The effect of endometriosis on the fertility of women

Endometriosis is defined by the presence of ectopic endometrial tissue outside the uterus, frequently located on pelvic organs such as the fallopian tubes and ovaries, and occasionally beyond the pelvic region. This condition manifests as dysmenorrhea, chronic pelvic pain, dyspareunia, and subfertility. Despite extensive research, the etiology and pathogenesis of endometriosis remain unclear, with laparoscopy being the definitive diagnostic method. The association between endometriosis and infertility has been extensively debated. Endometriosis can impair fertility by disrupting embryo implantation, altering hormone levels, and compromising oocyte quality. This literature review aims to examine the effects of endometriosis on female fertility. The review encompasses documents from clinical trials with control groups involving 196 to 22,416 reproductive-age participants (25-42 years), and case studies published over the past thirty-seven years from various regions (USA, Australia, Turkey, Africa, and Europe. Reputable databases such as BMJ, NEJM, Elsevier, AJR, Medline, and PubMed were utilized, with references compiled in the bibliography. A risk-benefit analysis indicates that up to 50% of women with endometriosis experience infertility. Consensus on treatment options remains elusive. The relationship between endometriosis and infertility is supported by studies of both fertile and infertile women, animal studies, donor sperm studies, and in vitro fertilization outcomes. Diagnostic methodologies based on endometrial changes are providing insights into potential mechanisms of infertility, especially in women with milder disease. However, clinical management of endometriosis-related infertility has not shown conclusive success beyond in vitro fertilization.

Endometriosis; Female fertility; Infertility; Diagnostic methodologies 1. Introduction Endometriosis is a prevalent condition characterized by the abnormal growth of endometrial cells outside the uterus. These aberrant growths are most commonly found in pelvic organs such as the ovaries, peritoneum, uterosacral ligaments, pouch of Douglas, and rectovaginal septum. Although rare, extra pelvic endometrial abnormalities can occur in locations such as the umbilicus and stomach. The presence of endometrial tissue in these areas can cause irritation, pain, and adhesions on the affected structures [23, 5]. World Journal of Biology Pharmacy and Health Sciences, 2024, 19(01), 320–331 321 Figure 1 Endometriosis locations [10] 1.1. Aetiology and Pathogenesis The etiology and pathogenesis of endometriosis remain largely unclear, although there is increasing evidence that it is a complex multifactorial disease with both genetic and environmental components contributing to its development [17].  Heritability: Individuals with a family history of endometriosis, particularly among first -degree relatives, are at a higher risk of developing t he condition [17, 9].  Retrograde menstruation flow: The most widely accepted theory for the pathophysiology of endometriosis suggests that endometrial cells are transported intra-abdominally from the uterine cavity through the fallopian tubes during menstr uation [6, 9]. Various risk factors may enable endometrial cells to survive in ectopic locations [6].  Adhesions: Surgical scar implantations may attach to endometrial cells, leading to the development of endometriosis [6].  Mu llerian metaplasia: This theory posits that coelomic epithelium transforms into endometrium -like cells [6, 9].  