Endometriosis is an estrogen dependent disease characterized by the growth of endometrial epithelium and stromal cells outside the uterine cavity. Lack of a clinical test results in a diagnostic delay of between 6-12 years. Recent studies suggest that miRNAs may be useful diagnostic tools; however, results remain equivocal. Use of different reference miRNA and definitions of control groups are factors postulated to contribute to the inconsistent findings in the literature. Serum samples were collected from women (n=53) undergoing laparoscopic surgery. Reference RNAs and symptomatic vs asymptomatic control groups were studied. Comparisons were made between cases and controls, controls and treated vs non-treated cases, and controls, endometriosis and adenomyosis. Data were compared by Mann Whitney U tests and Kruskal Wallis tests. A p value  0.05 was considered statistically significant. Our major finding was that reference RNA selection and categorization of patients influenced results. When using the most appropriate reference and comparing to asymptomatic controls, miR-9 was upregulated and miR-451a was downregulated in women with endometriosis. When using the most appropriate reference and comparing to symptomatic controls, miR-9 and 141 were downregulated in women with endometriosis. miR-9 and 141 were also downregulated in women receiving treatment. When using the most appropriate reference and comparing to women with adenomyosis, miR-451a, 20a and 122 were downregulated in women with endometriosis. While miRNA is the newest and has most promise as a diagnostic biomarker, miRNA expression results are extremely sensitive to multiple experimental variables. Literature continues to approach miRNA research using different definitions of control populations and different reference RNA. To replicate results and advance the search for miRNA as a diagnostic biomarker for endometriosis, a common methodology between labs will be necessary. / Thesis / Master of Science (MSc) / Endometriosis affects 10% of women within their reproductive lifespan. Since the gold standard for diagnosing endometriosis is laparoscopy, a diagnostic biomarker for endometriosis is of utmost importance. Currently there is no universally acceptable biomarker and circulating levels of miRNA appear to be promising but results have yet to be replicated. Replication of results may be dependent on reference RNA and definitions of control groups.

Endometriosis is a chronic estrogen-dependent gynecological disease where endometrial cells implant at inappropriate sites causing significant pelvic pain, decreased quality of life, and often infertility. It affects 10% of women of reproductive age, and there is no minimally invasive diagnostic test. Consequently the time to diagnosis, which occurs during laparoscopic surgery followed by pathological confirmation of disease, is prolonged and exceeds 11 years. During this time, the disease often worsens and women thus experience avoidable morbidity. Additionally, endometriosis is a financial burden on the healthcare system; its annual cost was $69.4 billion (U.S.) and $1.8 billion (Canada) in 2009. For these reasons, identifying a clinical marker remains a top priority. Although multiple putative markers have been identified and reviewed, emerging evidence suggests a relationship between neurotrophins and endometriosis. The neurotrophins are growth factors recognized for promoting neuronal differentiation, growth, and maintenance. Recently, they have been shown to induce pathways central to endometriosis including proliferation, adhesion, angiogenesis and resistance to apoptosis, in cultured neurons, epithelial cells, fibroblasts, and cancer cell lines. Although two studies have suggested elevated concentrations of brain-derived neurotrophic factor (BDNF) in the plasma and eutopic endometrium of women with endometriosis, relatively little is known about uterine BDNF. Herein, we demonstrate the conservation of BDNF and its high affinity receptor in the mammalian uterus, and show the upregulation of BDNF and its low affinity receptor by estradiol in the mouse uterus. Encouraged by our results, we assessed circulating BDNF for its ability to differentiate between women with and without endometriosis, as excess estradiol in endometriotic lesions might increase BDNF in women with disease. Our results revealed that circulating BDNF concentrations were significantly higher in women with endometriosis, particularly those with Stage I and II disease compared to controls. Furthermore, women with endometriosis undergoing ovarian suppression had significantly lower circulating BDNF than women not undergoing treatment, suggesting that BDNF may provide an opportunity to monitor patient response to treatment. Taken together, the data herein advances our limited knowledge of uterine neurotrophins, and supports a link between BDNF and endometriosis. I therefore strongly suggest that BDNF is a useful clinical marker of endometriosis, and encourage additional research to determine its role in the pathophysiology of disease. / Thesis / Doctor of Philosophy (PhD) / Endometriosis is a chronic condition that affects over 10% of women of reproductive age. Women with endometriosis suffer from debilitating pelvic pain and it takes approximately 12 years before they are diagnosed during surgery. This is in part because there is no blood test to diagnose disease. We are interested in using a protein called brain-derived neurotrophic factor (BDNF) that is linked to several of the pathways that are disturbed in women with endometriosis as a means of determining whether or not a woman has endometriosis. The key goals of this thesis are to show that BDNF is a protein which is found in the uterus of many species, that it is controlled by estrogen, and that it might be useful in diagnosing endometriosis and monitoring how well a patient is responding to endometriosis treatment.

