Origin Theories of Endometriosis
Where does endometriosis come from?
There are several theories as to why and when endometriosis develops, although none have been proven definitively. Latest research demonstrates endometriosis lesions can be found in embryos thus highlighting that it can be laid down before birth.
- Crispi, S., Piccolo, M. T., D’avino, A., Donizetti, A., Viceconte, R., Spyrou, M., … & Signorile, P. G. (2013). Transcriptional profiling of endometriosis tissues identifies genes related to organogenesis defects. Journal of cellular physiology, 228(9), 1927-1934. https://doi.org/10.1002/jcp.24358
“Our group has recently described the presence of ectopic endometrium in a consistent number of human female foetuses analysed by autopsy, reinforcing the hypothesis that endometriosis may be generated by defects during the organogenesis of the female reproductive trait….These data support the theory that embryological defects could be responsible of the endometriosis generation.”
Why does it matter?
Many treatments (such as hysterectomy) are based on the oldest theory of the origins of endometriosis (Sampson’s theory) that menstrual blood backflows into the pelvis and once there attaches and grows. However, this retrograde menstruation occurs in most women but only around 10% develop endometriosis. In addition, endometriotic lesions have distinct characteristics from that of regular endometrial tissue from the uterus. Hysterectomy can be useful for diseases of the uterus, such as fibroids or adenomyosis, but may not put an end to endometriosis symptoms or progression. Endometriosis is complicated and no one has the definitive answer, but new studies are highlighting new information that can help guide further care.
Links:
Studies:
- Sourial, S., Tempest, N., & Hapangama, D. K. (2014). Theories on the pathogenesis of endometriosis. International journal of reproductive medicine, 2014. https://doi.org/10.1155/2014/179515
In this study, the different theories of the origins of endometriosis as well as contributing factors are discussed. The authors state that “The aetiology of endometriosis is complex and multifactorial, where several not fully confirmed theories describe its pathogenesis.” The topics discussed does not imply that they are necessarily the CAUSE of endometriosis, but that they may CONTRIBUTE to the proliferation and to the symptoms of endometriosis. The authors discuss:
- retrograde menstruation (“the oldest…theory proposes that endometriosis occurs due to the retrograde flow of sloughed endometrial cells/debris via the fallopian tubes into the pelvic cavity during menstruation [18]. However, retrograde menstruation occurs in 76%–90% of women with patent fallopian tubes and not all of these women have endometriosis.”)
- metaplasia (“residual embryonic cells of the Wolffian or Mullerian ducts persist and develop into endometriotic lesions that respond to oestrogen”)
- hormones (“Oestrogen is the driving force of endometrial proliferation and ectopic lesions may have an increased responsiveness to oestrogen, thus enhancing the development of endometriosis”)
- oxidative stress and inflammation (“accumulation of ROS may contribute to the propagation and maintenance of endometriosis and associated symptoms”)
- immune dysfunction (“women with endometriosis have higher expression of cytokines and vascular endothelial growth factors in their peritoneal fluid, which promote proliferation of endometrial cells and angiogenesis”)
- apoptosis suppression and alteration of endometrial cell fate (“inhibition of the apoptosis of endometrial cells may also be mediated by the transcriptional activation of genes that normally promotes inflammation, angiogenesis, and cell proliferation”)
- genetics (“different types of endometriosis may be associated with altering different gene clusters that regulate specific cellular functional aberrations”)
- stem cells (“due to their natural ability to regenerate, these stem cells may give rise to new endometriotic deposits”)
The theory of endometriosis being laid down during development of the fetus is evidenced in different studies:
- Crispi, S., Piccolo, M. T., D’avino, A., Donizetti, A., Viceconte, R., Spyrou, M., … & Signorile, P. G. (2013). Transcriptional profiling of endometriosis tissues identifies genes related to organogenesis defects. Journal of cellular physiology, 228(9), 1927-1934. https://doi.org/10.1002/jcp.24358
- Laganà, A. S., Vitale, S. G., Salmeri, F. M., Triolo, O., Frangež, H. B., Vrtačnik-Bokal, E., … & Sofo, V. (2017). Unus pro omnibus, omnes pro uno: a novel, evidence-based, unifying theory for the pathogenesis of endometriosis. Medical hypotheses, 103, 10-20. https://doi.org/10.1016/j.mehy.2017.03.032
- Signorile, P. G., Baldi, F., Bussani, R., Viceconte, R., Bulzomi, P., D’Armiento, M., … & Baldi, A. (2012). Embryologic origin of endometriosis: analysis of 101 human female fetuses. Journal of Cellular Physiology, 227(4), 1653-1656. https://doi.org/10.1002/jcp.22888
- Schuster, M., & Mackeen, D. A. (2015). Fetal endometriosis: a case report. Fertility and sterility, 103(1), 160-162. Retrieved from https://www.sciencedirect.com/science/article/abs/pii/S0015028214022274
Genetic associations with endometriosis can be seen the following studies:
- European Society For Human Reproduction And Embryology. “Genetic Link To Endometriosis – Unique Icelandic Study Provides Further Proof.” ScienceDaily. ScienceDaily, 5 March 2002. www.sciencedaily.com/releases/2002/02/020228073008.htm
“… among sisters there was a 5.2-fold increase in the risk of being diagnosed with endometriosis”
- Dun, E. C., Taylor, R. N., & Wieser, F. (2010). Advances in the genetics of endometriosis. Genome medicine, 2(10), 75. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2988445/#!po=0.609756
(This study composites several previous studies on the familial tendencies for endometriosis.)
“They found a sixfold increased risk for first-degree relatives of women with laparoscopically confirmed diagnosis of endometriosis. Moen and Magnus [14] conducted a large Norwegian study composed of 522 cases, which supported the findings of earlier studies looking at familial aggregation; 3.9% of mothers and 4.8% of sisters of affected individuals had endometriosis compared with only 0.6% of sisters in the control group. Interestingly, this Norwegian study [14] also concluded that symptom severity was increased among women who had relatives with endometriosis, a conclusion originally reported in a smaller study by Malinak et al. [12].”
- Nouri, K., Ott, J., Krupitz, B., Huber, J. C., & Wenzl, R. (2010). Family incidence of endometriosis in first-, second-, and third-degree relatives: case-control study. Reproductive Biology and Endocrinology, 8(1), 85. https://pubmed.ncbi.nlm.nih.gov/20618992/
“Endometriosis was found in 8/136 (5.9%) first-degree relatives of patients and in 4/134 (3.0%) first-degree relatives of controls in the real-case analysis”
- 23andMe. (2017). New genetic variants found to influence endometriosis risk. Retrieved from https://blog.23andme.com/23andme-research/endometriosis/
“…the study identified 19 genetic variants associated with endometriosis, and many of those variants are also associated with other serious health conditions such as ovarian cancer, cardiovascular disease and high cholesterol….In this case the study found several variants in genes involved in sex hormone metabolism, specifically the genes GREB1, FN1, KDR, CCDC170, ESR1, SYNE1, and FSHB.”
- Stefansson, H., Geirsson, R. T., Steinthorsdottir, V., Jonsson, H., Manolescu, A., Kong, A., … & Stefansson, K. (2002). Genetic factors contribute to the risk of developing endometriosis. Human reproduction, 17(3), 555-559. Retrieved from https://academic.oup.com/humrep/article/17/3/555/642154
“CONCLUSIONS: This is the first population-based study using an extensive genealogy database to examine the genetic contribution to endometriosis. A genetic factor is present, with a raised risk in close and more distant relatives, and a definite kinship factor with maternal and paternal inheritance contributing.”