Lymph vascular emboli of endometrial cells: Endometrial cells may be transported to distant sites, such as the pleural cavity, through the lymphatic or circulatory systems [6].  Increased incidence of luteinized unruptured ovarian follicle syndrome (Trapped Oocyte): Patients with severe endometriosis and distorted pelvic anatomy exhibit a high rate of infertility, potentially due to abnormalities in oocyte development and tubal transport [6].  Early menarche or Late menopause: These complications may arise in response to hormonal changes during the menstrual cycle [1]. 1.2. Symptoms of Endometriosis Common signs and symptoms of endometriosis include [12, 5, 20]  Painful periods (Dysme norrhea): Pelvic pain and cramping may begin before and extend for several days into the menstrual period, often accompanied by lower back and abdominal pain.  Dyspareunia: Pain during or after sexual intercourse, which is a frequent symptom.  Pain with bowel movements or urination: These symptoms are most pronounced during menstruation.  Excessive bleeding: Patients may experience heavy menstrual periods or intermenstrual bleeding.  Infertility: Defined as the inability to conceive after one year (or more) of unprotected sexual intercourse. 1.3. Use of the Endometriosis Fertility Index The Endometriosis Fertility Index (EFI) is a tool designed to predict the likelihood of achieving pregnancy following surgery. Its utility is assessed for forecasting the capacity to conceive without assisted reproductive technology (ART) after laparoscopic surgery. A study conducted in France from 2013 to 2016 involved 196 infertile patients to evaluate the effectiveness of the EFI [3]. World Journal of Biology Pharmacy and Health Sciences, 2024, 19(01), 320–331 322 Figure 2 Endometriosis Fertility Index [11] The study population met the following criteria: 1.4. Criteria for Study Inclusion Participants in the study met the following criteria:  Infertility persisting for over 12 months  Presence of asymptomatic pelvic pain, dysmenorrhea, and/or deep dyspareunia  Normal or abnormal hysterosalpingogram results  Normo-ovulation or failure to conceive after three cycles of superovulation, with or without intrauterine insemination (IUI), used as first -line therapy for unexplained infertility  Laparoscopic diagnosis of endometriosis  Partner’s semen classified as normal according to World Health Organisation (WHO) criteria [3] 2. Results Among the 196 infertile women who underwent laparoscopic surgery for endometriosis -related infertility, the study yielded the following outcomes:  9 women (4.6%) were lost to follow -up.  26 women (13.2%) with an EFI score of 4 were referred directly to ART .  56 women (28.9%) with EFI scores of 5–6 received non-ART management for 3–6 months.  114 women (58.2%) with EFI scores of 7 or higher received non-ART management for up to 12 months.  73 women (37.2%) achieved pregnancy through non -ART management:  18 women (32.1%) had EFI scores of 5–6.  55 women (48.2%) had EFI scores of 7. The mean time to conceive for women with EFI scores of 5 –6 and 7 was 5.2 m onths (SD 2.8) and 3.9 months (SD 2.9), respectively [3]. World Journal of Biology Pharmacy and Health Sciences, 2024, 19(01), 320–331 323 In routine clinical practice, 149 women (76%) achieved pregnancy, with 37.2% after non-ART management and 38.8% after ART management. The 'baby take-home rate' was 57.1% [3]. The Endometriosis Ferti lity Index proved to be a valuable tool for predicting fertility outcomes in infertile patients undergoing surgery for endometriosis. Patients with a low EFI score should be promptly referred to ART to increase overall pregnancy rates [3]. 