L’endométriose est définie comme la présence de tissu endométrial et de stroma en dehors de la cavité utérine. Ses localisations les plus fréquentes sont le péritoine pelvien et les ovaires. L’endométriose infiltrante est classiquement décrite comme la présence de tissu endométriotique plus de cinq millimètres sous le péritoine pelvien ou la séreuse d’un organe. Histologiquement il s’agit d’une lésion endométriotique mais qui contrairement aux lésions ovariennes ou péritonéales contient significativement plus de muscle lisse et de fibrose et est davantage associée à la douleur. Les lésions infiltrantes peuvent être responsables de dysménorrhée, dyspareunie profonde et douleurs pelviennes chroniques sévères ayant un charactère hyperalgique tel qu’on peut le retrouver dans les douleurs neuropathiques. Ces douleurs nécessitent souvent la prise de quantités importantes d’antalgiques et ont des répercussions importantes sur la vie professionnelle, quotidienne et sexuelle des femmes atteintes. L’endométriose infiltrante présente un rapport histologique étroit avec les structures nerveuses du rétropéritoine ou les nerfs des organes atteints. Dans sa localisation rectovaginale il existe une relation histologique étroite entre les lésions d’endométriose et les nerfs ainsi qu’une correlation entre l’intensité de la douleur et le nombre de structures nerveuses envahies par l’endometriose ou engaînées dans la fibrose. Ces lésions infiltrantes expriment le «nerve growth factor» (NGF), une neurotrophine qui joue un rôle clé dans la genèse de l’hyperalgie et de la douleur. Les structures nerveuses du rétropéritoine pelvien expriment quant à elles le récepteur spécifique pour la neurotrophine NGF. Le système «NGF-récepteur spécifique» peut être responsable d’un chimiotactisme tissulaire entre les tissus sécrétant du NGF et les nerfs qui expriment le récepteur pour le NGF. Le système «NGF- récepteur spécifique» au sein de la relation endométriose-nerfs pourrait rendre compte du caractère hyperalgique des lésions endométriotiques infiltrantes ainsi, qu’expliquer pourquoi les lésions nodulaires n’apparaissent que dans les sites anatomiques richement innervés (ligaments utérosacrés, lame rectovaginale, paroi du rectum ou du côlon…) et pas ailleurs. Le traitement de première intention est chirurgical. Il convient d’être suffisamment agressif sur les lésions tout en engendrant le moins de séquelles postopératoires possibles sachant que nombre de ces femmes sont stériles. En cas d’atteinte digestive basse, les modalités de l’intervention sont dictées par l’extension et le degré d’infiltration de la paroi digestive. Dans le but de réaliser dans la majorité des cas une chirurgie minimalement invasive (laparoscopique) avec des cicatrices de petites tailles, nous avons développé une stratégie de traitement basée sur le degré d’infiltration de la paroi digestive. Dans ce cadre nous avons développé une technique laparo-assistée de résection colique segmentaire et de résection antérieure du rectum.