- Rahmioglu, N., Montgomery, G. W., & Zondervan, K. T. (2015). Genetics of endometriosis. Women’s health, 11(5), 577-586. Retrieved from https://journals.sagepub.com/doi/pdf/10.2217/whe.15.41
“The heritable component of endometriosis has been illustrated by many different studies [2–4]. Higher rates of endometriosis among relatives of endometriosis cases compared with controls was shown, with risk ratio compared with general population risk for sisters estimated at 5.2 and for cousins 1.6 in a population-based study in Iceland [3]. In addition, in a hospital-based study in the UK, consisting of 230 women with surgically confirmed endometriosis in 100 families, familial aggregation of endometriosis was shown [4]. However, estimates of familial aggregation in human populations are likely to be affected – to an unknown extent – by the fact that endometriosis is only reliably diagnosed through laparoscopy. The chance of being diagnosed with endometriosis may be influenced by having a family member already diagnosed with disease and it is difficult to get an accurate population-based estimate of disease risk [5]. Stronger evidence of heritability is provided by twin studies, that have shown higher concordance in monozygotic twins compared with dizygotic twins, a finding less likely to be affected by selection biases operating on diagnostic opportunity [6,7]. The largest twin study, among 3096 Australian female twins, estimated the heritable component of endometriosis at 51%.”
- Sapkota, Y., Attia, J., Gordon, S. D., Henders, A. K., Holliday, E. G., Rahmioglu, N., … & Scott, R. J. (2015). Genetic burden associated with varying degrees of disease severity in endometriosis. Mhr: Basic science of reproductive medicine, 21(7), 594-602. Retrieved from https://academic.oup.com/molehr/article/21/7/594/2459755
“For the minimal disease, genetic factors may contribute to a lesser extent than other disease categories. Mild and moderate endometriosis appeared genetically similar, making it difficult to tease them apart. Consistent with our previous reports, moderate and severe endometriosis showed greater genetic burden than minimal or mild disease.”
- Hansen, K. A., & Eyster, K. M. (2010). Genetics and genomics of endometriosis. Clinical obstetrics and gynecology, 53(2), 403. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4346178/
“Studies have demonstrated the familial nature of endometriosis and suggest that inheritance occurs in a polygenic/multifactorial fashion. Studies have attempted to define the gene or genes responsible for endometriosis through association or linkage studies with candidate genes or DNA mapping technology. A number of genomics studies have demonstrated significant alterations in gene expression in endometriosis….A number of studies have demonstrated the familial clustering of endometriosis and that first-degree relatives of affected women are 5 to 7 times more likely to have surgically confirmed disease….Other findings support polygenic/multifactorial inheritance of endometriosis. First endometriosis that occurs in families tends to be more severe compared to sporadic cases. This suggests that there is more genetic propensity or liability in individuals with severe disease, and hence there is more likelihood to have affected sibs or offspring. Other factors which suggest a genetic predisposition to endometriosis include the similar and earlier age of onset of symptoms in affected families. Twin studies have demonstrated a higher concordance for endometriosis in monozygotic versus dizygotic twins, which suggested increased heritability….
“Another method used to investigate for gene mutations or polymorphisms associated with endometriosis involves gene mapping….A number of candidate genes have been evaluated for their association with endometriosis and include genes involved in inflammation, steroid-synthesis, detoxification, hormone receptors, estrogen metabolism, growth factors, adhesion molecules, apoptosis, cell-cycle regulation, oncogenes, other enzymes and metabolic systems. These studies have a priori defined the gene of interest which is then tested for association in a case-control or in a linkage study in individuals from an affected family. Most of these studies have failed to support or confirm an association between the candidate gene and endometriosis with a few interesting exceptions….
“Another gene mapping technique which holds promise in investigating the inheritance of endometriosis is Genome-wide Association scans. This is a very powerful, hypothesis free technique using single nucleotide polymorphisms (SNPs) to evaluate the genome for risk-associated variations….Further studies will help define these associations and determine the significant genes involved in the pathogenesis of endometriosis….
“Whereas genetics refers to the heritability of a trait, genomics refers to how genes are expressed….All of the cells in our bodies contain the same set of chromosomes with the same set of genes, the genome, but each differentiated cell type expresses only a fraction of the total available genes….angiogenic factors, growth factors, and hormone receptor genes are also up-regulated in the genomic studies. 18 Perhaps the most interesting aspect of the gene expression studies is the highlighting of the up-regulation of inflammatory response gene.25, 33 The inflammatory nature of endometriosis has long been recognized32; the genomics studies further advance the concept that aberrant communication between ectopic endometrial cells and immune system cells participating in the inflammatory response contribute to the development and persistence of endometriosis. 25, 34 Collectively, the studies cited above support the hypothesis that endometriosis is the result of abnormal expression or regulation of certain key genes.”
Staging and Categories of Endometriosis
Staging
So you’ve been told your endometriosis is a certain stage, but what does that mean?
The most widely used staging system for endometriosis, the American Society of Reproductive Medicine’s (ASRM), is based on how it affects fertility, not how it affects symptoms. Others systems of classification/staging focus on fertility or how the anatomy is affected (such as the Enzian classification for deep endometriosis, the endometriosis fertility index (EFI), and the American Association of Gynecological Laparoscopists (AAGL) classification) (Johnson et al., 2017). These do not take into consideration the biochemical effects of endometriosis (Imanaka, 2020). None of the systems “predicts pelvic pain, response to medications, disease recurrence, risks for associated disorders, quality of life measures, and other endpoints important to women and health care providers for guiding appropriate therapeutic options and prognosis” (Johnson et al., 2017, para. 3).
The ASRM’s classification system “classifies the disease as minimal (Stage I), mild (Stage II), moderate (Stage III) or severe (Stage IV)” based on a point system for how deep lesions go, the number of lesions, if cysts are on the ovaries, and adhesions (Khine, Taniguchi, & Harada, 2016, para. 12). A newer staging system called the endometriosis fertility index (EFI) “was developed…to predict fecundity after endometriosis surgery” and “could be useful as a clinical tool for counseling patients with endometriosis after surgery about their fertility prognosis and eventual need for fertility treatment” (Khine, Taniguchi, & Harada, 2016, para. 13).
None of these predict how you will respond to treatments or predict the symptoms experienced. Some will have Stage IV but have minimal symptoms. Others will have “minimal” disease but severe symptoms.
Endometriosis is divided into three main phenotypes: ovarian endometrioma (OMA), superficial peritoneal endometriosis (SPE), and deep infiltrating endometriosis (DIE). Here we’ll briefly discuss SPE and DIE.
Categories of Endometriosis
Superficial peritoneal endometriosis
Superficial peritoneal endometriosis (SPE) is defined as lesions less than 5 mm deep (Daly, 2018). Although superficial, SPE can cause moderate to severe symptoms as well as infertility (Reis et al., 2020). The appearance or staging of endometriosis does not reflect the biochemical mechanisms of endometriosis (Imanaka, 2020).
Deep Infiltrating Endometriosis
“Deep infiltrating endometriosis (DIE) represents 15 to 30% of endometriosis cases and is defined as endometriosis infiltrating the peritoneum by more than 5 mm. DIE is characterized by nodules infiltrating the rectosigmoid, uterosacral ligaments (USL), vaginal fornix, rectovaginal septum (RVS) and/or bladder.”
(Daly, 2018, para. 1)
(For reference, a millimeter is 0.039 of an inch. 5 mm would be about the length of a pencil’s eraser.)
DIE is associated with severe pain, and it has been noted to be important to resect (i.e. remove) these lesions in order to treat the pain (Yi, Leng, Lang, Ll, & Zhang, 2012). Your surgeon should be skilled and work with a multi-disciplinary team if DIE is present, because it can affect areas such as the bowel and ureters (Yi et al., 2012). Your surgeon should also know that ovarian endometriosis (or endometriomas) is associated with pelvic endometriosis and DIE, and should be prepared to address endometriosis in other areas as well (Exacoutos et al., 2018).
“Of the 177 DIE patients, 336 lesions were proved both histologically and laparoscopically as DIE lesions. The anatomical distributions of all DIE endometriotic lesions (number of patients, percentage) were as follows: bladder (5, 1.58%), uterosacral ligament (95, 67.08%), cul-de-sac (37, 12.02%), recto-vaginal septum (40, 12.66%), rectum and rectosigmoid junction (9, 2.85%) and ureter (12 lesions, 3.80%). Twenty-seven (67.5%) recto-vaginal septum lesions infiltrated deeply into the vaginal fornix. The 139 deeply infiltrating lesions on uterosacral ligaments (USL) included 29 on the left side, 37 on the right side and 73 were bilateral. The bladder was only anterior pelvic lesions in the DIE patients. While posterior pelvic lesions were more widespread and more severe in this group of DIE patients.”