2.1. Effect of Endometriosis on Infertility 2.1.1. Endometriosis-Associated Infertility The prevalence of endometriosis is notably higher among women of Filipino, Indian, Japanese, and Korean descent [21]. Clinical manifestations of endometriosis vary based on the location of the ec topic endometrial tissue and can include dysmenorrhea, dyspareunia, chronic pelvic pain, and infertility, though some individuals may be asymptomatic. A significant challenge in the timely diagnosis and management of endometriosis is the lack of a clear correlation between symptoms and disease severity [21, 2]. Endometriosis is a leading cause of infertility through various mechanisms, although not all women with endometriosis experience difficulty conceiving [21, 2]. The primary mechanism involves altered anatomical structures. Pelvic adhesions impair oocyte release and ostial pickup, alter sperm motility, and affect myometrial contractions, leading to modified embryo transport and fertilization. Endometriosis can impact any stage of the reproductiv e process. Inflammatory cells in the peritoneal fluid and endometriomas have detrimental effects on oocytes, embryos, and sperm, impairing tubal function and reducing tubal mobility. This results in a lower fertilization rate in both natural and in vitro c ycles [8, 14]. Endometriosis negatively affects the physiology of granulosa cells, leading to increased apoptosis and altered steroidogenesis by decreasing aromatase expression. This causes an imbalance in estrogen production, resulting in lower estradiol concentrations during the preovulatory phase and at the LH surge. The follicular phase is prolonged in these patients, as the LH surge is delayed or biphasic, leading to altered postovulatory progesterone release, which may affect oocyte maturation [8, 21]. The impact of endometriosis on the endometrium is also significant. A 2012 study demonstrated that cells could migrate from ectopic endometrial implants back to the uterine endometrium. These migrating cells exhibit upregulation of the Wnt7A gene, which affects endometrial receptivity during the implantation window. The Wnt7A gene is associated with estrogen-mediated uterine development and implantation [14, 19]. Another important gene is Hoxa10, which is involved in endometrial regeneration. Women with e ndometriosis have lower levels of Hoxa10, potentially explaining the reduced implantation rates. Additionally, higher levels of matrix metalloproteinases, which cause persistent endometrial breakdown, and lower levels of αβ -integrin, which impair embryo attachment, further contribute to lower implantation rates [14]. 2.1.2. The Impact of Endometriosis on Early Embryo Morpho kinetics A study conducted in Turkey evaluated 82 In Vitro Fertilisation (IVF) cycles, including 53 cycles with endometriosis and 29 cycles with tubal factor infertility. A total of 439 embryos were assessed for embryo morpho kinetics [4]. The presence of endometriosis was confirmed through laparotomy or laparoscopy in 27 patients and via transvaginal ultrasonography (TVUSG) in 26 patients, given the high diagnostic accuracy of TVUSG (Savelli 2009). Post-laparoscopic surgery, the diagnosis of endometriosis was verified by expert pathologists. The study included patients with grade 3 – 4 endometriosis. The control group consisted of 30 women with l aparoscopically confirmed tubal factor infertility undergoing their first IVF attempt, with no evidence of endometriosis or hydrosalpinx at the time of laparoscopy. Clinical pregnancy was confirmed by the visualization of a gestational sac and foetal heart beat using