免疫系统包括一系列的免疫细胞和激活免疫反应的调节因子，正常的免疫系统可以保护机体免受各种病原体的侵害。免疫系统失调会导致各种各样的免疫性疾病，例如过敏，自身免疫性疾病和肿瘤。子宮内膜异位症是妇科常见慢性疾病之一，其特点为子宮内膜腺体和间质种植在子宮体以外部位。倒流的子宮内膜组织成功逃逸免疫系统的监控是成功种植的必要条件，然而其病理机制尚未研究清楚。 / 本研究探索了子宮内膜异位症小鼠模型24小时内腹腔免疫细胞的变化。我们发现大部分免疫细胞在子宮内膜组织移植24小时内显著降低，然而骨髓源性抑制细胞（MDSC）的比例大幅度增高。子宮内膜移植后6小时内已经有大量MDSC到达腹腔，并在子宮内膜粘附增生阶段都维持在高水平。子宮内膜异位诱导的腹腔MDSC包括两个细胞亚型，CD11b⁺Ly-6G⁺Ly-6C{U+02E1}{U+1D52}{U+02B7}粒细胞型MDSC (G-MDSC)　和CD11b⁺Ly-6G-Ly-6C{U+02B0}{U+2071}{U+1D4D}{U+02B0}单核细胞型MDSC (-MDSC)，二者都能够显著抑制T细胞增生，表明MDSC在早期子宮内膜异位症发展过程中介导了免疫抑制的发生。用Gr-1抗体去除子宮内膜异位症小鼠模型中的MDSC后，异位病灶的生长相比对照组受到显著抑制。同时，粒细胞集落刺激因子（G-CSF）在内膜组织移植后6小时内也明显增高，体内补充G-CSF会引起正常小鼠骨髓和周围血中MDSC的比例增高，这表明G-CSF可以诱导MDSC在骨髓中增生，并且在周围血中聚集。然而，G-CSF不能引起腹腔中MDSC增多，提示还有其他的因子参与了MDSC的趋化反应。 / 本研究表明MDSC在子宮内膜异位症发生发展过程中很可能通过类似于抑制肿瘤免疫反应的免疫抑制作用，而推动子宮内膜免疫逃逸过程，最终导致异位子宮内膜存活并生长。因此，MDSC可能成为研发子宮内膜异位症新治疗方案的靶点。 / Normal immune system keeps human bodies remain intact and unharmed in the midst of a vast universe of pathogens. The immune system includes a series of cells and molecules which worked together to initiate immune response. The dysfunction of immune cells or modulators results in various diseases, such as allergic diseases, autoimmune diseases and tumors. Endometriosis is a chronic gyneacological disorder characterized by the implantation of endometrial glands and stroma outside the uterus. The successful immune escape of retrograded endometrial cell from immune surveillance is one of the key steps in the development of endometriosis. The underlying mechanism is still unknown. / In this study, we observed the profiles of peritoneal immune cells and cytokines within 24 hours (h) after the transplantation of endometrial fragments in peritoneal cavity in mice. Most of the peritoneal immune cells decreased after the transplantation, except myeloid derived suppressor cells (MDSC) were significantly increased within 24 h. MDSC was increased in the peritoneal cavity as early as 6 h and maintained at high level when the endometrial fragments attached and proliferated in the following days. The increased MDSC have CD11b⁺Ly-6G⁺Ly-6C{U+02E1}{U+1D52}{U+02B7} granulocytic MDSC (G-MDSC) and CD11b⁺Ly-6G-Ly-6C{U+02B0}{U+2071}{U+1D4D}{U+02B0} monocytic MDSC (M-MDSC) phenotypes. Isolated peritoneal MDSC significantly suppressed T cell proliferation and activated arginase activity, suggesting the immunosuppression of MDSC during early development of endometriosis. Depletion of MDSC by Gr-1 antibody treatment significantly reduced the growth and development of endometriosis. Concurrently, granulocyte colony stimulating factor (G-CSF) was significantly increased as early as 6 h after transplantation. Supplementation of G-CSF in control mice increased MDSC percentage in bone marrow and peripheral blood, but not in peritoneal cavity. This suggests that G-CSF is responsible to induce the proliferation of MDSC in bone marrow and accumulation of MDSC in peripheral blood, but not recruitment into peritoneal cavity. Additional cytokines or chemokines may involve the mobilization of MDSC from peripheral blood to peritoneal cavity. / Our study suggested that MDSC may play an essential role in the immune escape and promote endometrial survival during early development of endometriosis, probably through the similar immunosuppression mechanisms as in cancer. MDSC may be a novel target to develop highly effective therapeutics for treatment of endometriosis. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Zhang, Tao. