{"paper_id":"36347398-fb41-4e37-9728-f7bdfc9abcdc","body_text":"162\nRevista Societăţii Române de Obstetrică și Ginecologie • Vol. LXXII • Nr. 4 • octombrie-decembrie 2024\nreview\nAndreea Rus1, Mihai Căpîlnă2, Ioana Hălmaciu3\n1. County Emergency Clinical Hospital Târgu-Mureș, Romania\n2. Department of Obstetrics and Gynecology, “George Emil Palade” University of Medicine, Pharmacy,  \nSciences and Technology, Târgu-Mureș, Romania\n3. Department of Radiology and Medical Imaging, “George Emil Palade” University of Medicine, Pharmacy, \nSciences and Technology, Târgu-Mureș, Romania\nCorresponding author:  Ioana Hălmaciu, e-mail: ioana.halmaciu@umfst.ro\nThe link between endometriosis and autoimmune \ndiseases: a myth or reality?\nABSTRACT\nBroadly speaking, endometriosis is defined as a chronic condition in which endometrial-like tissue grows outside of the uterus, \nprimarily affecting women of reproductive age. Although it can be asymptomatic, the main reasons for patients seeking \nmedical attention are pelvic pain and, most notably, infertility. Unfortunately, the diagnosis is often delayed, sometimes by as \nmuch as ten years. Recent theories suggest that there may be a link between endometriosis and autoimmune diseases such \nas Hashimoto’s thyroiditis, lupus or rheumatoid arthritis. In this literary review, we explore these possible connections, with a \nparticular focus on the demonstrated (or not) correlations between specific autoimmune conditions and endometriosis. Nu -\nmerous studies have examined this association, but, unfortunately, the results remain inconclusive. For example, only a few \nhave identified a clear and significant link between endometriosis and a particular autoimmune disease. Many of these studies \nare limited by small sample sizes, the lack of standardized diagnostic criteria, or retrospective study designs. Some genetic \nstudies have proposed the involvement of shared genes such as PTPN22 or specific HLA alleles, but the evidence in this area \nis also not yet robust. Still, there is general agreement that both endometriosis and autoimmune diseases involve immune \nsystem dysfunctions, particularly chronic inflammation and cytokine production. To gain a better understanding of the rela -\ntionship between these conditions, larger, prospective and well-controlled studies that follow patients over time are needed. \nIn the future, research may lead to the discovery of shared biological markers or the development of immunological therapies \ncapable of targeting both disorders.\nKeywords: endometriosis, autoimmune diseases, immunological factors\nREZUMAT\nÎn linii mari, definim endometrioza ca fiind o boală cronică în care ţesutul endometrial se dezvoltă în afara uterului, afectând \ncu predilecţie femeile aflate la vârsta fertilă. Deși poate fi asimptomatică, principalele simptome pentru care se prezintă paci -\nentele la medic sunt durerile pelviene și în special infertilitatea. Din păcate, diagnosticul este adesea întârziat chiar și cu zece \nani. Unele teorii recente susţin că ar putea exista o legătură între endometrioză și bolile autoimune, cum ar fi tiroidita Hashi -\nmoto, lupusul sau artrita reumatoidă. În acest review literar, analizăm aceste aspecte, dar mai ales ne focalizăm pe corelaţia \ndemonstrată dintre anumite boli autoimune și endometrioză. Există numeroase studii care au analizat această asociere, însă \nrezultatele sunt, din păcate, neconcludente. De exemplu, câteva cercetări au găsit o legătură clară și semnificativă între \nendometrioză și anumite boli autoimune, iar multe dintre ele sunt limitate de anumiţi factori, cum ar fi dimensiunile mici ale \neșantionului, lipsa unor criterii de diagnostic standard și designul retrospectiv al studiului. Alte studii genetice au propus im -\nplicarea anumitor gene comune, cum ar fi PTPN22 sau anumite alele HLA, dar dovezile nu sunt suficient de solide nici în această \nprivinţă. Totuși, putem ajunge la un acord universal că atât în endometrioză, cât și în bolile autoimune apar dereglări ale siste-\nmului imunitar, în special inflamaţia cronică și producţia de citokine. Pentru a înţelege mai bine legătura dintre aceste afecţiuni, \nar fi necesare studii mai mari, prospective și bine controlate, care să urmărească pacienţii pe termen lung. În viitor, cercetarea \nar putea conduce la descoperirea unor markeri biologici comuni sau la dezvoltarea unor terapii imunologice care să trateze \nambele afecţiuni.