TVUSG two weeks after serum Human Chorionic Gonadotropin (βhCG) measurement [4]. In all cycles, ejaculated spermatozoa were used. Exclusion criteria included women over 40 years of age, those with partners suffering from male factor infertility, individuals requiring preimplantation genetic diagnosis due to structural or numerical chromosomal errors, and patients with uterine anomalies or polycystic ovary syndrome [4]. The study's findings indicate that endometriosis significantly influences early morpho kinetic events and cell cycles [4]. World Journal of Biology Pharmacy and Health Sciences, 2024, 19(01), 320–331 324 Table 1 Embryo morpho kinetics data of the study and control groups, respectively [4] Study Group Control Group p-value No, of embryos 264 175 tPB2 6.51 ± 9.07 3.71 ± 1.98 p < 0.01 tPNa 12.50 ± 7.87 11.13 ± 174 p < 0.01 tPNf 25.90 ± 6.31 25.30 ± 7.87 NS t2 28.64 ± 5.24 28.25 ± 5.40 NS t3 38.02 ± 6.87 37.67 ± 6.33 NS t4 41.44 ± 7.35 40.19 ± 6.29 NS t5 50.51 ± 9.86 49.76 ± 10.41 NS t6 55.28 ± 10.14 53.77 ± 9.91 NS t7 58.11 ± 10.14 58.33 ± 10.28 NS t8 62.67 ± 11.80 61.45 ± 11.09 NS t9 71.57 ± 13.37 69.62 ± 1158 NS VP (tPNf-tPNa) 13.25 ± 6.23 14.87 ± 7.79 NS ECC1 (tPb2-12) 22.19 ± 8.23 24.56 ± 5.66 p < 0.01 cc2a (t3-t2) 9.37 ± 5.08 9.42 ± 4.89 NS ECC2 12.87 ± 5.47 12.02 ± 4.73 NS FCC3 22.56 ± 9.4.6 22.03 ± 9.30 NS 52(t4-t3) 3.40 ± 5.31 2,53 ± 4,24 p z 0.01 S3(t8t5) 12.40 ± 9.20 12.59 ± 10.01 NS GQE (%) 78 ± 41,2 93 ± 25,3 p < 0.01 Values are shown as mean±SD. Differences between means were tested by t-test for equality of means. NS = not significant GQE = Good Quality Embryos Table 2 Differences in morpho kinetic data in contro l and study groups with respect to good and poor embryo quality [4] GOOD POOR Study group Control group p-value Study group Control group p- value No. of embryos 207 163 57 12 tPB2 7.12 ± 9.91 3.69 ± 1.98 p < 0.01 4.27 ± 4.24 3.89 ± 1.96 NS tPNa 12.88 ±- 8.56 11.15 ±- 3.76 p < 0.05 11.10 ± 4.35 10.79 ± 3.48 NS tPNf 25.51 ± 6.46 25.99 ± 8.11 NS 27.29 ± 5.53 26.05 ± 3.36 N5 t2 27.85 ± 3.76 28.22 ± 5.49 N5 31.47 ± 8.12 28.60 ± 4.07 NS t3 37.10 ± 6.19 37.63 ± 6.20 NS 41.31 ± 8.15 38.07 ± 8.20 N5 t4 40.40 ± 6.60 40.03 ± 5.90 NS 45.18 ± 8.66 42.35 ± 10.36 NS t5 50.43 ± 10.04 49.23 ± 9.24 N5 50.75 ± 9.25 56.74 ± 19.83 NS t6 55.04 ± 10.17 53.54 ± 8.82 NS 56.46 ± 10.02 56.82 ± 19.82 NS World Journal of Biology Pharmacy and Health Sciences, 2024, 19(01), 320–331 325 t7 58.11 ± 10.12 58,32 ± 10.28 NS 58.25 ± 11.36 ND t8 62.66 ± 11.83 61.45 ± 11.09 N5 ND ND t9 71.56 ± 13.37 69.62 ± 11.57 NS ND ND VP (tPNf - tPNa) 12.61 ± 6.41 14.83 ± 7.96 p < 0.05 15.69 ± 4.82 15.26 ± 5.15 NS ECC1 (tPb2- t2) 21.18 ± 8.10 24.51 ± 5.75 p < 0.01 26.10 ± 7.60 25.15 ± 4.20 NS cc2a (t342) 9.24 ± 5.04 9.41 ± 4.77 NS 9.84 ± 5.23 9.47 ± 6.59 NS ECC2 12.54 ± 5.32 11.81 ± 4.45 NS 14.55 ± 6.01 15.40 ± 7.48 N5 ECC3 22.25 ± 9.46 22.02 ± 9.29 NS ND ND 52(t4-t3) 3.28 ± 5.18 2.40 ± 4.05 NS 3.87 ± 5.78 4.28 ± 6.20 NS 53(t8-15) 12.47 ± 9.17 12.58 ± 10.09 NS ND ND tPB2 7.12 ± 9.91 3.69 ± 1.98 p < 0.01 4.27 ± 4.24 3.89 ± 1.96 NS tPNa 12.88 ±- 8.56 11.15 ±- 3.76 p < 0.05 11.10 ± 4.35 10.79 ± 3.48 NS tPNf 25.51 ± 6.46 25.99 ± 8.11 NS 27.29 ± 5.53 26.05 ± 3.36 N5 t2 27.85 ± 3.76 28.22 ± 5.49 N5 31.47 ± 8.12 28.60 ± 4.07 NS t3 37.10 ± 6.19 37.63 ± 6.20 NS 41.31 ± 8.15 38.07 ± 8.20 N5 t4 40.40 ± 6.60 40.03 ± 5.90 NS 45.18 ± 8.66 42.35 ± 10.36 NS t5 50.43 ± 10.04 49.23 ± 9.24 N5 50.75 ± 9.25 56.74 ± 19.83 NS t6 55.04 ± 10.17 53.54 ± 8.82 NS 56.46 ± 10.02 56.82 ± 19.82 NS t7 58.11 ± 10.12 58,32 ± 10.28 NS 58.25 ± 11.36 ND t8 62.66 ± 11.83 61.45 ± 11.09 N5 ND ND t9 71.56 ± 13.37 69.62 ± 