(Yi et al., 2012, para. 15)
Ovarian Endometrioma
Endometriomas are a type of endometriosis found as a cyst on the ovary. It “contains thick, brown, tar-like fluid, which may be referred to as a ‘chocolate cyst'” (UpToDate, 2021). “Ovarian endometriomas are found in up to 44% of women with endometriosis, and are significantly associated with the presence of pelvic deep infiltrating endometriosis, ovarian adhesions, and pouch of Douglas obliteration” (Cranney, Condous, & Reid, 2017).
References
Cranney, R., Condous, G., & Reid, S. (2017). An update on the diagnosis, surgical management, and fertility outcomes for women with endometrioma. Acta obstetricia et gynecologica Scandinavica, 96(6), 633-643. Retrieved from https://obgyn.onlinelibrary.wiley.com/doi/full/10.1111/aogs.13114
Daly, S. (2018). Imaging in Endometrioma/Endometriosis. Medscape. Retrieved from https://emedicine.medscape.com/article/403435-overview#a1
Demco, L. (2000). Review of pain associated with minimal endometriosis. JSLS: Journal of the Society of Laparoendoscopic Surgeons, 4(1), 5. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3015350/
Exacoustos, C., De Felice, G., Pizzo, A., Morosetti, G., Lazzeri, L., Centini, G., … & Zupi, E. (2018). Isolated ovarian endometrioma: a history between myth and reality. Journal of minimally invasive gynecology, 25(5), 884-891. Retrieved from https://www.jmig.org/article/S1553-4650(18)30042-6/fulltext?fbclid=IwAR1yOvqvObWgpldiQ-VAwvju8uGNqQz0-edmbhZluYmDvTfanlCQJcniTEQ
Imanaka, S., Maruyama, S., Kimura, M., Nagayasu, M., & Kobayashi, H. (2020). Towards an understanding of the molecular mechanisms of endometriosis-associated symptoms. World Academy of Sciences Journal, 2(4), 1-1. Retrieved from https://www.spandidos-publications.com/10.3892/wasj.2020.53
Johnson, N. P., Hummelshoj, L., Adamson, G. D., Keckstein, J., Taylor, H. S., Abrao, M. S., … & Rombauts, L. (2017). World Endometriosis Society consensus on the classification of endometriosis. Human reproduction, 32(2), 315-324. Retrieved from https://academic.oup.com/humrep/article/32/2/315/2631390
Khine, Y. M., Taniguchi, F., & Harada, T. (2016). Clinical management of endometriosis-associated infertility. Reproductive medicine and biology, 15(4), 217-225. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5715862/
UpToDate. (2021). Endometriosis: Management of ovarian endometriomas. Retrieved from https://www.uptodate.com/contents/endometriosis-management-of-ovarian-endometriomas
Reis, F. M., Santulli, P., Marcellin, L., Borghese, B., Lafay-Pillet, M. C., & Chapron, C. (2020). Superficial peritoneal endometriosis: clinical characteristics of 203 confirmed cases and 1292 endometriosis-free controls. Reproductive Sciences, 27(1), 309-315. Retrieved from https://link.springer.com/article/10.1007/s43032-019-00028-1
Yi, D. A. I., Leng, J. H., Lang, J. H., LI, X. Y., & Zhang, J. J. (2012). Anatomical distribution of pelvic deep infiltrating endometriosis and its relationship with pain symptoms. Chinese medical journal, 125(2), 209-213. Retrieved from https://journals.lww.com/cmj/Fulltext/2012/01020/Anatomical_distribution_of_pelvic_deep.10.aspx
Endometriosis Overview
Endometriosis is an inflammatory disorder defined by the presence of glandular endometrial and stromal cells outside the uterine cavity (Becker, 2015). An estimated 11% of women have endometriosis with varying degrees of severity of symptoms and infertility; the severity of symptoms does not necessarily correlate with extent of lesions (McCance & Huether, 2014). Despite the high incidence of endometriosis, diagnosis is often delayed by 10 years due to symptoms being misdiagnosed or dismissed as normal menstrual cramps, by the lack of satisfactory biomarkers to diagnose, and by the definitive diagnostic standard being surgical visualization with histological confirmation (Ahn, Singh, & Tayade, 2017; Schliep, 2015). While endometriosis is a benign condition, it is related to higher incidence of ovarian carcinomas, autoimmune disorders, and cardiovascular disease (Kvaskoff, Mu, Terry, Harris, Poole, Farland, & Missmer, 2015).
Precipitating Factors
The cause of endometriosis is unknown, but it is likely to be multi-factorial, including environmental and genetic factors (Ashrafi, Sadatmahalleh, Akhoond, & Talebi, 2016). Being female is a significant risk factor as endometriosis is mainly seen in females; however, it has been in seen in men, usually those undergoing chemotherapy for prostate cancer (Jabr & Mani, 2014; Martin & Hauck, 1985). Several risk factors have been associated to be relational to endometriosis but not causative. Patient gravidity has been negatively associated with endometriosis with the thought that pregnancy provided suppression due to anovulation and amenorrhea as well as metabolic, hormonal, immune and angiogenesis changes (Maggiore et al., 2015). However, this lack of pregnancy can also be considered as a symptom as endometriosis is highly related to infertility with up to 50% of infertility cases being related to endometriosis (Dunselman et al., 2014).
A family history of endometriosis is also a risk factor, with one study reporting a rate of 56% of patients studied with endometriosis having a family history (Dun, Kho, Morozov, Kearney, Zurawin, & Nezhat, 2014). Some studies have reported the proportion of endometriosis cases due to genetic factors to be in the range of 52% (Rahmioglu, Nyholt, Morris, Missmer, Montgomery, & Zondervan, 2014; Chettier, Albertsen, & Ward, 2014). However, while multiple genetic aberrations have been identified, none have been proven conclusive enough to be a biomarker for endometriosis (Rahmioglu, Nyholt, Morris, Missmer, Montgomery, & Zondervan, 2014). One theory of the origin of endometriosis is Mullerian rests that allows for endometriosis to be laid down during fetal development and is associated with other Mullerian disorders (Acién & Velasco, 2013).
There is an increased risk of endometrial polyps with endometriosis (Wang, Zhang, & Liu, 2016; Zheng, Mao, Zhao, Zhao, Wei, & Liu, 2015). Evidence of similar pathologies, such as estrogen driven proliferation of tissue, between endometriosis and endometrial polyps are noted (Zheng, Mao, Zhao, Zhao, Wei, & Liu, 2015). This association with endometriosis and endometrial polyps is important in infertility (Galal, 2016). Other risk factors include early age of menarche, short menstrual cycles, long duration of menstrual flow, and defects in the uterus or fallopian tubes (Ashrafi, Sadatmahalleh, Akhoond, & Talebi, 2016).
Cellular Analysis
Endometriotic lesions on a cellular level are not the same as the endometrium as endometriotic lesions are capable of high estrogen production, high prostaglandin production, and have a resistance to progesterone (Cristescu, Velişcu, Marinescu, Pătraşcu, Traşcă, & Pop, 2013). This is important in the symptoms seen. The endometriotic lesions respond to estrogen which signals to increase lesion size, fluid volume, increased epithelial cell height, and epithelial cell proliferation (Burns, Rodriguez, Hewitt, Janardhan, Young, & Korach, 2012). However, the endometriosis lesions are capable of estrogen production, have decreased responsiveness to progesterone, can produce cytokines and prostaglandins, and are capable of angiogenesis and neurogenesis (Hey-Cunningham, Peters, Zevallos, Berbic, Markham, & Fraser, 2013; Reis, Petraglia, & Taylor, 2013; Bulun et al., 2012; Chaban, 2012). These capabilities of the endometriotic lesions are thought to be responsible for the symptoms noted with endometriosis.
