Endometriosis Overview

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*This is a scholastic paper on endometriosis shared with us.


by Heidi Hill 

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 


 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). 


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).  


  • 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). 


Acién, P., & Velasco, I. (2013). Endometriosis: a disease that remains enigmatic. ISRN obstetrics and gynecology, 2013

Ahn, S. H., Singh, V., & Tayade, C. (2017). Biomarkers in endometriosis: challenges and opportunities. Fertility and Sterility

Alvarez, P., Bogen, O., & Levine, J. D. (2014). Role of nociceptor estrogen receptor GPR30 in a rat model of endometriosis pain. PAIN®, 155(12), 2680-2686. 

Alvarez, P., Giudice, L. C., & Levine, J. D. (2015). Impact of surgical excision of lesions on pain in a rat model of endometriosis. European Journal of Pain, 19(1), 103-110. 

Anderson, C. B., Penson, D. F., & Barocas, D. A. (2015). Quality of Life Measures. In 

Management of Bladder Cancer (pp. 95-110). Springer New York. 

Angioni, S., Pontis, A., Dessole, M., Surico, D., Nardone, C. D. C., & Melis, I. (2015). Pain control and quality of life after laparoscopic en-block resection of deep infiltrating endometriosis (DIE) vs. incomplete surgical treatment with or without GnRHa administration after surgery. Archives of gynecology and obstetrics, 291(2), 363-370. 

Aredo, J. V., Heyrana, K. J., Karp, B. I., Shah, J. P., & Stratton, P. (2017, January). Relating Chronic Pelvic Pain and Endometriosis to Signs of Sensitization and Myofascial Pain and Dysfunction. In Seminars in Reproductive Medicine. Thieme Medical Publishers. 

Ashrafi, M., Sadatmahalleh, S. J., Akhoond, M. R., & Talebi, M. (2016). Evaluation of risk factors associated with endometriosis in infertile women. International journal of fertility & sterility, 10(1), 11. 

Avila, I., Filogônio, I. D. S., Costa, L. M. P., & Carneiro, M. M. (2016). Anatomical Distribution of Deep Infiltrating Endometriosis and Its Relationship to Pelvic Pain. Journal of Gynecologic Surgery, 32(2), 99-103. 

Becker, C. (2015). Diagnosis and management of endometriosis. Prescriber, 26(20), 17-21. 

Bulun, S. E., Monsavais, D., Pavone, M. E., Dyson, M., Xue, Q., Attar, E., … Su, E. J. (2012). 

Role of Estrogen Receptor-β in Endometriosis. Seminars in Reproductive Medicine

30(1), 39–45. http://doi.org/10.1055/s-0031-1299596 

Burns, K. A., Rodriguez, K. F., Hewitt, S. C., Janardhan, K. S., Young, S. L., & Korach, K. S. (2012). Role of estrogen receptor signaling required for endometriosis-like lesion establishment in a mouse model. Endocrinology, 153(8), 3960-3971. 

Brown, J., & Farquhar, C. (2015). An overview of treatments for endometriosis. Jama, 313(3), 


Bruner-Tran, K. L., Herington, J. L., Duleba, A. J., Taylor, H. S., & Osteen, K. G. (2013). Medical management of endometriosis: emerging evidence linking inflammation to disease pathophysiology. Minerva ginecologica, 65(2), 199. 

Chaban, V. (2012). Primary afferent nociceptors and visceral pain. INTECH Open Access Publisher. Retrieved from http://www.intechopen.com/books/endometriosis-basicconcepts-and-current-research-trends/primaryafferent-nociceptors-and-visceral-pain  

Chen, W. C., Lee, M. H., & Wu, H. C. (2016). Endometriosis is a risk factor of interstitial cystitis/bladder pain syndrome within short interval–A National Population-Based Study. 

Urological Science, 27(2), S41-S42. 

Chen, Y. L., Zheng, A., & Wan, Q. (2014). Selective estrogen receptor modulators (SERMs) for endometriosis. The Cochrane Library

Chettier, R., Albertsen, H. M., & Ward, K. (2014). Rare mutations in WNT signaling pathways are risk factors for endometriosis. Fertility and Sterility, 102(3), e9. 