11.57 NS ND ND VP (tPNf - tPNa) 12.61 ± 6.41 14.83 ± 7.96 p < 0.05 15.69 ± 4.82 15.26 ± 5.15 NS ECC1 (tPb2- t2) 21.18 ± 8.10 24.51 ± 5.75 p < 0.01 26.10 ± 7.60 25.15 ± 4.20 NS cc2a (t342) 9.24 ± 5.04 9.41 ± 4.77 NS 9.84 ± 5.23 9.47 ± 6.59 NS ECC2 12.54 ± 5.32 11.81 ± 4.45 NS 14.55 ± 6.01 15.40 ± 7.48 N5 ECC3 22.25 ± 9.46 22.02 ± 9.29 NS ND ND 52(t4-t3) 3.28 ± 5.18 2.40 ± 4.05 NS 3.87 ± 5.78 4.28 ± 6.20 NS 53(t8-15) 12.47 ± 9.17 12.58 ± 10.09 NS ND ND With these discoveries, it is clear that endometriosis dominatingly influences the term of the early morpho kinetic occasions and cell cycles. 2.1.3. Oocyte Quality in Women with Endometriosis-Associated Infertility Endometriosis significantly impacts clinical markers of oocyte quality, which is a critical factor in reproduction. This study aims to evaluate the quality of oocytes in women with inferti lity related to endometriosis. The investigation involved infertile women of reproductive age, ranging from 29 to 40 years, who underwent IVF and Intra -Cytoplasmic Sperm Injection (ICSI) procedures. Participants were divided into three groups:  Group I: 50 patients with recurrent unilateral endometriomas World Journal of Biology Pharmacy and Health Sciences, 2024, 19(01), 320–331 326  Group II: 50 patients with unilateral endometriomas after surgical treatment  Control Group: 30 patients with tubal factor infertility Clinical and morphological assessments of oocyte quality were performed i n all IVF/ICSI cycles [16, 18, 20,22, 24]. Table 3 Baseline Characteristics of Women with Infertility [16] Characteristics Group I in = 501 Group II (n=50) Control group (n = 30) Age, years 3336 ± 45 32.64±4,2 31.73 ± 421 Infertility duration 4.6 ± 2_4 4.2 ± 2.1 33±2.6 AMH 2.2 ± 13 2.1 ± 1,8 3.0±1.8 The number of antral follicles in the affected ovary 4.1 ± 15 5.4± 13 125±2.9 (at both sides) The number of antral follicles in the intact ovary 72±2.6 7.8 ± 23 Total number of nocytes recovered 8.8 ± 3.9 9.2±3.2 10.1 ±6.8 The number of high -quality oocytes obtained (oocyte in metaphase II) 4.1 ± 2_0 5.2 ± 2.6 9.6 ±3..5 Table 4 Characteristic of patients with endometriomas [16] Size of endometriomas Group I (n = SO) Group II (n = 50) >10mm 18 (36%) 24 (48%) 10-20 mm 20 (40%) 18 (36%) 20-30 mm 8 (16%) 6 (12%) 30-40 mm 4 (8%) 1 (2%) The findings of the investigation indicate a statistically significant increase in the number of immature oocytes at metaphase I (MI) and the germinal vesicle (GV) stage in patients with endometriosis-associated infertility compared to the control group (p < 0.005). Additionally, there was notable degeneration of oocytes in patients with endometriomas exceeding 3 cm in diameter. These results suggest that endometriomas negatively impact oocyte quality, and that even after cystectomy, endometriomas continue to have a detrimental effect on the ovaries [16, 18, 20, 22, 24]. Therefore, it can be concluded that endometriomas, both before and after surgical intervention, adversely affect ovarian quality [16, 18, 20, 22, 24]. 2.2. Chronic Niche Inflammation in Endometriosis Development Chronic inflammation within the tissue niche, particularly in the peritoneal cavity, ovaries, and uterus, plays a crucial role in the development of endometriosis [13]. 