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One of the most common symptoms of endometriosis is pelvic pain. This pain can occur during menstruation (dysmenorrhea), sex (dyspareunia), and/or be present chronically (Sinaii 2008; Schenken 2013; Porpora 1999). Approximately 75% of all women with symptomatic endometriosis will experience pain (Schenken 2013; Sinaii 2008). Interestingly, no clear correlation has been consistently observed between the extent of endometriosis and pain perception. In fact, some women with extensive endometriosis may only have minimal symptoms and vice-versa (Sinaii 2008). Other symptoms include low back pain, constipation, diarrhea, bloating, fatigue, and abnormal menstrual bleeding (Schenken 2013; Sinaii 2008). Bladder and bowel symptoms are typically cyclical, meaning they are usually worse around the time of menstruation (Giudice 2010).

The process by which endometriosis causes pelvic pain is complex and not entirely clear. Some of the hormonal and chemical changes caused by endometriosis could influence the growth of nerves into the ectopic endometrial tissue, leading to increased sensations of pain in the uterus (Triolo 2013; Burney 2012). The production of excess amounts of inflammatory mediators by endometriotic tissue contributes to increased pelvic pain as well (Triolo 2013; Bulun 2009). This is one of the reasons anti-inflammatory therapies, such as naproxen sodium and ibuprofen, offer effective pain relief for many endometriosis patients. These drugs are non-selective inhibitors of the COX-2 enzyme, which produces inflammatory mediators by metabolizing arachidonic acid (Bulun 2009). Interestingly, evidence suggests that progesterone can counter some of the molecular inflammatory actions that play a role in the development of endometriosis (Reis 2013).


Another manifestation of endometriosis is impaired fertility (Sinaii 2008). Healthy couples trying to become pregnant have a 15–20% chance each month of achieving a pregnancy. By comparison, women with endometriosis have a 2–10% chance of becoming pregnant each month. Between 25% and 50% of infertile women have endometriosis, and 30–50% of women with endometriosis have fertility problems (Bulletti 2010). Women with endometriosis are also less likely to have a live birth. In addition, endometriosis is associated with a higher rate of complications during pregnancy, including preeclampsia, preterm birth, abnormal vaginal bleeding, and an increased rate of a Caesarean-section delivery (Bulletti 2010; Falconer 2013; Sinaii 2008).

There are many theories as to how endometriosis causes infertility. The abnormal endometrial tissue could disrupt the anatomy of the pelvis, thus making ovulation, fertilization, and transport of the fertilized egg to the uterus more difficult (Bulletti 2010). Endometriosis can cause bands of scar tissue, called adhesions, to form between the female reproductive tract (uterus, ovaries, and fallopian tubes) and other organs in the pelvis and abdomen. This can also distort gynecological anatomy (Schenken 2012; Schenken 2013; Elsevier 2011). Endometriosis could also impair the function of the ovaries. Inflammation caused by endometriosis impairs sperm migration or the fertilization and implantation of the embryo into the uterus as well (Ziegler 2010). Other biochemicals, such as prostaglandins produced by abnormal endometrial tissue, could result in uterine contractions that make implantation difficult (Bulletti 2010). Also, resistance to progesterone and amplified estrogen production may also render the uterus unsuitable for supporting a pregnancy (Ziegler 2010).