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Classification and external resources
ICD-10 N80.
ICD-9 617.0
OMIM 131200
DiseasesDB 4269
MedlinePlus 000915
eMedicine med/3419 ped/677 emerg/165
MeSH D004715

Endometriosis (from endo, "inside", and metra, "womb") is a debilitating medical condition in females in which endometrial like cells appear and flourish in areas outside the uterine cavity, most commonly on the ovaries. The uterine cavity is lined by endometrial cells, which are under the influence of female hormones. These endometrial-like cells in areas outside the uterus (endometriosis) are influenced by hormonal changes and respond similarly as do those cells found inside the uterus. Symptoms often worsen in time with the menstrual cycle.

Endometriosis is typically seen during the reproductive years; it has been estimated that it occurs in roughly 5% to 10% of women.[1] Symptoms may depend on the site of active endometriosis. Its main but not universal symptom is pelvic pain in various manifestations. Endometriosis is a common finding in women with infertility.



Pelvic pain

A major symptom of endometriosis is recurring pelvic pain. The pain can be mild to severe cramping that occurs on both sides of the pelvis, to the lower back and rectal area and even down the legs. The amount of pain a woman feels is not necessarily related to the extent or stage (1 through 4) of endometriosis. Some women will have little or no pain despite having extensive endometriosis affecting large areas or having endometriosis with scarring. On the other hand, women may have severe pain even though they have only a few small areas of endometriosis. However, pain does typically worsen with severity. Symptoms of endometriosic-related pain may include [2]:

  • dysmenorrhea – painful, sometimes disabling cramps; pain may get worse over time (progressive pain), also lower back pains linked to the pelvis
  • chronic pelvic pain – typically accompanied by lower back pain or abdominal pain
  • dyspareunia – painful sex
  • dysuria – urinary urgency, frequency, and sometimes painful voiding


Many women with infertility have endometriosis. As endometriosis can lead to anatomical distorsions and adhesions (the fibrous bands that form between tissues and organs following recovery from an injury), the causality may be easy to understand; however, the link between infertility and endometriosis remains enigmatic when the extent of endometriosis is limited.[3] It has been suggested that endometriotic lesions release factors which are detrimental to gametes or embryos, or, alternatively, endometriosis may more likely develop in women who fail to conceive for other reasons and thus be a secondary phenomenon; for this reason it is preferable to speak of endometriosis-associated infertility[4] in such cases.


Other symptoms may be present, including:

  • nausea, vomiting, fainting, dizzy spells, vertigo[citation needed]
  • frequent or constant menstrual flow[citation needed]
  • chronic fatigue[citation needed]
  • heavy or long uncontrollable menstrual periods with small or large blood clots
  • some women may also suffer mood swings[citation needed]
  • extreme pain in legs and thighs
  • back pain
  • mild to extreme pain during intercourse
  • extreme pain from frequent[citation needed] ovarian cysts
  • pain from adhesions which may bind an ovary to the side of the pelvic wall, or they may extend between the bladder and the bowel,uterus, etc
  • extreme pain with or without the presence of menses
  • premenstrual spotting
  • mild to severe fever
  • headaches
  • depression
  • hypoglycaemia (low blood sugar)
  • anxiety

In addition, women who are diagnosed with endometriosis may have gastrointestinal symptoms that mimic irritable bowel syndrome

Patients who rupture an endometriotic cyst may present with an acute abdomen as a medical emergency.

Occasionally pain may also occur in other regions. Cysts can occur in the bladder (although rare) and cause pain and even bleeding during urination. Endometriosis can invade the intestine[citation needed] and cause painful bowel movements or diarrhea.

In addition to pain during menstruation, the pain of endometriosis can occur at other times of the month and doesn't have to be just on the date on menses. There can be pain with ovulation, pain associated with adhesions, pain caused by inflammation in the pelvic cavity, pain during bowel movements and urination, during general bodily movement i.e. exercise, pain from standing or walking, and pain with intercourse. But the most desperate pain is usually with menstruation and many women dread having their periods. Also the pain can start a week before menses, during and even a week after menses, or it can be constant. There is no known cure for endometriosis.[citation needed]


Endometriosis can affect any female, from premenarche to postmenopause, regardless of race or ethnicity or whether or not they have had children. It is primarily a disease of the reproductive years. Estimates about its prevalence vary, but 5–10% is a reasonable number, more common in women with infertility (20–50%) and women with chronic pelvic pain (about 80%).[5] As an estrogen-dependent process, it can persist beyond menopause and persists in up to 40% of patients following hysterectomy.[6]