2.3. Peritoneal Cavity The presence of peritoneal fluid in the peritoneal cavity results from the exudation of developing follicles and the corpus luteum. This fluid contains electrolytes, urea, steroidal hormones such as estrogen and progesterone, and other components like endometrial cells, macrophages, lymphocytes, and eryth rocytes. Some of these components have secretory functions; for instance, endometrial cells secrete glycodelin, and macrophages secrete cytokines and angiogenic factors [13]. Infertility in most cases of endometriosis is primarily due to chronic inflamma tion induced by the abnormal environment, such as the increased volume of peritoneal fluid. Significant changes in the immune system include the World Journal of Biology Pharmacy and Health Sciences, 2024, 19(01), 320–331 327 inhibition of T-cell-mediated cytotoxicity, decreased natural killer cell activity, and a rapid increase in pro-inflammatory cytokines and activated macrophages. These sudden changes create an oxidative and immunotolerant microenvironment conducive to endometriotic implantations [13]. Endometriotic implants secrete various substances, including estradiol, progest erone, monocyte chemoattractant protein (MCP)-1, transforming growth factor (TGF)-β, and vascular endothelial growth factor (VEGF). Additionally, pro- inflammatory cytokines such as interleukins (IL) -1, IL -6, and IL -8, and tumour necrosis factor alpha (TNF -α) are secreted. This mixture of secretions in the peritoneal fluid stimulates proliferative and angiogenic processes, contributing to the development and rapid progression of endometriosis [13]. The formation of endometriomas in the ovaries disrupts org an functionality and induces localized effects. The cystic fluid within endometriomas contains pro -inflammatory cytokines (IL-6 and IL-8), reactive oxygen species (ROS), TGF - β, and matrix metalloproteinases (MMPs). These components of cystic fluid alter th e surrounding tissue of nearby endometriomas, leading to decreased follicular density, increased fibrosis, and loss of cortical stroma. Caspase -3 immunostaining has revealed signs of atresia in early follicles in tissue biopsies from ovaries containing endometriomas [13]. TGF-β1 and ROS contribute to fibrosis and adhesion formation through the differentiation of myofibroblasts and the expression of profibrotic genes mediated by plasminogen activator inhibitor -1. The loss of ovarian stroma has a detrimental effect on follicle formation. Pathogenesis is marked by a reduced blood supply and depletion of specific growth factors that would normally be secreted by healthy stromal cells [13]. 2.4. Deep Infiltrating Endometriosis A retrospective cohort study was conducted to investigate the impact of previous surgery for endometriosis on assisted reproductive technology (ART) cumulative live -birth rates in patients with deep infiltrating endometriosis (DE). The study included 222 DE patients who underwent ART [7]. The diagnosis of DE was established based on strict imaging criteria and histological confirmation of the disease. Women with a prior history of surgery for endometriosis were included, and their ART outcomes were compared with those of patients without a history of such surgery [7]. The cohort selection process is detailed in Figure 3. From January 2008 to December 2016, a total of 222 DE patients underwent 440 ART cycles [7]. The patient characteristics are summarized in Table 4. It is noteworthy that in 1 49 cases (67.1%), DE was associated with ovarian endometrioma (OMA) lesions [7]. World Journal of Biology Pharmacy and Health Sciences, 2024, 19(01), 320–331 328 Figure 3 The process of the cohort selection [7] Table 4 provides detailed information on the patient characteristics and their ART outcomes. Figure 3 illustrates the cohort selection process, ensuring a comprehensive understanding of the study design and its findings [7]. World Journal of Biology Pharmacy and Health Sciences, 2024, 19(01), 320–331 329 