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2013. / Includes bibliographical references (leaves 102-128). / Abstracts also in Chinese. / Acknowledgements --- p.i / Publications --- p.iii / Academic Awards --- p.iii / List of tables and figures --- p.ix / List of abbreviations --- p.ix / Abstract --- p.xv / Chapter Chapter 1 --- Endometriosis --- p.1 / Chapter 1.1 --- Epidemiology --- p.1 / Chapter 1.1.1 --- Prevalence --- p.1 / Chapter 1.1.2 --- Risk factors --- p.2 / Chapter 1.1.2.1 --- Menstrual and reproductive factors --- p.2 / Chapter 1.1.2.2 --- Genetics --- p.3 / Chapter 1.1.2.3 --- Physical and habitual factors --- p.6 / Chapter 1.1.2.4 --- Environmental toxins --- p.6 / Chapter 1.1.2.5 --- Immune comorbidity --- p.7 / Chapter 1.2 --- Pathogenesis --- p.8 / Chapter 1.2.1 --- Retrograde menstruation --- p.8 / Chapter 1.2.2 --- Lymphatic or vascular spread --- p.9 / Chapter 1.2.3 --- Coelomic metaplasia and induction theory --- p.10 / Chapter 1.3 --- Pathophysiology --- p.11 / Chapter 1.3.1 --- Dysfunction of immune system --- p.11 / Chapter 1.3.2 --- Attachment and invasion --- p.12 / Chapter 1.3.3 --- Angiogenesis --- p.12 / Chapter 1.3.4 --- Oxidative stress --- p.13 / Chapter 1.4 --- Symptoms --- p.13 / Chapter 1.4.1 --- Pelvic pain --- p.14 / Chapter 1.4.2 --- Dysmenorrhea --- p.15 / Chapter 1.4.3 --- Dyspareunia --- p.15 / Chapter 1.4.4 --- Infertility --- p.16 / Chapter 1.5 --- Diagnosis --- p.16 / Chapter 1.5.1 --- Laparoscopy --- p.17 / Chapter 1.5.2 --- Laboratory tests --- p.17 / Chapter 1.5.3 --- Imaging --- p.18 / Chapter 1.5.4 --- Therapeutic diagnosis --- p.19 / Chapter 1.6 --- Treatment --- p.19 / Chapter 1.6.1 --- Hormonal therapy --- p.19 / Chapter 1.6.1.1 --- Combined oral contraceptives --- p.20 / Chapter 1.6.1.2 --- Progestogens --- p.20 / Chapter 1.6.1.3 --- Danazol --- p.21 / Chapter 1.6.1.4 --- GnRH Agonists --- p.22 / Chapter 1.6.1.5 --- Gestrinone --- p.23 / Chapter 1.6.2 --- Surgical treatment --- p.23 / Chapter 1.6.2.1 --- Conservative surgery --- p.24 / Chapter 1.6.2.2 --- Definitive surgery --- p.24 / Chapter 1.6.3 --- Treatment of endometriosis-related infertility --- p.25 / Chapter 1.6.4 --- New potential therapies --- p.25 / Chapter 1.6.4.1 --- Angiogenesis inhibitors --- p.26 / Chapter 1.6.4.2 --- Antioxidant therapy --- p.26 / Chapter 1.6.4.3 --- Immunomodulatory therapy --- p.27 / Chapter 1.6.4.3.1 --- Pentoxifylline --- p.27 / Chapter 1.6.4.3.2 --- TNF-α inhibitor --- p.28 / Chapter 1.6.4.3.3 --- Loxoribine --- p.28 / Chapter 1.6.4.4 --- Others --- p.29 / Chapter 1.7 --- Summary --- p.29 / Chapter Chapter 2 --- Immunology of Endometriosis --- p.30 / Chapter 2.1 --- Cell-mediated immunity --- p.30 / Chapter 2.1.1 --- Monocytes/Macrophages --- p.31 / Chapter 2.1.2 --- Dendritic cells --- p.32 / Chapter 2.1.3 --- T lymphocyte --- p.34 / Chapter 2.1.4 --- Natural killer cells --- p.34 / Chapter 2.1.5 --- T regulatory cells --- p.35 / Chapter 2.2 --- Humoral immunity --- p.37 / Chapter 2.3 --- Cytokines and growth factors --- p.39 / Chapter 2.3.1 --- Interleukin-1 --- p.39 / Chapter 2.3.2 --- Interleukin-6 --- p.40 / Chapter 2.3.3 --- Interleukin-8 --- p.41 / Chapter 2.3.4 --- Interleukin-12 --- p.42 / Chapter 2.3.5 --- Monocyte chemotactic protein-1 --- p.43 / Chapter 2.3.6 --- RANTES --- p.43 / Chapter 2.3.7 --- Tumor necrosis factor-α --- p.44 / Chapter 2.3.8 --- Vascular endothelial growth factor --- p.45 / Chapter 2.3.9 --- Growth factors --- p.46 / Chapter 2.3.9.1 --- Insulin-like growth factor --- p.46 / Chapter 2.3.9.2 --- Transforming growth factor beta --- p.46 / Chapter 2.3.9.3 --- Platelet derived