Endometriosis and Smoking

This condition is associated with tobacco smoking in women. The risk of a cyst turning to be ovarian cancer is extremely high in such conditions especially in women in their 30's. Ovarian cysts may indicate advanced endometriosis and often is associated with reduced fertility or infertility.Smoking causes decreased estrogens with breakthrough bleeding and shortened luteal phases. Smokers have an earlier than normal (by about 1.5-3 years) menopause which suggests that there is some toxic affect of smoking on the follicles directly. Chemically, nicotine has been shown to concentrate in cervical mucous and metabolites have been found in follicular fluid and been associated with delayed follicular growth and maturation. Finally, there is some affect on tubal motility because smoking is associated with an increased incidence of ectopic pregnancy as well as an increased spontaneous abortion rate.

Endometriosis and Pregnancy

Aging, however, brings with it many effects that will decrease fertility. Depletion over time of ovarian follicles affects menstrual regularity. Endometriosis has more time to produce scarring of the ovary and tubes so they cannot move freely or it can even replace ovarian follicular tissue if ovarian endometriosis persists and grows. Leiomyomata (fibroids) can slowly grow and start causing endometrial bleeding that disrupts implantation sites or distorts the endometrial cavity which affects carrying a pregnancy in the very early stages. Abdominal adhesions from other intraabdominal surgery, or ruptured ovarian cysts can also affect tubal motility needed to sweep the ovary and gather an ovulated follicle (egg).

Endometriosis in postmenopausal women does occur and has been described as an aggressive form of this disease characterized by complete progesterone resistance and extraordinarily high levels of aromatase expression.[7] In less common cases, girls may have endometriosis symptoms before they even reach menarche.[8][9]


Endometriosis bears no relationship to endometrial cancer. Current research has demonstrated an association between endometriosis and certain types of cancers, notably ovarian cancer, non-Hodgkin's lymphoma and brain cancer.[10][11][12] Endometriosis often also coexists with leiomyoma or adenomyosis, as well as autoimmune disorders. A 1988 survey conducted in the US found significantly more Hypothyroidism, fibromyalgia, chronic fatigue syndrome, autoimmune diseases, allergies and asthma in women with endometriosis compared to the general population.[13]

Pathology and locations

Endoscopic image of endometriotic lesions at the peritoneum of the pelvic wall.
Micrograph of the wall of an endometrioma. All features of endometriosis are present (endometrial glands, endometrial stroma and hemosiderin-laden macrophages. H&E stain.

Active endometriosis produces inflammatory mediators that cause pain and inflammation, as well as scarring or fibrosis of surrounding tissue. Triggers of various kinds, including menses, toxins, and immune factors, may be necessary to start this process. Typical endometriotic lesions show histologic features similar to endometrium, namely stroma, endometrial epithelium, and glands that respond to hormonal stimuli. Older lesions may display no glands but hemosiderin deposits as residual. To the eye, lesions can appear dark blue or powder-burn black and vary in size; red, white, yellow, brown or non-pigmented. Some lesions within the pelvis walls may not be visible to the eye, as normal-appearing peritoneum of infertile women reveals endometriosis on biopsy in 6–13% of cases.[14] Additionally other lesions may be present, notably endometriomas of the ovary, scar formation, and peritoneal defects or pockets. Endometrioma on the ovary of any significant size (Approx. 2 cm +) must be removed surgically because hormonal treatment alone will not remove the full endometrioma cyst, which can progress to acute pain from the rupturing of the cyst and internal bleeding. Endometrioma is sometimes misdiagnosed as ovarian cysts.

Early endometriosis typically occurs on the surfaces of organs in the pelvic and intra-abdominal areas. Health care providers may call areas of endometriosis by different names, such as implants, lesions, or nodules. Larger lesions may be seen within the ovaries as endometriomas or "chocolate cysts", "chocolate" because they contain a thick brownish fluid, mostly old blood. Endometriosis may trigger inflammatory responses leading to scar formation and adhesions.

Endoscopic image of endometriotic lesions in the Pouch of Douglas and on the right sacrouterine ligament.

Most endometriosis is found on these structures in the pelvic cavity where it can produce mild, moderate, and/or severe pain felt in the pelvis and/or lower back areas. The pain is often more severe before, during, and/or after the menstrual period:

Bowel endometriosis affects approximately 10% of women with endometriosis, and can cause severe pain with bowel movements.