Cristescu, C., Velişcu, A. N. D. R. E. E. A., Marinescu, B., Pătraşcu, A. N. C. A., Traşcă, E. T., & Pop, O. T. (2013). Endometriosis–clinical approach based on histological findings. 

Rom J Morphol Embryol, 54(1), 91-97. 

DeBevoise, T. M., Dobinsky, A. F., McCurdy-Robinson, C. B., McGee, C. M., McNeely, C. E., Sauder, S. K., & Sullivan, K. D. (2015). Pelvic floor physical therapy: More than Kegels. 

Womens Healthcare, 3(2), 34-41. 

Demco, L. (2000). Review of pain associated with minimal endometriosis. JSLS: Journal of the 

Society of Laparoendoscopic Surgeons, 4(1), 5. 

Donnelly, L., & Yeung, P. (2015). Diagnostic challenges in a young woman with endometriosis: the value of excision. Journal of Endometriosis, 7(1), 42-45. 

dos Bispo, A. P. S., Ploger, C., Loureiro, A. F., Sato, H., Kolpeman, A., Girão, M. J. B. C., & Schor, E. (2016). Assessment of pelvic floor muscles in women with deep endometriosis. 

Archives of gynecology and obstetrics, 294(3), 519-523. 

Dun, E. C., Kho, K. A., Morozov, V. V., Kearney, S., Zurawin, J. L., & Nezhat, C. H. (2014). Endometriosis in adolescents. JSLS: Journal of the Society of Laparoendoscopic Surgeons, 19(2). 

Dunselman, G. A. J., Vermeulen, N., Becker, C., Calhaz-Jorge, C., D’Hooghe, T., De Bie, B., … 

& Prentice, A. (2014). ESHRE guideline: management of women with endometriosis. 

Human Reproduction, 29(3), 400-412. 

Ek, M., Roth, B., Ekström, P., Valentin, L., Bengtsson, M., & Ohlsson, B. (2015). 

Gastrointestinal symptoms among endometriosis patients—A case-cohort study. BMC women’s health, 15(1), 59. 

Erasmo, I., & Ferrero, S. (2015). Management of Dysmenorrhea in Women with Endometriosis. 


Estay, M. C., Sepulveda, P., Astorga, A. R., Wilkens, A. M., Schoijet, I. M., Bozzo, P., … & Varela, C. (2015). “Urinary tract endometriosis: Detection and evaluation of deep infiltration with MRI. European Society of Radiology. Retrieved from https://www.researchgate.net/profile/Ignacio_Maldonado_Sch/publication/301677311_U


Fraser, I. S., & Berkley, K. J. (2013). Session 64: Endometriosis-associated pain. Human 

Reproduction, 28(suppl 1), i103-i103. 

Galal, A. F. (2016). Should hysteroscopy be combined with laparoscopy in endometriosis associated infertility?. Reprodução & Climatério, 31(2), 63-67. 

Gezer, A., & Oral, E. (2015). Progestin therapy in endometriosis. Women’s Health, 11(5), 643-

Gingold, J. A., & Falcone, T. (2016). Retroperitoneal anatomy during excision of pelvic side wall endometriosis. Journal of endometriosis and pelvic pain disorders, 8(2), 62. 

Godin, R., & Marcoux, V. (2015). Vaginally Administered Danazol: An Overlooked Option in the Treatment of Rectovaginal Endometriosis?. Journal of Obstetrics and Gynaecology Canada, 37(12), 1098-1103. 

Gonçalves, A. V., Barros, N. F., & Bahamondes, L. (2016). The Practice of Hatha Yoga for the Treatment of Pain Associated with Endometriosis. The Journal of Alternative and Complementary Medicine

Gordon, M. (2014). Manual of nursing diagnosis (13th ed.). Burlington, MA: Jones & Bartlett 


Gupta, S., Harlev, A., Agarwal, A., Al Safaar, A., Gupta, A., & Hack, G. (2015). Oxidative Stress and Endometriosis. In Endometriosis (pp. 23-36). Springer International 


Habiba, M., & Benagiano, G. (2016). The Incidence and Clinical Significance of Adenomyosis. 

In Uterine Adenomyosis (pp. 9-43). Springer International Publishing. 

Halpern, G., Schor, E., & Kopelman, A. (2015). Nutritional aspects related to endometriosis. 

Revista da Associação Médica Brasileira, 61(6), 519-523. 