\nCuvinte-cheie: endometrioză, boli autoimune, factori imunologici\nIntroduction\nEndometriosis is a chronic medical condition in which \nendometrial tissue grows outside the uterus, affecting \napproximately 8-10% of women of reproductive age. It \ncommonly causes pelvic pain or infertility, although in \nmany cases it may remain asymptomatic (1-3). Despite its \nhigh prevalence, the condition is often underdiagnosed, \nwith many women waiting an average of 7 to 10 years \nbefore receiving a proper diagnosis (4).\nThe exact cause of endometriosis remains unknown, \nthough potential contributing factors include genetics, \nimmune system dysfunction, and retrograde menstru -\nation. It is believed that endometrial cells may change \ntheir direction, going backwards through the fallopian \n\n163\nobstetrica și ginecologia\nRus et al. The link between endometriosis and autoimmune...\ntubes, adhere to peritoneal surfaces, and begin to proli -\nferate wherever they end up, triggering an inflammation \nreaction in the abdominal cavity (5,6) . These cells are \nhormone-sensitive and respond to the cyclical hormonal \nchanges during menstruation, leading to inflammation, \npain, scarring and, more often, fertility issues. Symp -\ntoms vary depending on the location of the ectopic \ntissue but typically include pelvic pain, particularly \nsevere dysmenorrhea during menstruation as a hallmark \nsign. Many women also report pain during intercourse, \npainful urination and cyclic digestive discomfort. Addi -\ntionally, endometriosis is linked to heavy or irregular \nmenstrual bleeding, which can lead to complications \nsuch as anemia and chronic fatigue. One of the most \nconcerning issues is its well-documented association \nwith infertility, as studies suggest that up to 40% of \nwomen experiencing difficulty conceiving may have \nendometriosis (7), an alarming amount. \nOther symptoms like chronic fatigue, nausea, bloating \nand digestive problems, can further complicate diagno -\nsis, often mimicking other disorders such as irritable \nbowel syndrome.\nThe impact of endometriosis extends beyond phy -\nsical symptoms. Chronic pain can drastically reduce \nthe quality of life, interfering with a woman’s ability to \nwork, maintain social relationships and engage in daily \nactivities. Its persistent nature is also linked to increa -\nsed rates of anxiety, depression and emotional distress. \nMoreover, endometriosis places a substantial burden \non healthcare systems due to the need for frequent me -\ndical visits, surgeries, and long-term treatment plans. \nThe management typically requires a multidisciplinary \napproach involving pain control, hormonal therapies \nand, in severe cases, surgical interventions like lapa -\nroscopy or even hysterectomy.\nGiven these challenges, early diagnosis and appro -\npriate management are critical. Increasing awareness \nand improving access to healthcare resources may help \nreduce diagnostic delays and improve quality of life for \naffected individuals. Further research is also essential to \nbetter understand the underlying causes of the disease \nand to develop improved treatment options.\nAn equally important aspect is how endometriosis \nis diagnosed. The diagnosis generally relies on a com -\nbination of clinical history, physical examination and \nimaging studies. While transvaginal ultrasound is often \nthe first-line imaging method, magnetic resonance ima -\nging (MRI) has emerged as a valuable tool for confirming \ndiagnosis and assessing disease extent. MRI provides \nhigh-resolution images of pelvic structures and can accu -\nrately identify endometriotic lesions, including deeply \ninfiltrating endometriosis, ovarian endometriomas and \nrectovaginal nodules. Studies have shown MRI to have \na sensitivity exceeding 90% in detecting endometriotic \nlesions, making it increasingly useful, especially when \nultrasound findings are inconclusive, by offering better \nresolution and a broader field of view. Its multiplanar \ncapabilities allow for detailed mapping of the disease, \nwhich is essential for surgical planning and improving \npatient outcomes.