The location of the lesions and the presence of adhesions can also affect the symptomology seen (Lu, Zhang, Jiang, Zou, & Li, 2014). Most symptoms arise from a chronic inflammatory state, noxious chemical release such as prostaglandins, musculoskeletal sequelae, and/or adhesions. An estimated 30-50% of patients with endometriosis are infertile due to the inflammatory environment and physical abnormalities such as adhesions (Koga, Yoshino, Hirota, Hirata, Harada, & Osuga, 2014).
Pain:
- Chronic pelvic pain:
Chronic pelvic pain is strongly associated with endometriosis (Donnelly & Yeung, 2015). Pain with endometriosis is related to increased inflammation, nociceptors, and noxious stimuli (Alvarez, Bogen, & Levine, 2014; McKinnon, Bertschi, Bersinger, & Mueller, 2015). Morotti, Vincent, Brawn, Zondervan, and Becker (2014) note higher nerve fiber production and density, increased neurotrophins, and the location of lesions in proximity to areas such as the bowel to be contributory to pain in endometriosis. These nerve fibers are found within and near the endometriotic lesions as well as in the peritoneum and endometrium of those with endometriosis (Fraser & Berkley, 2013). In patients with endometriosis, increased pro-inflammatory estrogen unchecked by antiinflammatory progesterone (due to progesterone resistance) has also been hypothesized to be problematic in endometriosis pain (Bruner-Tran, Herington, Duleba, Taylor, & Osteen, 2013; Cristescu, Velişcu, Marinescu, Pătraşcu, Traşcă, & Pop, 2013). The peritoneal fluid of endometriosis patients has been noted to have higher amounts of tumor necrosis factor-α, several interleukins, RANTES, monocytes, and prostaglandins (Aredo, Heyrana, Karp, Shah, & Stratton, 2017). Cristescu, Velişcu, Marinescu, Pătraşcu, Traşcă, and Pop (2013) describe an “overproduction of estrogen in endometriotic stromal cells with high local production of prostaglandins” (p. 95) as well as overproduction of prostaglandins PGE2 and PGF2-alpha not only in the endometriotic lesions but also in the uterus. Pain can be either cyclical or acyclical. Pelvic floor muscle dysfunction has been shown to be pathologic in pain with endometriosis patients (Raimondo et al., 2016). Most often hypertonicity of the pelvic floor is implicated in the musculoskeletal pain experienced (Aredo, Heyrana, Karp, Shah, & Stratton, 2017).
- Dysmenorrhea:
Dysmenorrhea is a classic signal for endometriosis. Erasmo and Ferrero (2015) state that “in patients suffering from dysmenorrhea, the incidence of endometriosis ranges from 40% to 60% and the 70% of adolescents who experience dysmenorrhea are diagnosed with endometriosis” (p. 63). Erasmo and Ferrero (2015) note the pain to be visceral and somatic. They also indicate that inflammation, prostaglandins, nerve growth factors, deep infiltrating lesions, and increased uterine contractility to be causes of dysmenorrhea in endometriosis (Erasmo & Ferrero, 2015).
- Intermenstrual pain
Pain between menstruations can be caused by the factors already mentioned of inflammation, nociceptors, noxious stimuli, and musculoskeletal dysfunctions.
- Pain during exercise
The location of the lesions, the presence of adhesions, and other factors such as pelvic floor dysfunction, trigger points, and muscles spasms can all factor into pain with exercise (Hartmann & Sarton, 2014; Aredo, Heyrana, Karp, Shah, & Stratton, 2017). High impact exercises can affect the tonicity of the pelvic floor. Adhesions can cause pulling sensations as well as musculoskeletal imbalances.
- Fatigue:
Pain is one factor leading to fatigue (Morotti, Vincent, Brawn, Zondervan, & Becker, 2014). Luisi et al. (2015) also noted hormonal alterations, chronic inflammation and impaired immune function as causes of fatigue in endometriosis.
- Menstrual:
- Premenstrual spotting:
Spotting for greater than two days prior to menstruation has been associated as a strong indicator for endometriosis (Heitmann, Langan, Huang, Chow, & Burney, 2014). Although hormonal and inflammatory alterations could play a part in spotting, in this case, the presence of an endometrial polyp is the most likely cause of spotting in this patient (Thubert, Demoulin, Lamazou, Rivain, Trichot, Faivre, & Deffieux, 2014).
- Menorrhagia
While dysmenorrhea is defined as a classic sign of endometriosis, menorrhagia is more often associated with conditions that frequently coexist with endometriosis. Adenomyosis, leiomyomas, and endometrial polyps are often comorbidities of endometriosis and have the primary symptom of menorrhagia (Habiba & Benagiano, 2016; Nezhat et al, 2016; Thubert, Demoulin, Lamazou, Rivain, Trichot, Faivre, & Deffieux, 2014). It may also be noted that polycystic ovarian syndrome is also frequently seen in endometriosis patients which can contradict this symptom (Likes & Lessey, 2014).
- Gastrointestinal:
- Dyschezia
Elevated prostaglandin levels within the peritoneal fluid are seen in patients with endometriosis, and these prostaglandins affect gastrointestinal motility (McAllister, Giourgas, Faircloth, Leishman, Bradshaw, & Gross, 2016). The irritation of the gastrointestinal tract from the cytokines released can also contribute to dyschezia, particularly seen if lesions are located within the posterior cul de sac (Avila, Filogônio, Costa, & Carneiro, 2016). Hypertonic pelvic floor muscles can contribute to the pain and spasms felt upon defecation (Preil, Belkin, & Goldstein, 2016).
- Bloating
The exact cause of the bloating experienced with endometriosis is unknown. Some contribute it to the inflammatory process while others cite the coexistence of irritable bowel syndrome; however, many patients experience gastrointestinal symptoms cyclically which might indicate the inflammatory and/or hormonal impact (Ek, Roth, Ekström, Valentin, Bengtsson, & Ohlsson, 2015). Ek, Roth, Ekström, Valentin, Bengtsson, and Ohlsson (2015) identify mast cells as possible contributors from the inflammatory spectrum, but they also point out that hormonal receptors in the gastrointestinal tract could also explain the symptoms.
- Alternating constipation/diarrhea
Again, prostaglandins and inflammatory markers are contributory to altered bowel function as is pelvic floor muscular dysfunction. Endometriosis on or near the bowel has been seen as contributory to bowel symptoms, even to the extent of bowel obstruction due to lesion growth (Ruffo et al., 2014).
- Urinary:
- Pain on micturition
While endometriosis of the urinary tract is rare, the most common site is the bladder (Knabben, Imboden, Fellmann, Nirgianakis, Kuhn, & Mueller, 2015). Estay et al. (2015) describes bladder symptoms as cyclical dysuria, dyspareunia, or resembling recurrent cystitis, and more rarely hematuria. Estay et al. (2015) described ureteral obstruction from endometriosis lesions presenting more as the loss of kidney function including anuria and hydronephrosis. Knabben, Imboden, Fellmann, Nirgianakis, Kuhn, and Mueller (2015) point out that bladder symptoms are usually symptomatic whereas ureteral are often not symptomatic. Again, irritation of the urinary tissue from the inflammatory markers described above can cause symptoms, particularly of the bladder. Endometriosis of the ureters would present more from obstruction due to lesion growth versus inflammation. In this case, endometriosis of the bladder would be suspected, however interstitial cystitis would need to be ruled out as it is frequently seen in endometriosis patients as well (Chen, Lee, & Wu, 2016).
- Examination:
- Tenderness with palpation
Tenderness can be due to pelvic floor muscular dysfunction and/or to lesion location (Yamamoto, Carillo, & Howard, 2014). Particularly tenderness is noted in the rectovaginal area, bladder, and close to the uterosacral ligaments in many patients with endometriosis (Nourmoussavi, Bodmer‐Roy, Mui, Mawji, Williams, Allaire, & Yong, 2014; Yamamoto, Carillo, & Howard, 2014; Williams et al., 2016). If a patient had been sexually active, the symptom of dyspareunia might also have been described. In addition to the contributory causes of inflammation, muscular dysfunction, and adhesions, Williams et al. (2016) also describe increased nerve bundle density noted in endometriosis patients with dyspareunia. This could also cause pain upon pelvic examination.