growth factor --- p.46 / Chapter 2.3.9.4 --- Macrophage-colony stimulating factor --- p.47 / Chapter 2.3.9.5 --- Hepatocyte growth factor --- p.47 / Chapter 2.4 --- Molecular modulations in immune response --- p.47 / Chapter 2.4.1 --- NF-κB Signaling pathway --- p.47 / Chapter 2.4.2 --- NF-κB activation in endometriosis --- p.48 / Chapter 2.4.3 --- NF-κB activation in endometriosis associated peritoneal immune response --- p.50 / Chapter 2.5 --- The relationship between estrogen and immune response --- p.51 / Chapter 2.5.1 --- Effect of estrogen on immune cells and cytokines --- p.51 / Chapter 2.5.2 --- Effect of hormone treatment on immune response --- p.52 / Chapter 2.6 --- Summary --- p.53 / Chapter Chapter 3 --- Study Hypothesis and Objectives --- p.55 / Chapter 3.1 --- Hypothesis and aims --- p.56 / Chapter 3.2 --- Objectives --- p.56 / Chapter Chapter 4 --- Methodology --- p.57 / Chapter 4.1 --- Experimental design --- p.57 / Chapter 4.2 --- Cell-mediated immunity --- p.58 / Chapter 4.2.1 --- Experimental endometriosis in vivo --- p.58 / Chapter 4.2.2 --- Collection of peritoneal fluid, peritoneal cells and endometrial fragments --- p.59 / Chapter 4.2.3 --- Quantification of peritoneal immune cells --- p.59 / Chapter 4.3 --- MDSC functional analysis --- p.60 / Chapter 4.3.1 --- T cell suppression --- p.60 / Chapter 4.3.1.1 --- Collection and sorting of MDSC and T cells --- p.60 / Chapter 4.3.1.2 --- T cell proliferation assay --- p.61 / Chapter 4.3.2 --- Arginase production of MDSC --- p.62 / Chapter 4.3.2.1 --- Isolation of peritoneal G-MDSC and M-MDSC --- p.62 / Chapter 4.3.2.2 --- Arginase assay --- p.63 / Chapter 4.3.3 --- WrightGiemsa staining --- p.64 / Chapter 4.4 --- Kinetics of G-MDSC and M-MDSC --- p.64 / Chapter 4.4.1 --- Collection of peripheral mononuclear cells --- p.64 / Chapter 4.4.2 --- Collection of bone marrow cells --- p.65 / Chapter 4.5 --- MDSC depletion --- p.65 / Chapter 4.5.1 --- Interventions --- p.65 / Chapter 4.5.2 --- Sample collection --- p.66 / Chapter 4.5.3 --- BrdU staining --- p.66 / Chapter 4.6 --- Peritoneal cytokines and chemokines profile --- p.66 / Chapter 4.6.1 --- Cytokines antibody array --- p.66 / Chapter 4.6.2 --- Chemokines antibody array --- p.67 / Chapter 4.6.3 --- Data analysis of array --- p.68 / Chapter 4.6.4 --- ELISA validation --- p.69 / Chapter 4.6.5 --- Histology and immunohistochemistry --- p.69 / Chapter 4.6.5.1 --- Histology --- p.69 / Chapter 4.6.5.2 --- Immunohistochemistry --- p.70 / Chapter 4.7 --- MDSC proliferation and mobilization --- p.71 / Chapter 4.8 --- Statistics --- p.71 / Chapter Chapter 5 --- Results --- p.72 / Chapter 5.1 --- Histology of endometrial fragment --- p.72 / Chapter 5.2 --- Immune cell profiles --- p.72 / Chapter 5.3 --- Identification of MDSC --- p.73 / Chapter 5.3.1 --- T cell proliferation assay --- p.73 / Chapter 5.3.2 --- Arginase production --- p.74 / Chapter 5.3.3 --- Wright-Giemsa staining --- p.75 / Chapter 5.4 --- Kinetics of G-MDSC and M-MDSC --- p.75 / Chapter 5.5 --- MDSC depletion --- p.76 / Chapter 5.5.1 --- Gr-1 antibody depletion --- p.76 / Chapter 5.5.2 --- Size and weight of endometriotic lesions --- p.76 / Chapter 5.5.3 --- Growth and development of endometriotic lesions --- p.77 / Chapter 5.5.4 --- T cells and macrophages --- p.77 / Chapter 5.6 --- Cytokines and chemokines profiles --- p.78 / Chapter 5.6.1 --- Cytokine and chemokine profiles --- p.78 / Chapter 5.6.2 --- ELISA validation --- p.79 / Chapter 5.6.3 --- Cytokines expression in endometriotic lesions --- p.79 / Chapter 5.7 --- Proliferation and mobilization of MDSC by cytokine --- p.80 / Chapter Chapter 6 --- Discussion --- p.81 / Chapter 6.1 --- MDSC in early endometriosis --- p.81 / Chapter 6.1.1 --- Identification of MDSC --- p.81 / Chapter 6.1.1.1 --- Terminology of MDSC --- p.81 / Chapter 6.1.1.2 --- Subsets of MDSC --- p.81 / Chapter 6.1.1.3 --- Characteristics of MDSC --- p.82 / Chapter 6.1.2 --- MDSC in cancer --- p.83 / Chapter 6.1.2.1 --- Expansion and accumulation of MDSC in cancer --- p.83 / Chapter 6.1.2.2 --- Suppressive mechanisms of MDSC in cancer --- p.84 / Chapter 6.1.2.3 --- Suppressive mechanisms of MDSC subsets --- p.89 / Chapter 6.1.3 --- MDSC in inflammation --- p.90 / Chapter 6.1.4 --- MDSC in endometriosis --- p.90 / Chapter 6.2 --- Other immune cells in early endometriosis --- p.92 / Chapter 6.3 --- Cytokines and chemokines in early endometriosis --- p.93 / Chapter 6.4 --- Potentials of the study --- p.94 / Chapter 6.4.1 --- Potentials for new therapy --- p.95 / Chapter 6.4.1.1 --- Facilitating differentiation of MDSC --- p.95 / Chapter 6.4.1.2 --- Inhibiting MDSC proliferation --- p.96 / Chapter 6.4.1.3 --- Eliminating MDSC --- p.97 / Chapter 6.4.1.4 --- Blockade of MDSC suppressive function --- p.97 / Chapter 6.4.2 --- Potentials for new biomarkers --- p.97 / Chapter 6.5 --- Limitations of the study --- p.98 / Chapter 6.5.1 --- Lack of human study --- p.98 / Chapter 6.5.2 --- Lack of stable cell line --- p.98 / Chapter 6.5.3 --- Unknown mechanisms of MDSC in endometriosis --- p.99 / Chapter 6.5.4 --- Signaling pathway --- p.99 / Chapter Chapter 7 --- Conclusion and future plan --- p.100 / Reference --- p.102 / Chapter Appendices: --- Tables & Figures --- p.128

Bakgrund: Endometrios är en kronisk inflammatorisk sjukdom som uppskattas drabba 10 procent av alla personer med livmoder i fertil ålder. Sjukdomen har setts påverka flera aspekter i livet och kan orsaka stort lidande hos individen. Syfte: Syftet med denna litteraturöversikt var att undersöka hur personer med endometrios upplever att olika aspekter livskvaliteten påverkas av sjukdomen. Metod: Litteraturöversikten baserades på vetenskapliga artiklar publicerade i databaserna PubMed och CINAHL. Efter kvalitetsgranskning av 23 artiklar återstod 17, varav två kvalitativa och 15 kvantitativa. Resultaten från de inkluderade studierna gick sedan igenom och delades upp under rubriker utifrån de aspekter av livskvalitet som framkom. Huvudresultat: Endometrios visades ha en negativ påverkan på de drabbades liv och vardag. Kvinnor med endometrios skattade signifikant lägre generell livskvalitet och hälsorelaterad livskvalitet än kvinnor utan sjukdomen. De vanligast förekommande symtomen var olika typer av smärta vilka sågs ha en signifikant negativ påverkan på livskvaliteten och det dagliga livet, som nedsatt produktivitet inom arbete och utbildning. Endometrios innebar även psykiska begränsningar i form av antingen minskat generellt välmående eller sämre emotionell funktion. Gällande socialt nätverk visade flera studier att kvinnor med endometrios upplevde en negativ påverkan på relationer och/eller deras sociala liv. Normalisering och okunskap kunde bidra till försening i diagnos och påverkan på livskvalitet. Även vårdpersonalens kunskap inom ämnet ansågs vara otillräcklig i många fall. Slutsats: Kvinnor med endometrios hade lägre livskvalitet än kvinnor utan sjukdomen. Vidare forskning kring sjukdomen kan förbättra behandling och påskynda diagnostisering, vilket kan påverka den