\nResults \nFor the first time in history, in 1987, Gleicher was the \nfirst to propose that endometriosis might be classified \nas an autoimmune disease, noting that it fulfills many \ndiagnostic criteria: polyclonal B cell activation, immu -\nnologic abnormalities in T and B cell function, increased \napoptosis, tissue damage and multiorgan involvement (9).\nEpidemiological studies suggest a higher prevalence \nof autoimmune disorders among women with endo -\nmetriosis (10), pointing toward a shared mechanisms \nsuch as hormonal influences, systemic inflammation \nand genetic predisposition (11,12) . Sadly, the diagnosis is \noften delayed by up to 10 years from the onset of pelvic \npain (13). Autoimmune conditions frequently associated \nwith endometriosis are widely discussed in the scientific \nliterature due to their overlapping pathogenic features, \nprimarily involving immune dysregulation and chronic \ninflammation. Among these, Hashimoto’s thyroiditis, \nan autoimmune condition in which the immune system \nattacks the thyroid gland, leading to hypothyroidism, \nis commonly observed in women with endometriosis. \nSeveral studies have reported a significantly higher pre -\nvalence of Hashimoto’s disease in this patient population, \nsuggesting a possible immunological link between the \ntwo diseases. Chronic inflammation and the presence \nof autoantibodies are hallmarks of both conditions, \nwhich may account for their increased co-occurrence (14). \nMoreover, research has highlighted a distinct cytokine \nprofile, with significantly elevated production of IL-1 β, \nIL-6 and TNF- α in both endometriotic and endometrial \ntissues. These differences between tissue types indicate \na dysregulated cytokine environment in women with \nendometriosis, compared to healthy controls, mediators \nthat play a central role in the pathophysiology of both \nautoimmune thyroiditis (15) and endometriosis (16). \nSystemic lupus erythematosus (SLE), another well-\nknown autoimmune disorder characterized by wide -\nspread inflammation and immune dysfunction, is also \nmore commonly seen in women with endometriosis. \nThis may be due to overlapping immune dysregulati -\non, including abnormal T cell activity and cytokine \nproduction. SLE is marked by a hyperactive immune \nresponse, which may align with the mechanisms driving \nectopic endometrial growth (17). The chronic inflamma -\ntory environment, elevated autoantibody levels, and \nimmune complexes may contribute to the progression \nof both diseases, suggesting that immune modulation \ncould serve as a potential therapeutic target (18). Notably, \nboth SLE and endometriosis have been associated with \npregnancy complications such as miscarriage and in -\ntrauterine fetal demise (19).\nOne of the largest cohort studies, based on Taiwan’s \nNational Health Insurance Database and including over \none million participants, found a clear association betwe -\nen endometriosis and SLE, strengthening the case for a \nlink between the two (20) .\nRheumatoid arthritis (RA), a systemic autoimmune \ndisorder that primarily affects the joints but also in -\nvolves systemic inflammation, has also been linked to \nendometriosis. The connection likely stems from shared \n\n164\nRevista Societăţii Române de Obstetrică și Ginecologie • Vol. LXXII • Nr. 4 • octombrie-decembrie 2024\nreview\ninflammatory pathways, particularly involving cytokines \nsuch as TNF- α and IL-6, which are the core to the patho -\ngenesis of both diseases. Studies suggest that women \nwith RA are more likely to have endometriosis and vice \nversa. Research by Gogacz et al. (2021) found elevated \nlevels of IL-6 and TNF- α in patients with endometriosis \n– key markers also implicated in RA (21). Both diseases \nalso share associations with HLA  gene polymorphisms, \nindicating a potential genetic susceptibility (22).