- Diagnostic laparoscopic findings:
- Glands and stroma in the pelvic cavity
Endometriosis is diagnosed by the visualization and preferably the histological confirmation of endometrial glands and/or stroma outside of the uterus (Cristescu, Velişcu, Marinescu, Pătraşcu, Traşcă, & Pop, 2013). Visually, endometriosis can vary from the clear, white, red, tan, and black colorations that may be very small to blister like formations to polypoid masses (Kondi-Pafitis, 2012). Kondi-Pafitis (2012) describes the histological presentation as “one or more endometrioid glands surrounded by stromal cells, resembling the endometrial stromal cells of the proliferative phase…. consistent with inactive or irregular proliferative endometrium, although typical proliferative or secretory changes may be observed” (p. 106). Kondi-Pafitis (2012) also notes that inflammatory cells and fibrosis may be present. An older study, but worth noting, performed by Demco (2000) utilized patients under conscious sedation to perform pain mapping of the lesions. The study found that the different colored lesions produced different amounts of pain, that the pain extended beyond the visible border of the lesion, and that palpation of the endometriotic lesions produced “cramps” (Demco, 2000). This information is important in understanding the symptomology and in treating the disease.
o Endometrial polyp
As noted previously, endometrial polyps are frequently seen with endometriosis (Wang, Zhang, & Liu, 2016; Zheng, Mao, Zhao, Zhao, Wei, & Liu, 2015). Estrogen driven proliferation of tissue is seen in endometrial polyps as well as endometriosis (Zheng, Mao, Zhao, Zhao, Wei, & Liu, 2015).
Medical Management
Pharmalogical
Hormonal: Balancing hormones is reasoned to be beneficial in alleviating symptoms; however, it does not rid the patient of the disease. Most efforts are concentrated on lowering estrogen in order to alleviate symptoms, particularly pain. Birth control pills, progestins, gonadotropin-releasing hormone antagonists, aromatase inhibitors, selective estrogen receptor modulators, and oral and intravaginal danazol are different hormonal therapies trialed to decrease symptoms and slow progression of the disease. However, some of these therapies have limited evidence and many have untoward side effects, so much so that some are only recommended if all other medical and surgical options fail (Tosti, Biscione, Morgante, Bifulco, Luisi, & Petraglia, 2016; Dunselman, et al., 2014; Brown & Farquhar, 2015). Also note that the resistance to progesterone seen in endometriosis lesions can cause some patients to be refractive to the effect of progestins (Cristescu, Velişcu, Marinescu, Pătraşcu, Traşcă, & Pop, 2013). In the following order, depending on patient tolerance, hormonal therapy could be trialed:
- Oral contraceptives: Oral contraceptives are useful for dysmenorrhea, reduction of pelvic pain, and reduction in the recurrence rate for endometriomas (ovarian cyst endometriosis) (Zorbas, Economopoulos, & Vlahos, 2015).
- Progestins (oral, intrauterine, injections): These can be useful for pain reduction (Gezer & Oral, 2015).
- Gonadotropin-releasing hormone analogs: These are as effective as other hormonal methods for endometriosis pain, but associated with a significant reduction in bone mineral density (Jeng, Chuang, & Shen, 2014). The most commonly prescribed is sold under the brand name Lupron, who recommends a lifetime maximum of 12 months of treatment (Lupron, n.d.).
- Danazol: Danazol is useful for decreasing pain and lowering inflammation (shown via a lowered CA-125) (Szubert, Suzin, Duechler, Szuławska, Czyż, & KowalczykAmico, 2014). However, danazol can have strong androgenic side effects (deepening of voice, facial hair growth) (Godin & Marcoux, 2015). Vaginally administered danazol might help decrease the pain and the nodule size in rectovaginal endometriosis (Godin & Marcoux, 2015).
- Aromatase inhibitors: These are only used if other hormonal methods and surgical therapies have failed but can be useful for pain (Hashim, 2014).
- Selective estrogen receptor modulators: Their effectiveness and safety are not established and have shown an increased risk for thromboembolism, vaginal dryness, rash and abdominal cramps (Chen, Zheng, & Wan, 2014).
Surgical
As discussed, surgical visualization is the definitive method for diagnosing endometriosis. Surgical intervention within the diagnostic surgery is preferable and is aimed at removing the endometriotic lesions. Surgical treatment can help prevent the reoccurrence of endometriosis without the use of hormones afterwards (Jovanovic, Dikic, Janković-Raznatovic, Savija, & Radaković, 2015). While ablation of endometriosis has been utilized extensively, newer data suggests excising the lesions may lead to a better long term outcome for patients. Ablation may or may not destroy the full thickness of the lesion while excision allows for better margins and provides samples for histological study.
A randomized, double-blind, five year follow up study concluded that surgical intervention was effective for at least up to five years and demonstrated that in some areas excision was more effective than ablation (Healey, Cheng, & Kaur, 2014). Excision is preferred in order for all tissue to be sent for histological review and confirmation (Dunselman et al., 2014; Donnelly & Yeung, 2015). Complete excision of deep infiltrating endometriosis has shown better outcomes versus incomplete surgical removal coupled with postoperative hormonal therapy (Angioni, Pontis, Dessole, Surico, Nardone, & Melis, 2015). Mackenzie (2015) suggests that excision be the standard of care for bowel endometriosis. Several other studies also suggest that excision is the preferable treatment method (Laganà, 2016; Alvarez, Giudice, & Levine, 2015; Koninckx, Donnez, & Brosens, 2016; Gingold & Falcone, 2016).
Other
- Dietary: Several dietary changes are suggested to alleviate symptoms. A diet rich in vegetables, fruit, and omega-3 fatty acids is recommended due to the oxidative stress created by the chronic inflammatory state (Gupta, Harlev, Agarwal, Al Safaar, Gupta, & Hack, 2015; Halpern, Schor, & Kopelman, 2015). Celiac disease has been connected with endometriosis through inflammatory markers and genetics and a gluten free diet has been shown to decrease painful symptoms (Santoro et al., 2014; Mormile & Vittori, 2013; Marziali, 2012). A study cites the role of inflammation and oxidative stress from endometriosis as factors leading to an increase in the risk of coronary heart disease in endometriosis patients, therefore a heart healthy diet would be beneficial as well (Mu, Rich-Edwards, Rimm, Spiegelman, & Missmer, 2016). A low fat diet is suggested as high fat consumption has been associated with increased inflammatory markers (Heard, Melnyk, Simmen, Yang, Pabona, & Simmen, 2016). Due to the frequent diagnosis of irritable bowel syndrome in endometriosis patients, a low FODMAPs diet is suggested (Moore, Gibson, & Burgell, 2014).
- Physical Activity: As noted, endometriosis patients can be susceptible to pelvic musculoskeletal disorders, so physical therapy with a women’s health qualified physical therapist would be beneficial (DeBevoise, Dobinsky, McCurdy-Robinson, McGee, McNeely, Sauder, & Sullivan, 2015). This might include retraining of the pelvic floor muscles to prevent spasms, reestablishing musculoskeletal balance, trigger point therapy, and other pain relieving modalities (dos Bispo et al., 2016). Yoga therapy has been shown to decrease menstrual pain and increase quality of life (Yonglitthipagon et al., 2017; Gonçalves, Barros, & Bahamondes, 2016).
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Does Endometriosis Cause Infertility? Covering the Basics
Table of contents
- Learn More About the Connections Between Endometriosis and Infertilit y
- What is Endometriosis
- Endometriosis and Fertility: Exploring the Connection
- What Happens When Endometriosis Does Cause Infertility?