Hartmann, D., & Sarton, J. (2014). Chronic pelvic floor dysfunction. Best Practice & Research 

Clinical Obstetrics & Gynaecology, 28(7), 977-990. 

Hashim, H. A. (2014). Potential role of aromatase inhibitors in the treatment of endometriosis. 

Int J Womens Health, 6, 671. 

Heard, M. E., Melnyk, S. B., Simmen, F. A., Yang, Y., Pabona, J. M. P., & Simmen, R. C. (2016). High-Fat diet promotion of endometriosis in an immunocompetent mouse model is associated with altered peripheral and ectopic lesion redox and inflammatory status. 

Endocrinology, 157(7), 2870-2882. 

Healey, M., Cheng, C., & Kaur, H. (2014). To excise or ablate endometriosis? A prospective randomized double-blinded trial after 5-year follow-up. Journal of minimally invasive gynecology, 21(6), 999-1004. 

Heitmann, R. J., Langan, K. L., Huang, R. R., Chow, G. E., & Burney, R. O. (2014). 

Premenstrual spotting of≥ 2 days is strongly associated with histologically confirmed endometriosis in women with infertility. American journal of obstetrics and gynecology

211(4), 358-e1. 

Hey-Cunningham, A. J., Peters, K. M., Zevallos, H. B., Berbic, M., Markham, R., & Fraser, I. S. (2013). Angiogenesis, lymphangiogenesis and neurogenesis in endometriosis. Front Biosci (Elite Ed), 5, 1033-56. 

Jabr, F. I., & Mani, V. (2014). An unusual cause of abdominal pain in a male patient: 

Endometriosis. Avicenna journal of medicine, 4(4). 

Jeng, C. J., Chuang, L., & Shen, J. (2014). A comparison of progestogens or oral contraceptives and gonadotropin-releasing hormone agonists for the treatment of endometriosis: a systematic review. Expert opinion on pharmacotherapy, 15(6), 767-773. 

Jovanovic, A. M., Dikic, S. D., Janković-Raznatovic, S., Savija, J., & Radaković, J. (2015). The 

Importance of the Surgical Approach in the Prevention of Recurrence of Endometriosis. 

Journal of Gynecologic Surgery, 31(2), 71-77. 

Knabben, L., Imboden, S., Fellmann, B., Nirgianakis, K., Kuhn, A., & Mueller, M. D. (2015). Urinary tract endometriosis in patients with deep infiltrating endometriosis: prevalence, symptoms, management, and proposal for a new clinical classification. Fertility and sterility, 103(1), 147-152. 

Koga, K., Yoshino, O., Hirota, Y., Hirata, T., Harada, M., & Osuga, Y. (2014). Infertility 

Treatment of Endometriosis Patients. In Endometriosis (pp. 431-443). Springer Japan. 

Kondi-Pafitis, A. (2012). Pathological Aspects of Endometriosis. INTECH Open Access 

Publisher. Retrieved from http://cdn.intechopen.com/pdfs-wm/36756.pdf  

Koninckx, P. R., Donnez, J., & Brosens, I. (2016). Microscopic endometriosis: impact on our understanding of the disease and its surgery. Fertility and Sterility, 105(2), 305-306. 

Kvaskoff, M., Mu, F., Terry, K. L., Harris, H. R., Poole, E. M., Farland, L., & Missmer, S. A. (2015). Endometriosis: a high-risk population for major chronic diseases?. Human reproduction update, dmv013. 

Laganà, A. S., Vitale, S. G., Trovato, M. A., Palmara, V. I., Rapisarda, A. M. C., Granese, R., … & Chiofalo, B. (2016). Full-thickness excision versus shaving by laparoscopy for intestinal deep infiltrating endometriosis: rationale and potential treatment options. 

BioMed Research International, 2016

Likes, C. E., & Lessey, B. A. (2014). Coexistence of polycystic ovary syndrome and endometriosis in women with infertility. Journal of Endometriosis and Pelvic Pain Disorders, 6(2), 78-83. 

Lu, Z., Zhang, W., Jiang, S., Zou, J., & Li, Y. (2014). Effect of lesion location on endometriotic adhesion and angiogenesis in SCID mice. Archives of gynecology and obstetrics, 289(4), 823-830. 