\nMultiple sclerosis (MS), a neuroinflammatory auto -\nimmune disease affecting the central nervous system, \nhas also been linked to endometriosis in several epi -\ndemiological studies. Sinaii et al. (2002) showed that \nwomen with endometriosis are up to seven to 24 times \nmore likely to develop autoimmune diseases, including \nMS, compared to the general population (23) . While the \nphenotypes of these conditions differ, they share an \nunderlying autoimmune foundation. Macrophages, for \ninstance, play a critical role in the initiation and progres -\nsion of endometriosis by mistakenly promoting repair \nof ectopic endometrial tissue rather than clearing it. Si -\nmilarly, in MS, macrophages contribute to pathogenesis \nby attacking the myelin sheath and oligodendrocytes (24). \nMoreover, there is clear evidence confirming that both \ndiseases are characterized by systemic inflammation \nand immune dysregulation, including an elevated Th1/\nTh2 cell ratio and increased IFN- γ activity, factors that \nsuggest a potential link between them (25) . Nonetheless, \nthere is still limited evidence in the medical field expla -\nining the molecular, immunological, or defense mecha -\nnisms shared by these two conditions, and assessing \nthe common molecular pathways and their components \nmay help clarify the association between endometriosis \nand MS (26) .\nSome studies also explore a potential link betwe -\nen Sjögren’s syndrome and endometriosis. Sjögren’s \nsyndrome is an autoimmune disorder that primarily \naffects the exocrine glands, leading to dryness of the eyes \nand mouth. Research has shown a higher prevalence of \nSjögren’s syndrome among women with endometriosis. \nBoth conditions are associated with systemic inflamma -\ntion, autoantibody production, and immune dysfunction. \nA study by Dmowski et al. (1994) suggested that the two \ndiseases share a similar immune profile, with elevated \nlevels of anti-SSA and anti-SSB antibodies commonly \nfound in both (27) . Additionally, both endometriosis and \nSjögren’s syndrome involve dysregulated T cell activity \nand cytokine production, which may help explain their \nconnection. More recent studies further support the \nbidirectional relationship between endometriosis and \nSjögren’s syndrome, potentially driven by dendritic cell \nmaturation and fibrosis signaling pathways (28) .\nGastrointestinal symptoms such as bloating, con -\nstipation and diarrhea are commonly reported among \nwomen with endometriosis. Research also indicates a \nhigher prevalence of irritable bowel syndrome (IBS) \nand celiac disease in these patients. Sinaii et al. (2002) \nobserved that women with endometriosis often present \nwith gastrointestinal symptoms likely exacerbated by \nimmune-mediated intestinal inflammation (29). The over -\nlap between celiac disease and endometriosis may be \nexplained by shared immune dysfunction, particularly \ninvolving T cell activation and inflammatory cytokine \nproduction. Santoro et al. (2014), in their study on celiac \ndisease in Italian women with endometriosis, reported \na potential association between the two conditions, \nhighlighting an increasing trend in the prevalence of \nceliac disease among women affected by endometriosis. \nAlthough the results were not statistically significant (30), \nit is noteworthy that numerous studies in recent years \nhave explored this connection and yielded similar fin -\ndings (31,32) . The growing interest in this relationship stems \nfrom the shared characteristics of both celiac disease \nand endometriosis, particularly with respect to their un -\nderlying etiology and ongoing inflammatory processes.\nCommon pathogenic mechanisms between \nendometriosis and autoimmune diseases\nTo summarize the information presented above re -\ngarding each pathology, we first note the shared mecha -\nnism between endometriosis and autoimmune disea -\nses: immune system dysfunction. In endometriosis, the \nimmune system fails to eliminate ectopic endometrial \ntissue, leading to its persistence and proliferation outside \nits normal location. Similarly, autoimmune diseases are \ncharacterized by the immune system attacking autoan -\ntigens, causing tissue damage. Key immune dysfunctions \nobserved in both conditions include:\nn  Impaired natural killer (NK) cell function, leading to \ninadequate elimination of abnormal cells (33).