- Other Data on Endometriosis and Reproduction
- Diagnosing Endometriosis: A Multifaceted Approach
- Managing Endometriosis: A Multidisciplinary Approach
- Dietary and Lifestyle Considerations
- Endometriosis and Pregnancy: Potential Complications
- Mental Well-Being and Psychological Impact of Fertility Treatment for Endo Patients
- Endometriosis and Fertility: Navigating the Journey
Learn More About the Connections Between Endometriosis and Infertility
An endometriosis (endo) diagnosis can be a frightening thing. Very frightening. While this inflammatory condition can be binary or non-binary, women of childbearing age are prone to issues with reproduction due to endo. So does endometriosis cause infertility? Keep reading as I break down the basics of this topic. In this comprehensive guide, I will delve into the complex interplay between endometriosis and fertility, exploring the condition’s impact, treatment options, and strategies to overcome potential obstacles on the journey to parenthood. I will also discuss the emotional impact of this condition on patients.
What is Endometriosis
Endometriosis is a chronic inflammatory condition. In this disease, endometrial-like lesions implant on tissues and organs throughout the abdomen and pelvis, even elsewhere in the body! These lesions contain glands and stroma, similar to the endometrium (the tissue that lines the uterine walls), causing chronic inflammatory reactions.
Endometriosis lesions produce many substances and even make their own estrogen, which, as a result, causes a variety of issues locally and systemically. Pain is one of the most common symptoms, though silent endo exists as well. Please continue reading this article to learn more about endometriosis.
Endometriosis and Fertility: Exploring the Connection
While endometriosis does not automatically equate to infertility, there is a well-documented association between the two. Approximately 30% to 50% of individuals with endometriosis experience fertility challenges, though the reasons behind this link are not fully understood. Several potential mechanisms have been proposed:
- Anatomical Distortions: Endometriosis can cause physical distortions in the reproductive anatomy, leading to scarring, adhesions, and obstructions in the fallopian tubes or ovaries, hindering the fertilization process.
- Inflammatory Response: The lesions can trigger an inflammatory response, creating an inhospitable environment for fertilization and implantation.
- Hormonal Imbalances: Endometriosis may disrupt the delicate hormonal balance required for ovulation and implantation, potentially impacting fertility.
- Egg Quality: Some research suggests that endometriosis may adversely affect egg quality, further complicating the conception process.
Despite these potential challenges, it’s important to note that more than 70% of individuals with mild to moderate endometriosis can conceive naturally, offering hope for those seeking to start a family.
What Happens When Endometriosis Does Cause Infertility?
It can. 25 to 50% of women with infertility have endometriosis, and 30 to 50% of women with endometriosis have infertility. However, it is very encouraging to know that most women with endometriosis can become pregnant.
This statistic is significant. Many younger women with this disorder feel psychological effects due to the possibility of not being able to have kids. Not all patients carry this sentiment. Growing numbers of people do not want to have children. However, for those who do, these thoughts and emotions about fertility can be devastating. Then, endometriosis patients who do conceive often worry about the pregnancy and subsequent delivery of the baby.
Other Data on Endometriosis and Reproduction
Studies have also demonstrated that the enzyme aromatase may also play a role in endometriosis and infertility. There is an abnormally high level of this enzyme in the endometrium and endometriosis lesions in patients with endometriosis. In the uterus, this enzyme may affect both natural endometrial development and its receptivity for the implantation of the fetus.
Progesterone is another hormone that may play a role in implantation failure. Resistance to this enzyme can affect reproduction, as it is necessary for a normal pregnancy. In some studies, progesterone receptors displayed abnormalities and caused dysregulation in the endometrial layer of the uterus in patients with endometriosis. Levels of progesterone should increase with pregnancy, but with endometriosis, this process is delayed and can cause an unopposed estrogen state that cannot sustain fertility.
Diagnosing Endometriosis: A Multifaceted Approach
Diagnosing endometriosis can be a complex process, as the symptoms can mimic those of other conditions. The diagnostic journey often begins with a physical examination and an evaluation of the individual’s medical history. If endometriosis is suspected, additional tests may be recommended, such as:
- Ultrasound: An abdominal or transvaginal ultrasound can help identify cysts (endometriomas), possibly endometriosis lesions (this is not common but an up-and-coming area of research), as well as the potential impact on the organs themselves or other abnormalities in the reproductive organs.
- Laparoscopy: Considered the gold standard for diagnosing endometriosis, a laparoscopy involves a minimally invasive surgical procedure where a small camera is inserted into the abdomen, allowing the surgeon to visually inspect the pelvic organs and take tissue samples if necessary.
While the severity of endometriosis is often classified into stages (minimal, mild, moderate, or severe) based on the extent and location of the endometrial growths, it’s important to note that the stage does not necessarily correlate with the intensity of symptoms or the degree of fertility challenges.
Managing Endometriosis: A Multidisciplinary Approach
The management of endometriosis typically involves a multidisciplinary approach, combining medical and surgical interventions tailored to the individual’s unique circumstances and fertility goals. Treatment options may include:
- Pain Management: Over-the-counter or prescription pain medications, such as non-steroidal anti-inflammatory drugs (NSAIDs) or hormonal contraceptives, can help alleviate the discomfort associated with endometriosis.
- Hormone Therapy: Hormonal treatments, such as birth control pills, progestin-only therapy, or gonadotropin-releasing hormone (GnRH) agonists, may have some impact on suppressing the growth of endometriosis and managing symptoms, though these options are only short-term while on the medications and can have some serious side effects.
- Surgery: Laparoscopic or robotic surgery is recommended to remove endometriosis, scar tissue, or cysts, potentially improving fertility outcomes.
- Assisted Reproductive Technologies (ART): In cases where natural conception remains challenging, assisted reproductive technologies like in vitro fertilization (IVF) or intrauterine insemination (IUI) may be recommended.
It’s crucial to work closely with a multidisciplinary team, including reproductive endocrinologists, gynecologists, and fertility specialists, to develop a personalized treatment plan that addresses both the management of endometriosis symptoms and the individual’s fertility goals.
Dietary and Lifestyle Considerations
While there is no definitive evidence that specific dietary or lifestyle changes can cure endometriosis or improve fertility outcomes, maintaining a healthy lifestyle can contribute to overall well-being and potentially alleviate some symptoms. Recommendations may include:
- Balanced Diet: Consuming a diet rich in fresh fruits, and vegetables, minimizing grains, especially gluten, and lean proteins can provide essential nutrients and support overall health.
- Exercise: Regular physical activity, such as low-impact exercises like walking or swimming, can help manage stress and promote overall well-being.
- Stress Management: Engaging in stress-reducing activities like meditation, yoga, or deep breathing exercises can help promote relaxation and reduce the impact of stress on fertility.
- Supplements: While the evidence is limited, some individuals report benefits from taking supplements for pain relief, reducing inflammation, and improving their quality of life.
It’s essential to consult with a healthcare professional before making significant dietary or lifestyle changes, especially if you are undergoing fertility treatments or considering assisted reproductive technologies.
Endometriosis and Pregnancy: Potential Complications
While endometriosis does not necessarily preclude a successful pregnancy, it’s important to be aware of potential complications that may arise. Some of the risks associated with endometriosis during pregnancy include:
- Placenta Previa: Endometriosis may increase the risk of placenta previa, a condition where the placenta partially or completely covers the cervix, potentially leading to bleeding and complications during pregnancy or delivery.
- Miscarriage: Research findings on the link between endometriosis and miscarriage have been mixed, with some studies suggesting an increased risk while others found no significant association.
- Ectopic Pregnancy: Endometriosis may increase the risk of ectopic pregnancy, where the fertilized egg implants outside the uterus, typically in the fallopian tube.
It’s essential to work closely with your healthcare provider to monitor and manage any potential complications that may arise during pregnancy if you have endometriosis.
Mental Well-Being and Psychological Impact of Fertility Treatment for Endo Patients
Living with endometriosis can be a challenging and emotionally taxing experience, particularly for those struggling with fertility issues. The physical pain, emotional distress, and potential financial burdens associated with treatment can take a toll on an individual’s mental well-being. It’s crucial to prioritize self-care and seek support from mental health professionals, support groups, or counseling services if needed.