Endometriosis may spread to the cervix and vagina or to sites of a surgical abdominal incision.

Less commonly lesions can be found on the diaphragm. Diaphragmatic endometriosis is rare, most always on the right hemidiaphragm, and may inflict cyclic pain of the right shoulder just before and during menses. Rarely, endometriosis can be extraperitoneal and is found in the lungs and CNS.[15]

Pleural implantations are associated with recurrent right pneumothoraces at times of menses, termed catamenial pneumothorax.

Endometriosis may also present with skin lesions in cutaneous endometriosis.


Endoscopic image of a ruptured chocolate cyst in left ovary.

Complications of endometriosis include:

Infertility can be related to scar formation and anatomical distortions due to the endometriosis; however, endometriosis may also interfere in more subtle ways: cytokines and other chemical agents may be released that interfere with reproduction.

Complications of endometriosis include bowel and ureteral obstruction resulting from pelvic adhesions. Also, peritonitis from bowel perforation can occur.


A health history and a physical examination can in many patients lead the physician to suspect endometriosis. Surgery is the gold standard in diagnosis. However, most insurance plans will not cover surgical diagnosis unless the patient has already attempted to become pregnant and failed.

Micrograph an endometrioma. H&E stain.

Use of imaging tests may identify endometriotic cysts or larger endometriotic areas. It also may identify free fluid often within the cul-de-sac. The two most common imaging tests are ultrasound and magnetic resonance imaging (MRI). Normal results on these tests do not eliminate the possibility of endometriosis. Areas of endometriosis are often too small to be seen by these tests.

The only way to diagnose endometriosis is by laparoscopy or other types of surgery with lesion biopsy. The diagnosis is based on the characteristic appearance of the disease, and should be corroborated by a biopsy. Surgery for diagnoses also allows for surgical treatment of endometriosis at the same time.

Although doctors can often feel the endometrial growths during a pelvic exam, and your symptoms may be telltale signs of endometriosis, diagnosis cannot be confirmed without performing a laparoscopic procedure. Often the symptoms of ovarian cancer are identical to those of endometriosis. If a misdiagnosis of endometriosis occurs due to failure to confirm diagnosis through laparoscopy, early diagnosis of ovarian cancer, which is crucial for successful treatment, may have been missed.[17]


Surgically, endometriosis can be staged I–IV (Revised Classification of the American Society of Reproductive Medicine).[18] The process is a complex point system that assesses lesions and adhesions in the pelvic organs, but it is important to note staging assesses physical disease only, not the level of pain or infertility. A patient with Stage I endometriosis may have little disease and severe pain, while a patient with Stage IV endometriosis may have severe disease and no pain or vice versa. In principle the various stages show these findings:

  • Stage I (Minimal)
Findings restricted to only superficial lesions and possibly a few filmy adhesions
  • Stage II (Mild)
In addition, some deep lesions are present in the cul-de-sac
  • Stage III (Moderate)
As above, plus presence of endometriomas on the ovary and more adhesions
  • Stage IV (Severe)
As above, plus large endometriomas, extensive adhesions.


An area of research is the search for endometriosis markers. These markers are substances made by or in response to endometriosis that health care providers can measure in the blood or urine. If markers are found, health care providers could diagnose endometriosis by testing a woman's blood or urine which might show high levels of estrogen or low levels of progesterone, and reduce the need for surgery. The antigen CA-125 is known to be elevated in many patients with endometriosis[19] but is not specifically indicative of endometriosis.

Research is also being conducted on potential genetic markers associated with endometriosis so that a saliva-based diagnostic may replace surgical procedures for basic diagnosis.[20] However, this research remains very preliminary and the diagnostic standard continues to be surgical intervention.

Potential causes

While the exact cause of endometriosis remains unknown, many theories have been presented to better understand and explain its development. These concepts do not necessarily exclude each other.

