernandes LFC,\nAbrão MS, Kho RM. Extrapelvic endometriosis: A systematic\nreview. Journal of Minimally Invasive Gynecology. 2020; 27:\n373–389. https://doi.org/10.1016/j.jmig.2019.10.004.\n[12] Raffi L, Suresh R, McCalmont TH, Twigg AR. Cutaneous en-\ndometriosis. International Journal of Women’s Dermatology.\n2019; 5: 384–386. https://doi.org/10.1016/j.ijwd.2019.06.025.\n[13] Gonzalez RH, Singh MS, Hamza SA. Cutaneous endometriosis:\nA case report and review of the literature. The American Journal\nof Case Reports. 2021; 22: e932493. https://doi.org/10.12659/\nAJCR.932493.\n[14] Zhang P , Sun Y , Zhang C, Y ang Y , Zhang L, Wang N, et al .\nCesarean scar endometriosis: presentation of 198 cases and lit-\nerature review. BMC Women’s Health. 2019; 19: 14. https:\n//doi.org/10.1186/s12905-019-0711-8 .\n[15] Al Hoshan M S, Shaikh A A. A classical case of cesarean scar\nendometriosis in a 35-year-old woman presenting with cyclical\nabdominal pain: A case report. The American Journal of Case\nReports. 2023; 24: e940200-1. https://doi.org/10.12659/AJCR\n.940200.\n[16] Koninckx PR, Fernandes R, Ussia A, Schindler L, Wattiez A,\nAl-Suwaidi S, et al. Pathogenesis based diagnosis and treatment\nof endometriosis. Frontiers in endocrinology. 2021; 12: 745548.\nhttps://doi.org/10.3389/fendo.2021.745548.\n[17] Wyatt J, Fernando SM, Powell SG, Hill CJ, Arshad I, Probert\nC, et al . The role of iron in the pathogenesis of endometrio-\nsis: A systematic review. Human Reproduction Open. 2023; 3:\nhoad033. https://doi.org/10.1093/hropen/hoad033.\n[18] Sing SS, Taylor H, Giudice I, Lessey BA, Abrao MS, Kotarski\nJ, et al . Primary efficacy and safety results from two-double\nblind, randomized, placebo controlled studies of elagolix, an\noral gonadotropin-releasing hormone antagonist, in women with\nendometriosis-associated pain. Journal of Obstetrics and Gynae-\ncology Canada. 2017; 39: 401.\n[19] Ozel L, Sagiroglu J, Unal A, Unal E, Gunes P , Baskent E, et al.\nAbdominal wall endometriosis in the cesarean section surgical\nscar: A potential diagnostic pitfall. The Journal of Obstetrics and\nGynaecology Research. 2012; 38: 526–530. https://doi.org/10.\n1111/j.1447-0756.2011.01739.x.\n[20] Amer S. Endometriosis. Obsterics, Gynaecology & Reproduc-\ntive Medicine. 2008; 5: 126–133. https://doi.org/10.1016/j.og\nrm.2008.03.003.\n[21] Draghi F, Cocco G, Richelmi FM, Schiavone C. Abdominal wall\n10\n\n\nsonography: A pictorial review. Journal of Ultrasound. 2020;\n23: 265–278. https://doi.org/10.1007/s40477-020-00435-0 .\n[22] Goker A, Sarsmaz K, Pekindil G, Kandiloglu AR, Kuscu NK.\nRectus abdominis muscle endometriosis. Journal of the College\nof Physicians and Surgeons–Pakistan. 2014; 24: 944–946.\n[23] Bartłomiej B, Małgorzata S, Karolina F, Anna S. Caesarean scar\nendometriosis may require abdominoplasty. Clinical Medicine\nInsights. Case Reports. 2021; 14: 11795476211027666. https:\n//doi.org/10.1177/11795476211027666.\n[24] Nepali R, Upadhyaya Kafle S, Pradhan T, Dhamala JN. Scar\nendometriosis: A rare cause of abdominal pain. Dermatopathol-\nogy. 2022; 9: 158–163. https://doi.org/10.3390/dermatopatholo\ngy9020020.\n[25] Alnafisah F, Dawa SK, Alalfy S. Skin endometriosis at the cae-\nsarean section scar: A case report and review of the literature.\nCureus. 2018; 10: e2063. https://doi.org/10.7759/cureus.2063.\n[26] Tatli F, Gozeneli O, Uyanikoglu H, Uzunkoy A, Y alcın HC, Oz-\ngonul A, et al. The clinical characteristics and surgical approach\nof scar endometriosis: A case series of 14 women. Bosnian\nJournal of Basic Medical Sciences. 2018; 18: 275–278. https:\n//doi.org/10.17305/bjbms.2018.2659.\n[27] Taburiaux L, Pluchino N, Petignat P , Wenger JM.\nEndometriosis- associated abdominal wall cancer: A poor prog-\nnosis? International Journal of Gynecologic Cancer. 2015; 25:\n1633–1638. https://doi.org/10.1097/IGC.0000000000000556.\n[28] Ferrandina G, Palluzzi E, Fanfani F, Gentileschi S, V alentini AL,\nMattoli MV ,et al. Endometriosis-associated clear cell carcinoma\narising in caesarean section scar: A case report and review of the\nliterature. World Journal of Surgical Oncology. 2016; 14: 300.\nhttps://doi.org/10.1186/s12957-016-1054-7 .\n[29] Cullen TS. Adeno-Myoma Uteri Diffisum Benignum (pp. 133–\n157). Johns Hopkins Press: NY , U.S.A. 1897.\n[30] Koninckx PR, Ussia A, Adamyan L, Tahlak M, Keckstein J,\nWattiez A, et al . The epidemiology of endometriosis is poorly\nknown as the pathophysiology and diagnosis are unclear. Best\nPractice & Research. Clinical Obstetrics & Gynaecology. 2021;\n71: 14–26. https://doi.org/10.1016/j.bpobgyn.2020.08.005.\n[31] Mabrouk M, Raimondo D, Mastronardi M, Raimondo I, Del\nForno S, Arena A, et al. Endometriosis of the appendix: when to\npredict and how to manage-a multivariate analysis of 1935 en-\ndometriosis cases. Journal of Minimally Invasive Gynecology.\n2020; 27: 100–106. https://doi.org/10.1016/j.jmig.2019.02.015.\n11","source_license":"CC0","license_restricted":false}