Furthermore, you and your partner can do these things to help prepare for these possible feelings:
- Prepare and be ready for the emotional journey ahead.
- Cope with grief and loss associated with unsuccessful prior attempts or miscarriages.
- Develop strategies for coping with the news of other people’s births and pregnancies.
- Keep the communication lines between you and your partner open and discuss feelings throughout the entire process.
Endometriosis and Fertility: Navigating the Journey
The path to parenthood for individuals with endometriosis can be challenging, but it’s important to remember that fertility challenges are not insurmountable. By working closely with a multidisciplinary team of healthcare professionals, exploring various treatment options, and maintaining a positive outlook, many individuals with endometriosis can achieve their dream of starting a family.
It’s crucial to be proactive in seeking support and guidance from healthcare providers, as well as accessing resources and support networks specifically designed for those navigating endometriosis and fertility challenges. Organizations like the American Society for Reproductive Medicine (ASRM) and Endometriosis UK offer valuable information, resources, and advocacy support for individuals on this journey.
While endometriosis may present obstacles, embracing a comprehensive approach that addresses both the condition and fertility goals can increase the chances of a successful outcome. With perseverance, the right medical support, and a commitment to self-care, the dream of parenthood can become a reality for many individuals with endometriosis.
REFERENCES
https://www.pennmedicine.org/updates/blogs/fertility-blog/2016/august/endometriosis-and-fertility
https://www.endometriosis-uk.org/endometriosis-fertility-and-pregnanc
Updated: August 9, 2024
Endometrioma 101: Understanding Deep Ovarian Endometriosis
Table of contents
- Your Guide to Ovarian Endometrioma: Treatment, Symptoms, Doctors, Etc.
- What is Endometriomas (Deep Ovarian Endometriosis)?
- Recurrence of The Lesions Following Surgery
- Clinical Impact of Endometriomas (in Women of Reproductive Age)
- Major Concerns:
- Treatment and Surgery Options
- Final Thoughts and Question for Readers
Your Guide to Ovarian Endometrioma: Treatment, Symptoms, Doctors, Etc.
Endometrioma (deep ovarian endometriosis) can be difficult to treat due to controversies and challenges surrounding the best approaches, treatment, and diagnosis. Many of these hurdles result from misunderstandings about the condition and underlying disease process – deep ovarian endometriosis.
If you suffer from these ovarian endometriosis lesions, our sincere thoughts go out to you. Often known as “chocolate cysts,” some consider endometriomas as the most severe threat to a woman’s reproductive system (aside from cancerous tumors found in the reproductive tract). Furthermore, these lesions don’t always respond well to medical treatment and can potentially ruin the health of ovarian tissue. This article will help you understand endometrioma, symptoms, and deep ovarian endometriosis treatment.
What is Endometriomas (Deep Ovarian Endometriosis)?
Endometriomas happen when endometrial-like tissue grows inside the ovary or sometimes outside. Endometrioma is very common and affects between 17-44% of endo patients. Endometriomas are typically an advanced form of endometriosis, meaning stage three or four.
Surgery is often necessary to remove the endometriomas. However, eliminating endometrioma cysts and capsules is an advanced procedure and needs excellent skills. This surgery can potentially lead to partial or complete loss of ovarian function, especially if done by less experienced surgeons. These cystic masses can cause extreme challenges for women undergoing fertility treatments, i.e., assisted reproductive technologies (ART).
Endometriomas are dark-fluid-filled cavities, and they can present in a variety of shapes and sizes. An ultrasound can show suspected cases of endometrioma, but confirmation needs surgery and histology. Therefore, getting a diagnosis of endometrioma can be riddled with challenges.
Recurrence of The Lesions Following Surgery
On our social media accounts, we receive many questions about the topic of endometrioma recurrence. We took to Instagram to get the responses from endometriosis specialists about this recurrence. Here are some of their responses:
Dr. Jon Einarsson:
“It depends on several factors including the age of the patient, method of surgery, the experience of the surgeon, etc. In the literature, recurrence rates of over 30% have been reported, although I have personally not seen that high of recurrence risk.”
Dr. Abhishek Mangeshikar
“We’ve had ovarian recurrence rates of less than 10 percent in our two years of follow-ups of about 85 patients with ovarian endometriomas.”
“What’s important is to completely free the ovary and excise the peritoneum or uterosacral ligament it was adherent to, apart from excising the cyst. This will truly help reduce recurrence rates compared to just doing a cyst excision and leaving peritoneal disease behind.”
Dr. Ram Cabrera
“I share the same opinion, in my center, our recurrence rate is less than 8% a good technique and excision of all zone of endometrioma even peritoneal improve outcomes, also as previously said it depends on many factors like endometrioma size, multiple endometriomas, and post-op treatment.”
Dr. Gabriel Mitroi
“We have a very low recurrence rate. This is because often, during surgery, only the visible endometrioma cysts are removed. Anything under 2 cm is out of our visual field.”
Clinical Impact of Endometriomas (in Women of Reproductive Age)
Endometriomas does not cause infertility in all women it affects. However, studies show that between 25% to 50% of women with infertility have endometriosis, and 30% to 50% of women with endometriosis have infertility. However, that does not mean that endometrioma will necessarily cause infertility in women of reproductive age, especially when diagnosed and treated early with the best-practice treatments that have evolved over the years.
One of the leading fertility challenges is that ovarian lesions affect the number of eggs in ovarian tissue. Endometrioma can also impair the maturation of the egg and cause the woman to have a lower antral follicle count (AFC) and Anti-Müllerian hormone (AMH). Also, women with endometriomas often have high follicle-stimulating hormone (FSH) levels.
Major Concerns:
- Intense pelvic pain
- Possible infertility
- Decrease ovarian function
- It can place women of child-bearing age at a higher risk of cancer
Treatment and Surgery Options
Treatment for endometriomas will vary from person to person. The number of lesions and the staging of the disease progress are just a couple of the factors that will influence the right treatment plan for you.
Treatment for Females of Reproductive Ages
Many OB-GYNS and other healthcare providers still practice old treatments for endometriosis that don’t effectively manage the disorder. It’s a complicated condition. Thus, there are many myths and misconceptions about endometriosis.
Women of reproductive ages who wish to maintain fertility should have a fertility specialist in their multidisciplinary endometriosis team. Women with endometriomas may respond to some of the following treatments:
Non-surgical treatments: These treatment options are temporary choices to manage pain and complications in the short term.
- Medication therapy
- Observation
Surgical treatment: this may include:
- Drainage
- Laser ablation
- Capsule excision (the procedure of choice for most top experts)
Final Thoughts and Question for Readers
Have you had to deal with endometrioma? If so, please share how it has impacted your endo journey.
Endometriosis Myths & Facts: Dispelling the Misconceptions
Table of contents
- Debunking the Myths About Endometriosis & Exploring the Facts
- Overview of Endometriosis
- Why is it Difficult to Diagnose Endometriosis?
- Myth #1: Severe Period Pain is Normal
- Myth #2: A Hysterectomy Cures Endometriosis
- Myth #3: Endometriosis Only Affects the Pelvic Area
- Myth #4: Endometriosis Symptoms are Simply a “Heavy Period”
- Myth #5: Douching Causes Endometriosis
- Myth #6: Having an Abortion Can Cause Endometriosis
- Myth #7: You’re Too Young to Have Endometriosis
- Myth #8: Endometriosis Can Be Prevented
- Myth #9: Endometriosis is Always Painful
- Myth #10: Pregnancy is a Cure for Endometriosis
- Myth #11: Menopause Cures Endometriosis
- Myth #12: Hormonal Therapy Cures Endometriosis
- Myth #13: Endometriosis is Cancer
- Myth #14: Tubal Endometriosis Always Causes Infertility
- Myth #15: Endometriosis Symptoms Are the Results of Emotional Distress (It Is All in Your Head)
- We Want Your Input
Debunking the Myths About Endometriosis & Exploring the Facts
One in ten women worldwide is affected by endometriosis, also known as “endo,” for short. While this number is an estimate, the actual figures may be higher. Not only is the person with this inflammatory disorder affected, so are the family members and people around her due to the often debilitating effects of this disease. Endometriosis facts are important because it is complex and often misunderstood even though it’s a common disorder. Because of this, there are many myths and misconceptions regarding endometriosis prognosis, treatment, causes, symptoms, diagnosis, complications, etc.