Luisi, S., Pizzo, A., Pinzauti, S., Zupi, E., Centini, G., Lazzeri, L., … & Petraglia, F. (2015). Neuroendocrine and stress-related aspects of endometriosis. Neuroendocrinology Letters, 36(1). 

Lupron. (n.d.). Women: Endometriosis. Retrieved from http://www.lupron.com/  

Martin Jr, J. D., & Hauck, A. E. (1985). Endometriosis in the male. The American surgeon

51(7), 426-430. 

Maggiore, U. L. R., Ferrero, S., Mangili, G., Bergamini, A., Inversetti, A., Giorgione, V., … & Candiani, M. (2015). A systematic review on endometriosis during pregnancy: diagnosis, misdiagnosis, complications and outcomes. Human reproduction update, dmv045. 

Marziali, M., Venza, M., Lazzaro, S., Lazzaro, A., Micossi, C., Stolfi, V. M., … & Pozza, E. (2012). CURRENT ISSUE MINERVA CHIRURGICA. Minerva Chirurgica, 67(6), 499504. 

McAllister, S. L., Giourgas, B. K., Faircloth, E. K., Leishman, E., Bradshaw, H. B., & Gross, E. R. (2016). Prostaglandin levels, vaginal innervation, and cyst innervation as peripheral contributors to endometriosis-associated vaginal hyperalgesia in rodents. Molecular and Cellular Endocrinology, 437, 120-129. 

Mackenzie, M. W. (2015). Simple Excision Technique for Complex Endometriosis. Journal of 

Minimally Invasive Gynecology, 22(6), S139. 

McKinnon, B. D., Bertschi, D., Bersinger, N. A., & Mueller, M. D. (2015). Inflammation and nerve fiber interaction in endometriotic pain. Trends in Endocrinology & Metabolism, 26(1), 11-21. 

Moore, J., Gibson, P. R., & Burgell, R. (2014). Low FODMAP diet–Efficacy in managing abdominal symptoms in patients with endometriosis. Journal of Nutrition & Intermediary Metabolism, 1, 14. 

Mormile, R., & Vittori, G. (2013). Celiac Disease, Hepatitis B Vaccine Nonresponse and 

Endometriosis: What is the Link? J Vaccines Vaccin 4: 187. doi: 10.4172/21577560.1000187 Page 2 of 2 Volume 4• Issue 4• 1000187 J Vaccines Vaccin ISSN: 21577560 JVV an open access journal Disease Unresponsive to the Intramuscular Vaccination Schedule: A Pilo t Study. AM J Gastroenterol, 105, 2117-2119. 

Morotti, M., Vincent, K., Brawn, J., Zondervan, K. T., & Becker, C. M. (2014). Peripheral changes in endometriosis-associated pain. Human reproduction update, dmu021. 

Mu, F., Rich-Edwards, J., Rimm, E. B., Spiegelman, D., & Missmer, S. A. (2016). 

Endometriosis and risk of coronary heart disease. Circulation: Cardiovascular Quality and Outcomes, 9(3), 257-264. 

Nourmoussavi, M., Bodmer‐Roy, S., Mui, J., Mawji, N., Williams, C., Allaire, C., & Yong, P. J. (2014). Bladder base tenderness in the etiology of deep dyspareunia. The journal of sexual medicine, 11(12), 3078-3084. 

Nezhat, C., Li, A., Abed, S., Balassiano, E., Soliemannjad, R., Nezhat, A., … & Nezhat, F. 

(2016). Strong Association Between Endometriosis and Symptomatic Leiomyomas. 

JSLS: Journal of the Society of Laparoendoscopic Surgeons, 20(3). 

Preil, R. N., Belkin, Z. R., & Goldstein, A. T. (2016). Medical Therapies for the Treatment of Overactive Pelvic Floor. In The Overactive Pelvic Floor (pp. 255-263). Springer International Publishing. 

Rahmioglu, N., Nyholt, D. R., Morris, A. P., Missmer, S. A., Montgomery, G. W., & Zondervan, K. T. (2014). Genetic variants underlying risk of endometriosis: insights from metaanalysis of eight genome-wide association and replication datasets. Human reproduction update, 20(5), 702-716. 