  1. Estrogens: Endometriosis is a condition that is estrogen-dependent and thus seen primarily during the reproductive years. In experimental models, estrogen is necessary to induce or maintain endometriosis. Medical therapy is often aimed at lowering estrogen levels to control the disease. Additionally, the current research into aromatase, an estrogen-synthesizing enzyme, has provided evidence as to why and how the disease persists after menopause and hysterectomy.
  2. Retrograde menstruation: The theory of retrograde menstruation, first proposed by John A. Sampson, suggests that during a woman's menstrual flow, some of the endometrial debris exits the uterus through the fallopian tubes and attaches itself to the peritoneal surface (the lining of the abdominal cavity) where it can proceed to invade the tissue as endometriosis. While most women may have some retrograde menstrual flow, typically their immune system is able to clear the debris and prevent implantation and growth of cells from this occurrence. However, in some patients, endometrial tissue transplanted by retrograde menstruation may be able to implant and establish itself as endometriosis. Factors that might cause the tissue to grow in some women but not in others need to be studied, and some of the possible causes below may provide some explanation, e.g., hereditary factors, toxins, or a compromised immune system. It can be argued that the uninterrupted occurrence of regular menstruation month after month for decades is a modern phenomenon, as in the past women had more frequent menstrual rest due to pregnancy and lactation. Sampson's theory certainly is not able to explain all instances of endometriosis, and it needs additional factors such as genetic or immune differences to account for the fact that many women with retrograde menstruation do not have endometriosis. In addition, at least one study found that endometriotic lesions are biochemically very different from transplanted ectopic tissue, which casts doubt on Sampson's theory.[21]
  3. Müllerianosis: A competing theory states that cells with the potential to become endometrial are laid down in tracts during embryonic development and organogenesis. These tracts follow the female reproductive (Mullerian) tract as it migrates caudally (downward) at 8–10 weeks of embryonic life. Primitive endometrial cells become dislocated from the migrating uterus and act like seeds or stem cells. This theory is supported by foetal autopsy.[22]
  4. Coelomic Metaplasia: This theory is based on the fact that coelomic epithelium is the common ancestor of endometrial and peritoneal cells and hypothesizes that later metaplasia (transformation) from one type of cell to the other is possible, perhaps triggered by inflammation.[1] This theory is further supported by laboratory observation of this transformation.[23]
  5. Genetics: Hereditary factors play a role. It is well recognized that daughters or sisters of patients with endometriosis are at higher risk of developing endometriosis themselves; for example, low progesterone levels may be genetic, and may contribute to a hormone imbalance. There is an about 10-fold increased incidence in women with an affected first-degree relative.[5] A 2005 study published in the American Journal of Human Genetics found a link between endometriosis and chromosome 10q26.[24] One study found that in female siblings of patients with endometriosis the relative risk of endometriosis is 5.7:1 versus a control population.[25]
  6. Transplantation: It is accepted that in specific patients endometriosis can spread directly. Thus endometriosis has been found in abdominal incisional scars after surgery for endometriosis. It can also grow invasively into different tissue layers, i.e., from the cul-de-sac into the vagina. On rare occasions endometriosis may be transplanted by blood or by the lymphatic system into peripheral organs such as the lungs and brain.
  7. Immune system: Research is focusing on the possibility that the immune system may not be able to cope with the cyclic onslaught of retrograde menstrual fluid. In this context there is interest in studying the relationship of endometriosis to autoimmune disease, allergic reactions, and the impact of toxins.[26] It is still unclear what, if any, causal relationship exists between toxins, autoimmune disease, and endometriosis.
  8. Environment: There is a growing suspicion that environmental factors may cause endometriosis, specifically some plastics and cooking with certain types of plastic containers with microwave ovens.[27] Other sources suggest that pesticides and hormones in our food cause a hormone imbalance.
  9. Birth Defect: In rare cases where imperforate hymen does not resolve itself prior to the first menstrual cycle and goes undetected, blood and endometrium are trapped within the uterus of the patient until such time as the problem is resolved by surgical incision. Many health care practitioners never encounter this defect, and due to the flu-like symptoms it is often misdiagnosed or overlooked until multiple menstrual cycles have passed. By the time a correct diagnosis has been made, endometrium and other fluids have filled the uterus and fallopian tubes with results similar to retrograde menstruation resulting in endometriosis. The initial stage of endometriosis may vary based on the time elapsed between onset and surgical procedure.

Cause of pain

The way endometriosis causes pain is the subject of much research. Because many women with endometriosis feel pain during or around their periods and may spill further menstrual flow into the pelvis with each menstruation, some researchers are trying to reduce menstrual events in patients with endometriosis.

Endometriosis lesions react to hormonal stimulation and may "bleed" at the time of menstruation. The blood accumulates locally, causes swelling, and triggers inflammatory responses with the activation of cytokines. It is thought that this process may cause pain.