fysiska, psykiska och sociala funktionen hos individen. Detta kan minska kostnaderna vid såväl sjukskrivning som lägre arbetsproduktivitet samt frekventa vårdbesök relaterade till feldiagnostisering och vårdfördröjning. / Background: Endometriosis is a chronic inflammatory disease estimated to occur in 10 percent of the population with uterus of reproductive age. The disease has been observed to affect many aspects of life and causing great suffering for the individual. Aim: The aim of this literature review is to examine how people with endometriosis are experiencing how different aspects of quality of life is affected by the disease. Method: The literature review was based on scientific articles published in PubMed and CINAHL. After examining the quality of 23 articles 17 remained, including two qualitative and 15 quantitative studies. The results of the included studies were broken down and assorted into subgroups depending on which aspects of quality of life mentioned. Main Results: The result showed that endometriosis had a negative impact on the daily lives of those suffering of the disease. Women with endometriosis stated significantly lower overall quality of life and health-related quality of life than women without the disease. The most commonly reported symptoms were different types of pain which had a significant negative impact on quality of life and daily life, such as reduced work and education productivity. Endometriosis could also lead to mental limitations as decreased general wellbeing or emotional function. Regarding the social aspects, multiple studies showed that women with endometriosis experienced that the disease had a negative influence on relationships and/or their social life. Normalization and insufficient knowledge about the disease could contribute to delay in diagnosis and impact the quality of life. The knowledge of health care personnel was also seen inadequate in many cases. Conclusion: Women with endometriosis had lower quality of life than women without the disease. Further research could improve treatment and speed up diagnosis, affecting the physical, psychological and social functioning of the individual. This could reduce the costs from both sick leave and decreased work productivity as well as frequent health care visits related to misdiagnosis and delay of treatment.

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Endometriosis is a painful and debilitating chronic gynaecological condition experienced by women in their reproductive years. This illness impacts on their fertility rate and on their general quality of life. Current research into the lived experience and perceived quality of life of women living with Endometriosis is lacking. Considering the prevalence of this condition, an understanding of women's lived experiences and the processes from which meaning is generated is essential to assist women and their families in coping with Endometriosis. Illness representation theory provided some insight into the meaning making processes involved in understanding and coping with a chronic illness. A phenomenological study was conducted to explore women with Endometriosis' lived experiences and the pervasiveness of this condition in terms of their perceived quality of life. I argued that dynamic relationships exist between the women's personal, social and medical worlds and that these interactions provide the context for the creation of women's lived experiences of Endometriosis. / Thesis (M.A.)-University of KwaZulu-Natal, 2005.