Raimondo, D., Youssef, A., Mabrouk, M., Del Forno, S., Martelli, V., Pilu, G., … & Seracchioli, 

  1. (2016). Pelvic Floor Muscle Dysfunction at 3d/4d Transperineal Ultrasound in Patients with Deep Infiltrating Endometriosis: A Pilot Study. Ultrasound in Obstetrics & Gynecology

Reis, F. M., Petraglia, F., & Taylor, R. N. (2013). Endometriosis: hormone regulation and clinical consequences of chemotaxis and apoptosis. Human reproduction update, 19(4), 406-418. 

Riazi, H., Tehranian, N., Ziaei, S., Mohammadi, E., Hajizadeh, E., & Montazeri, A. (2015). Clinical diagnosis of pelvic endometriosis: a scoping review. BMC women’s health, 15(1), 39. 

Ruffo, G., Scopelliti, F., Manzoni, A., Sartori, A., Rossini, R., Ceccaroni, M., … & Falconi, M. (2014). Long-term outcome after laparoscopic bowel resections for deep infiltrating endometriosis: a single-center experience after 900 cases. BioMed research international, 2014

Santoro, L., Campo, S., D’Onofrio, F., Gallo, A., Covino, M., Campo, V., … & Montalto, M. (2014). Looking for celiac disease in Italian women with endometriosis: a case control study. BioMed research international, 2014

Schliep, K. C., Chen, Z., Stanford, J. B., Xie, Y., Mumford, S. L., Hammoud, A. O., … & Peterson, C. M. (2015). Endometriosis diagnosis and staging by operating surgeon and expert review using multiple diagnostic tools: an inter‐rater agreement study. BJOG: An International Journal of Obstetrics & Gynaecology

Szubert, M., Suzin, J., Duechler, M., Szuławska, A., Czyż, M., & Kowalczyk-Amico, K. (2014). Evaluation of selected angiogenic and inflammatory markers in endometriosis before and after danazol treatment. Reproduction, Fertility and Development, 26(3), 414-420. 

Thubert, T., Demoulin, G., Lamazou, F., Rivain, A. L., Trichot, C., Faivre, E., & Deffieux, X. (2014). Menometrorrhagia. La Revue du praticien, 64(4), 531-539. 

Tosti, C., Biscione, A., Morgante, G., Bifulco, G., Luisi, S., & Petraglia, F. (2016). Hormonal therapy for endometriosis: from molecular research to bedside. European Journal of Obstetrics & Gynecology and Reproductive Biology

Wang, N., Zhang, Y., & Liu, B. (2016). Demographic and clinical features of endometrial polyps in patients with endometriosis. BioMed research international, 2016

Wang, W., Li, R., Fang, T., Huang, L., Ouyang, N., Wang, L., … & Yang, D. (2013). 

Endometriosis fertility index score maybe more accurate for predicting the outcomes of in vitro fertilisation than r-AFS classification in women with endometriosis. Reproductive Biology and Endocrinology, 11(1), 112. 

Williams, C., Hoang, L., Yosef, A., Alotaibi, F., Allaire, C., Brotto, L., … & Yong, P. J. (2016). Nerve bundles and deep dyspareunia in endometriosis. Reproductive Sciences, 23(7), 892-901. 

Yamamoto, M. P., Carillo, J. F., & Howard, F. M. (2014). Chronic Abdominal Pain of 

Gynecologic Causes: Diagnosis. Chronic Abdominal Pain: An Evidence-Based, 

Comprehensive Guide to Clinical Management. New York, New York: Springer.  

Yonglitthipagon, P., Muansiangsai, S., Wongkhumngern, W., Donpunha, W., Chanavirut, R., Siritaratiwat, W., … & Janyacharoen, T. (2017). Effect of yoga on the menstrual pain, physical fitness, and quality of life of young women with primary dysmenorrhea. Journal of Bodywork and Movement Therapies

Zheng, Q. M., Mao, H. L., Zhao, Y. J., Zhao, J., Wei, X., & Liu, P. S. (2015). Risk of endometrial polyps in women with endometriosis: a meta-analysis. Reproductive Biology and Endocrinology, 13(1), 103. 

Zorbas, K. A., Economopoulos, K. P., & Vlahos, N. F. (2015). Continuous versus cyclic oral contraceptives for the treatment of endometriosis: a systematic review. Archives of gynecology and obstetrics, 292(1), 37-43.