Table 5 Patients’ characteristics in the general population (n = 222) [7] DE, deep infiltrating endometriosis; OSIS, endometriosis; OMA, endometrioma; FSH, follicle -stimulating hormone; AFC, antral follicle count; AMH, anti- Mu llerian hormone a Continuous data are presented as mean ± standard deviation; categorical data are presented as number (percentages). Abbreviation ART - Assisted Reproductive Technology DE - Deep infiltrating Endometriosis EFI - Endometriosis Fertility Index GV - Germinal Vesicle ICSI - Intra-Cytoplasmic Sperm Injection IL - Iinterleukins IUI - Intra-Uterine Insemination IVF - In Vitro Fertilisation LH - Luteinizing Hormone MCP - Monocyte Chemoattractant Protein MMPs - Matrix MetalloProteinases OMA - Ovarian Endometrioma ROS - Reactive Oxygen Species TGF - Transforming Growth Factor TNF-α - Tumor Necrosis Factor alpha TVUSG - Trans-Vaginal UltraSonography VEGF - Vascular Endothelial Growth Factor WHO - World Health Organisation World Journal of Biology Pharmacy and Health Sciences, 2024, 19(01), 320–331 330 βhCG - Human Chorionic Gonadotropin 3. Conclusion  Heterogeneity of Endometriosis: Endometriosis is a complex and heterogeneous disorder that affects various aspects of the reproductive cycle, including mechanical, molecular , and genetic factors.  Pathophysiological Factors Affecting Infertility: Several key pathophysiological factors contribute to infertility associated with endometrioma. Inflammatory changes in the peritoneal cavity can alter sperm -oocyte interaction. Distorted pelvic anatomy may impair oocyte release and utero -tubal transport. Additionally, ovarian endometriomas can adversely affect ovarian reserve and oocyte quality.  Impact of Pro -inflammatory Microenvironment: The pro -inflammatory microenvironment in the ectopic endometrium can alter endometrial resp onsiveness, further contributing to infertility.  Predictors of Reproductive Outcomes: While endometrioma is significantly associated with infertility, ovarian reserve status and response to ovarian stimulation are more critical predictors of reproductive o utcomes than the mere presence of endometrioma.  Individualized Treatment Approaches: In vitro fertilization (IVF) is the most effective treatment for infertility in endometriosis patients. However, treatment decisions should be individualized, considering the patient’s age, ovarian reserve, other causes of infertility, duration of infertility, and male factors.  Multidisciplinary Management: The management of patients with endometriosis -related infertility should involve a multidisciplinary team to address the complex and multifaceted nature of the disorder Compliance with ethical standards Statement of informed consent Informed consent was obtained from all individual participants included in the study.

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Nat Rev Endocrinol. 2014 May;10(5):261-75. doi: 10.1038/nrendo.2013.255. Epub 2013 Dec 24. PMID: 24366116. [23] Vercellini, P., Vigano ̀ , P., Somigliana, E. et al. Endometriosis: pathogenesis and treatment. Nat Rev Endocrinol 10, 261–275 (2014). https://doi.org/10.1038/nrendo.2013.255 [24] . Xu B, Guo N, Zhang XM, Shi W, Tong XH, Iqbal F, Liu YS. Oocyte quality is decreased in women with minimal or mild endometriosis. Sci Rep. 2015 May 29;5:10779. doi: 10.1038/srep10779. PMID: 26022105; PMCID: PMC4448226 Authors short Biography Roshika Nirmani Habarawa Batuwattage Fernando graduated from Riga Stradins University with a Doctor of Medicine (MD) degree in 2020. Currently working in the Diagnostics Radiology Department at Daugavpils Regional Hospital in Latvia.