Focusing on the disease itself often ignores the vicious cycles of stress, fatigue, pain, doctor visits, flare-ups, and loss of productivity experienced by the patient. These factors can lead to a decreased quality of life. Worse is that endometriosis facts come behind outdated treatment options, myths, and misconceptions about this disorder. It takes an average of eight to ten years for a patient to be diagnosed with endometriosis. One of the biggest problems with the misconceptions about endo is that they can prevent women from seeking treatment. Keep reading as we review endometriosis facts and debunk the myths.
Overview of Endometriosis
Endometriosis is a pelvic disorder characterized by endometriosis tissue similar but not the same as the tissue inside the uterus, growing elsewhere. Typically, the growth occurs outside the uterus, ovaries, fallopian tubes, cervix, the surface of the bladder, bowel, and distant organs.
Endometriosis growths can cause pain, scarring, and sometimes infertility. Pain from endometriosis is usually the result of menstrual bleeding from the tissues. Unlike the endometrium inside your uterus, blood that comes from endo tissue outside this organ has no means of escaping the body. This blood causes increased pressure and inflammation, which can result in pain that’s often debilitating. If you would like to learn more information about endometriosis, please read our introduction article, “Endometriosis 101: Covering the Basics.”
Why is it Difficult to Diagnose Endometriosis?
Studies show that it can take an average of seven years or more for a woman to get an endometriosis diagnosis. Why is this? Endometriosis signs and symptoms are often similar to other conditions, such as irritable bowel syndrome or pelvic inflammatory disease (PID). Therefore, it’s often mistaken for another illness. Furthermore, the myths and misconceptions we discuss below also prevent a lot of women from seeking help. For this reason, it’s crucial to get the endometriosis facts clear. Keep reading as we debunk the myths and state the facts.
Myth #1: Severe Period Pain is Normal
Nineteenth-century doctors were often perplexed by “women’s problems.” As a result, women were often discounted as being unstable mentally. While the attitudes and thoughts have improved since, some of those old beliefs persist, including those regarding period pain.
Many patients with endometriosis hear that their severe period pain is “normal.” Pain and cramping are normal during menstruation. However, the pain should not be so intense that it interferes with functioning or impacts the quality of life. If your period pain is so severe that you cannot carry out daily activities, you should seek an endometriosis expert.
Myth #2: A Hysterectomy Cures Endometriosis
Endometriosis growths are tissues “similar” to those inside of the uterus. It is not the same tissue. Simply removing the uterus and/or ovaries without excising any endometriotic implants growing outside the uterus will not cure it.
Myth #3: Endometriosis Only Affects the Pelvic Area
Locations within the pelvis, such as the surface of the uterus, bladder, or fallopian tubes, are the most common locations where endometriosis growths occur. However, endo can occur elsewhere in the body. In some cases, endometriosis growths have been present in distant organs, such as the lungs.
Myth #4: Endometriosis Symptoms are Simply a “Heavy Period”
Bleeding during menstruation can be heavy at times. However, it should not exceed the saturation of a pad or tampon in one hour. If you experience that degree of bleeding, you should bring this up with your healthcare provider. The fact is that many women with endometriosis experience abnormally heavy flow due to the excess tissue.
Myth #5: Douching Causes Endometriosis
No scientific evidence links douching with the development of endometriosis.
Myth #6: Having an Abortion Can Cause Endometriosis
No scientific evidence demonstrates that having an abortion causes endometriosis. Those who claim otherwise might be confusing endometritis and endometriosis.
Myth #7: You’re Too Young to Have Endometriosis
A common misconception is that endometriosis is rare or doesn’t occur in young women and teenagers. As a result, many doctors do not consider an endometriosis diagnosis in young women with typical symptoms. Endometriosis facts demonstrate that teenagers and women in their early 20s can have the disorder. Most people with endometriosis state they experienced endo symptoms during adolescence.
Myth #8: Endometriosis Can Be Prevented
It’s not clearly understood what causes endometriosis. Therefore, there are no proven ways to prevent this inflammatory condition. Anything else is purely speculation at this point.
Myth #9: Endometriosis is Always Painful
Not all women with endometriosis experience pain. Studies show that some women with advanced stages of endometriosis do not experience pain as a symptom.
Myth #10: Pregnancy is a Cure for Endometriosis
This misconception about endometriosis is slowly beginning to fade. However, not quickly enough! Pregnancy fluctuates hormones in the female body, which can temporarily suppress some symptoms of endometriosis. However, these symptoms usually recur for most patients following the pregnancy. Therefore, it’s not a cure.
Myth #11: Menopause Cures Endometriosis
Endometriosis symptoms often occur during menstruation, but many women experience them long after periods stop. Following menopause, the body still produces small amounts of hormones, and the endometriosis tissue still responds to them, thus causing pain. For many women, the symptoms of endometriosis may improve after menopause, but that does not mean it’s a cure. Depending on the case, it might be necessary to remove endometriosis implants or adhesions even after menopause.
Myth #12: Hormonal Therapy Cures Endometriosis
Doctors have been treating endometriosis for years using hormonal therapy drugs. However, these medications do not have long-term effects on the disease itself. Hormones can help relieve the symptoms temporarily and even shrink the growths, but they do not cure endometriosis.
Myth #13: Endometriosis is Cancer
Endometriosis growths are not cancerous. To date, there is little evidence that shows endometriosis directly causes cancer. However, some types of cancers are more common in women who have endometriosis. Endometrial cancer is also known as uterine cancer. Many studies have examined the relationship between the two, and one showed that merely 0.7 percent of patients with endometriosis had endometrial cancer at the 10-year follow-up. Therefore, endometriosis does not equal cancer, but it may increase the risk of cancer.
Myth #14: Tubal Endometriosis Always Causes Infertility
Tubal endometriosis is not very common, and it does not always cause infertility. Does endometriosis cause infertility? It can be in many cases, but the mechanisms of infertility in endometriosis remain multifactorial. Can you get pregnant with endometriosis? It is possible, and many women do – especially with proper treatment early on.
Myth #15: Endometriosis Symptoms Are the Results of Emotional Distress (It Is All in Your Head)
Yes. People have heard many times that emotional distress could be the cause of their endometriosis and pain. This statement is false. The fact is, endometriosis is a highly complex disorder with many underpinnings. Those with endometriosis often experience emotional distress as an impact of the symptoms such as pain and infertility. But emotional distress it’s not the cause of endometriosis symptoms.
Endometriosis quick facts:
1- There is no blood test available for the diagnosis of endometriosis.
Mehedintu C, J Med Life, 2014
2- The diagnosis of endometriosis starts by taking a good history from patients, and performing a detailed physical exam including pelvic exam. In some cases, a doctor might ask for MRI and Ultrasound to have a more thorough picture. But the ultimate diagnosis is only possible with laparoscopic /robotic surgery and taking a biopsy for histopathology. There is no blood test that can tell if you have endometriosis.
3- Studies show that those with endometriosis have an increased risk of developing depression and anxiety disorders.
Chen LC, et al, J Affect Disord, 2016
4- Pelvic pain due to endo occurs a day part of an inflammatory cycle which can affect the pelvic organs and functions such as sitting, sex, bowel movements and even urination. Pelvic floor physical therapy can help with restoring balance to the pelvic floor muscles.
Dr. Juan Michelle Martin, Endometriosis Physical Therapist.
5- “The most common clinical signs of endometriosis are menstrual irregularities, chronic pelvic pain, dysmenorrhea (painful periods), dyspareunia (painful sex), and infertility.”
Lagana AS, et al, Int J Womens Health. 2017
We Want Your Input
Are there any endometriosis myths or misconceptions we did not list here? Let us know in the comments below!