\nn  Hyperactivation of macrophages, contributing to ex -\ncessive inflammatory responses (34).\nn  Dysregulation of T-helper (Th1, Th17) cells and regula -\ntory T cells (Tregs), resulting in chronic inflammation \nand immune imbalance (35) .\nSecondly, both pathologies are marked by chronic \ninflammation, a distinctive feature of both endometri -\nosis and autoimmune diseases. In endometriosis, the \nperitoneal fluid and ectopic lesions show elevated levels \nof inflammatory mediators, and, similarly, auto  immune \ndiseases, such as rheumatoid arthritis and systemic \nlupus erythematosus, are driven by persistent in  flam -\nmation. Chronic inflammation plays a central role in \nboth conditions. In endometriosis, this inflammation is \ncharacterized by increased cytokine levels and heighte -\nned macrophage activity in the peritoneal fluid, contri -\nbuting to the proliferation and implantation of ectopic \nendometrial cells. A study published in the Journal of \nReproductive Immunology  highlighted elevated concen -\ntrations of proinflammatory cytokines in the peritoneal \nfluid of endometriosis patients, such as interleukin-6 \n(IL-6) and tumor necrosis factor-alpha (TNF- α), which \ncan stimulate endometrial cell proliferation (36). Additi -\nonally, research has also shown increased macrophage \nactivity in the peritoneal fluid of women suffering from \nthis disease, with cells secreting growth factors and \ncytokines that promote the implantation and growth \nof endometrial lesions (37).\nCytokine imbalances also play a crucial role in both \nconditions, causing immune dysregulation and accelera -\n\n165\nobstetrica și ginecologia\nting inflammation. Specific cytokines involved include \nIL-17 and IL-23, both elevated in both endometriosis and \nautoimmune diseases, contributing to chronic activation \nof the immune system, TNF- α and IL-1 β, which promote \ninflammation and tissue destruction. Additionally, oxi -\ndative stress leads to cellular damage, DNA mutations, \nand perpetuates inflammatory responses (38).\nIn endometriosis, over time, multiple theories have \nemerged, one of which is the autoimmune theory. Emer -\nging evidence supports the hypothesis that endometri -\nosis may have an autoimmune component. Features of \nautoimmune diseases observed in endometriosis include \nthe presence of autoantibodies, such as anti-nuclear \nantibodies and anti-endometrium antibodies (39).\nAnother link between the two studied pathologies is \nthe genetic and epigenetic factors that contribute to the \ndevelopment of both endometriosis and autoimmune \ndiseases through shared genetic susceptibility, with \nspecific gene variants related to immune function and \ninflammation (e.g., HLA genes, IL-6, TNF genes). Family \nclustering suggests a hereditary predisposition to both \nconditions. Epigenetic changes, such as DNA methylation \nand histone acetylation, influence immune cell behavior \nand cytokine production.\nControversies and limitations of existing \nresearch\nA systematic review conducted in 2019 examined 26 \ncross-sectional, case-control and cohort studies pu -\nblished on the association between endometriosis and \nautoimmune diseases. The studies that quantified the \nassociation between endometriosis and multiple auto -\nimmune diseases generally had poor quality of evidence \ndue to a high risk of bias in most study designs and sta -\ntistical analyses. Only five of the 26 studies supported a \nstatistically significant association between endometri -\nosis and at least one autoimmune disease (40) .\nSince endometriosis is a potentially hereditary di -\nsease, several genetic studies have been conducted to \ninvestigate the association between autoimmune ge -\nnes and endometriosis (41). Among these studies, genes \nsuch as PTPN22  have been associated with rheumatoid \narthritis (RA) and, by extension, with endometriosis. \nAdditionally, HLA alleles, commonly associated with \nautoimmune diseases, have been reported in association \nwith endometriosis. However, these studies generally \nincluded small sample sizes, poorly defined ethnicities, \nand limited genotyping. It is important to note that \nthese autoimmune genes have not been reported in \nrobust, large-scale genome-wide association studies of \nendometriosis (42).