Objetivos: Determinar las características clínico-quirúrgicas y anatomopatológicas de las pacientes con endometriosis pélvicas sometidas a cirugía laparoscópica en el Hospital Nacional Arzobispo Loayza en el periodo comprendido entre Enero de 2010 y Diciembre del 2012. Material y métodos: La muestra seleccionada estuvo comprendida por 206 pacientes operadas por vía laparoscópica en el periodo que corresponde al estudio. Los instrumentos empleados estuvieron conformados por una ficha de recolección de datos convenientemente elaborada para los fines de estudio. Resultados: la media de la edad de los pacientes fue 32.5+/-5.4 años; siendo la mínima de 19 años y la máxima de 46 años. En cuanto a las características clínicas de las pacientes con endometriosis pélvicas sometidas a cirugía laparoscópica encontramos que el 81.4 % de las pacientes tuvo infertilidad; dolor pélvico crónico el 22.5 %, dismenorrea el 22.5 %; dispareunia el 11.8 %; dolor palpable el 12.7 %, tacto vaginal doloroso el 15.7 %. En cuanto a los hallazgos operatorios de pacientes con endometriosis pélvicas sometidas a cirugía laparoscópica encontramos que a nivel uterino hubo una mayor frecuencia de focos endometriósicos en un 34.9 %, a nivel de trompas hubo una mayor frecuencia de adherencias; a nivel de ovarios también hubo una mayor frecuencia de adherencias y focos endometriósicos; a nivel del Douglas hubo una mayor frecuencia de focos endometriósicos en un 20.4 %. Conclusión: Hay una relación estadísticamente significativa de endometriosis en fondo de saco anterior con dispareunia; de endometriosis en ovario derecho con dolor palpable; endometriosis en ovario izquierdo con masas pélvicas; y de endometriosis en los ligamentos anchos con tacto vaginal doloroso. (P<0.05)

Thesis (Ph. D.)--University of Texas at Austin, 2004. / Supervisors: Mary A. Steinhardt and Nell H. Gottlieb. Vita. Includes bibliographical references.

Chronic inflammation is associated with a dysregulation of the immune response. Inflammation is also associated with decreased reproductive capacity in women, however an exact mechanism has yet to be identified. Physiological states such as obesity and disease states such as endometriosis are both associated with chronic inflammation, an insufficient immune response, and infertility in women; therefore these two conditions serve as excellent models to study the effects of inflammation on reproductive function. Early indications of inflammation may aid in early detection of immune dysregulation associated with different physiological and pathological conditions. One way to measure immune balance between pro- and anti-inflammatory states in the female urogenital tract is by observing changes in the bacterial species that populate the mucosal surface. Commensal bacteria that make up the microbiome play a critical role in the development and maturation of the immune system in humans. Because these microbes and the host’s immune system are constantly influencing each other, several immunological conditions and disease states have been shown to have an altered microbial profile than that of healthy individuals. The goal for this study was to examine how triggers of inflammation alter the peripheral immune response, urogenital microbial communities, and reproductive function. Specifically, our aims were to 1) use an animal model of obesity to determine whether this physiological model of inflammation decreases immune protection of the urogenital microbiome and alters ovarian function; and 2) use endometriosis as a disease model of inflammation to assess whether the presence of endometriotic lesions alters urogenital microbial dynamics, and also whether surgical intervention restores commensal bacterial profiles to that of a non-disease state. The results of this study revealed that the urogenital microbial community dynamics were altered in both our obese and disease models of inflammation compared to their respective controls. In the obesity study, we also found that our obese model had decreased markers of inflammation, which may be due to dietary composition. In the endometriosis study, we observed that patients with disease had a unique urogenital microbiome profile and that surgery had an effect in shifting the urogenital microbial profiles of several patients. Overall, our long-term goal is to determine whether the urogenital microbiome is a good indicator of immune stress and if alternative therapies can alter microbial community dynamics, eliminate immune stress associated with disease. Ultimately we are looking at the microbiome as an indicator of overall immune health and implementing alternative diagnostic and treatment strategies to immune diseases that affect reproductive function in women.