\nRegarding the association between endometriosis and \nautoimmune thyroiditis (Hashimoto’s disease), a study \npublished in Gynecologic and Obstetric Investestigation \nin 2024 showed that, while higher rates of Hashimoto’s \nthyroiditis were found in women with endometriosis \ncompared to those without, and women with higher \nTSH levels, there was no significant impact on fertility \nand reproductive outcomes related to the coexistence \nof endometriosis and thyroid disease (43). Furthermore, \nregarding the association with systemic lupus erythema -\ntosus (SLE), studies have shown that women diagnosed \nwith endometriosis, regardless of whether they received \nsurgical treatment, did not show a statistically signifi -\ncant difference in the risk of SLE (44) .\nIn a controversial state, a Danish cohort study did not \nsupport the same association as the studies mentioned \nbefore. This study analyzed 9191 patients whose endome -\ntriosis was diagnosed by laparoscopy or laparotomy (45) , \nand no significant associations were found between \nendometriosis and SLE (standardized incidence ratio \n= 1.1; 95% CI; 0.6-2.1). However, the study did report a \nmodest increase in the risk of SLE.\nCurrent studies exploring the relationship between \nendometriosis and autoimmune diseases face several \nlimitations, which influence their results and validity. \nSome limitations include small sample sizes, which re -\nduce the statistical power of findings. A limited number \nof participants makes it difficult to generalize findings \nto the broader population, especially for identifying rare \nautoimmune diseases or associations with endometrio -\nsis. Another issue is the lack of consistent diagnostic cri -\nteria, as there is no universally accepted set of diagnostic \ncriteria for endometriosis or autoimmune diseases. This \ninconsistency between studies can lead to variability \nin how these conditions are identified, classified and \nevaluated, contributing to differing results and inter -\npretations in the literature. Many studies examining the \nrelationship between endometriosis and autoimmune \ndiseases are retrospective, relying on the review of past \nmedical data or patient records, which may introduce \nrecall bias and confounding factors. These studies often \nlack the control over variables that prospective studies \nwould provide, affecting the clarity of findings. On a \ndifferent note, most studies fail to account for other \npotential confounding factors such as environmental \nexposure, genetic predisposition, or hormonal influences \nthat may contribute to the development of autoimmu -\nne diseases and endometriosis, and these factors are \ncrucial for understanding the underlying mechanisms \nand potential interactions but are often not sufficiently \ncontrolled. Another limitation we were able to identify \nis the cross-sectional nature of many studies, meaning \nthey only capture the relationship between endometri -\nosis and autoimmune diseases at a single point in time, \nwhich limits the ability to establish causality or to track \nthe progression of both conditions over time.\nConclusions and future research directions\nCurrent studies suggest an association between en -\ndometriosis and various autoimmune diseases, such as \nsystemic lupus erythematosus, rheumatoid arthritis \nand autoimmune thyroiditis. These autoimmune con -\nditions occur more frequently in women diagnosed with \nendometriosis, suggesting a potential link between the \ntwo. However, most studies do not provide sufficient \nevidence to establish a direct causality between the \ntwo conditions, and much of the research is limited \nby factors such as small sample sizes and the lack of \nuniform diagnostic criteria.\nRus et al. The link between endometriosis and autoimmune...\n\n166\nRevista Societăţii Române de Obstetrică și Ginecologie • Vol. LXXII • Nr. 4 • octombrie-decembrie 2024\nreview\nAn important point is that immune dysfunctions ob -\nserved in endometriosis, such as immune cell activation \nand the production of inflammatory cytokines, may \ncontribute to the development of autoimmune diseases. \nIt is also possible that the presence of endometriosis may \nworsen or alter the course of preexisting autoimmune \nconditions. In this regard, it is proposed that endo -\nmetriosis and autoimmune diseases may interact in a \nbidirectional manner, with each condition influencing \nthe pathogenesis of the other.\nTo address the limitations of current studies, more \nresearch is needed with a more thorough and controlled \napproach. The first step should be to make sure future \nstudies are prospective and long-term, so that we can \ntrack the progress of patients with endometriosis and \nbetter understand whether these women are at a higher \nrisk of developing autoimmune conditions as they age. \nSuch a study design could provide valuable insights into \nrisk factors and help identify the critical moments when \nthese conditions might develop.\nAdditionally, to ensure consistency in future research, \nit is crucial that diagnostic criteria for both endometri -\nosis and autoimmune diseases are standardized. This \nwould make it easier to compare different studies and \nhelp avoid significant differences in how these conditi -\nons are diagnosed.\nAnother important direction is exploring the shared \nimmunological mechanisms between endometriosis and \nautoimmune diseases. In-depth studies of the immune \nresponse at the cellular level, particularly on how chronic \ninflammation and uncontrolled immune system activa -\ntion contribute to the progression of both conditions, \ncould lead to the identification of new biomarkers for \ndiagnosis and treatment. Furthermore, this research \ncould pave the way for novel immunomodulatory ther -\napies that could improve both endometriosis and auto -\nimmune diseases.\nLarge, well-designed cohort studies with confounding \ncontrol and mediation quantification, as well as genetic \nand biological studies, are needed to provide additional \ninsights into whether endometriosis is a risk factor for \nor a consequence of autoimmune diseases, and whether \nthese two types of disorders share pathophysiological \nmechanisms despite appearing independently. Such per -\nspectives could offer opportunities for the development \nof new nonhormonal drugs, such as immunomodulators, \nor the repurposing of existing immunomodulatory ther -\napies for endometriosis (46) .\nAlthough current research suggests a link between \nendometriosis and autoimmune diseases, many unresol -\nved questions remain. Future studies must address the \ncurrent limitations, include larger participant groups, \nand use standardized diagnostic methods to better \nunderstand the interaction between these conditions. \nIdentifying common mechanisms and developing tar -\ngeted therapies could have a significant impact on the \ntreatment of patients with concurrent endometriosis \nand autoimmune diseases.\nIn our opinion, the relationship between endometriosis \nand autoimmune diseases is an extremely important yet \ncomplex area of research that requires further studies \nto clearly understand the mechanisms linking them. It \nis evident that there is a correlation between the two \nconditions, and women with endometriosis seem to have \nan increased risk of developing autoimmune diseases. \nHowever, it is still challenging to establish a direct \ncausality, and research to date is limited due to small \nsample sizes, the lack of uniform diagnostic criteria, \nand the retrospective design of many studies.\nDespite these limitations, we believe that the existing \nstudies provide a promising direction for the future, es -\npecially regarding exploring the shared immunological \nmechanisms between endometriosis and autoimmune di -\nseases. Immune mechanisms such as chronic inflamma -\ntion and immune dysregulation may play a crucial role \nin the development of both conditions, and identifying \nnew biomarkers and immunomodulatory therapies co -\nuld significantly improve the available treatments.   n\nREFERENCES\n1. Ha HK, Lim YT, Kim HS, Suh TS, Song HH, Kim SJ. 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Obstet Gynecol . 2002;100(4):702-12.\nREFERENCES\nRus et al. The link between endometriosis and autoimmune...","source_license":"CC0","license_restricted":false}