Pain can also occur from adhesions (internal scar tissue) binding internal organs to each other, causing organ dislocation. Fallopian tubes, ovaries, the uterus, the bowels, and the bladder can be bound together in ways that are painful on a daily basis, not just during menstrual periods.


While there is no cure for endometriosis,[citation needed] in many patients menopause (natural or surgical) will abate the process. In patients in the reproductive years, endometriosis is simply managed: the goal is to provide pain relief, to restrict progression of the process, and to relieve infertility if that should be an issue. In younger women with unfulfilled reproductive potential, surgical treatment tends to be conservative, with the goal of removing endometrial tissue and preserving the ovaries without damaging normal tissue. In women who do not have need to maintain their reproductive potential, hysterectomy and/or removal of the ovaries may be an option; however, this will not guarantee that the endometriosis and/or the symptoms of endometriosis will not come back, and surgery may induce adhesions which can lead to complications.

In general, patients are diagnosed with endometriosis at time of surgery, at which time ablative steps can be taken. Further steps depend on circumstances: patients without infertility can be managed with hormonal medication that suppress the natural cycle and pain medication, while infertile patients may be treated expectantly after surgery, with fertility medication, or with IVF.

Sonography is a method to monitor recurrence of endometriomas during treatments.

Treatments for endometriosis in women who do not wish to become pregnant include:

Hormonal medication

  • Progesterone or Progestins: Progesterone counteracts estrogen and inhibits the growth of the endometrium. Such therapy can reduce or eliminate menstruation in a controlled and reversible fashion. Progestins are chemical variants of natural progesterone.
  • Avoiding products with xenoestrogens, which have a similar effect to naturally produced estrogen and can increase growth of the endometrium.
  • Hormone contraception therapy: Oral contraceptives reduce the menstrual pain associated with endometriosis.[28] They may function by reducing or eliminating menstrual flow and providing estrogen support. Typically, it is a long-term approach. Recently Seasonale was FDA approved to reduce periods to 4 per year. Other OCPs have however been used like this off label for years. Continuous hormonal contraception consists of the use of combined oral contraceptive pills without the use of placebo pills, or the use of NuvaRing or the contraceptive patch without the break week. This eliminates monthly bleeding episodes.
  • Danazol (Danocrine) and gestrinone are suppressive steroids with some androgenic activity. Both agents inhibit the growth of endometriosis but their use remains limited as they may cause hirsutism and voice changes.
  • Gonadotropin Releasing Hormone (GnRH) agonist: These agents work by increasing the levels of GnRH. Consistent stimulation of the GnRH receptors results in downregulation, inducing a profound hypoestrogenism by decreasing FSH and LH levels. While effective in some patients, they induce unpleasant menopausal symptoms, and over time may lead to osteoporosis. To counteract such side effects some estrogen may have to be given back (add-back therapy). These drugs can only be used for six months at a time.
    • Lupron depo shot is a GnRH agonist and is used to lower the hormone levels in the woman's body to prevent or reduce growth of endometriosis. The injection is given in 2 different doses a once a month for 3 month shot with the dosage of (11.25 mg) or a once a month for 6 month shot with the dosage of (3.75 mg).[29]
  • Aromatase inhibitors are medications that block the formation of estrogen and have become of interest for researchers who are treating endometriosis.[30]

Other medication

  • NSAIDs Anti-inflammatory. They are commonly used in conjunction with other therapy. For more severe cases narcotic prescription drugs may be used. NSAID injections can be helpful for severe pain or if stomach pain prevents oral NSAID use.
  • MST Morphine sulphate tablets and other opioid painkillers work by mimicking the action of naturally occurring pain-reducing chemicals called endorphins. There are different long acting and short acting medications that can be used alone or in combination to provide appropriate pain control.
  • Diclofenac in suppository or pill form. Taken to reduce inflammation and as an analgesic reducing pain.


Procedures are classified as

  • conservative when reproductive organs are retained,
  • semi-conservative when ovarian function is allowed to continue, and
  • radical when the uterus and ovaries are removed.

Conservative therapy consists of removal, excision or ablation of endometriosis, adhesions, resection of endometriomas, and restoration of normal pelvic anatomy as much as is possible.[3]

Radical therapy in endometriosis removes the uterus (hysterectomy) and tubes and ovaries (bilateral salpingo-oophorectomy) and thus the chance for reproduction. Radical surgery is generally reserved for women with chronic pelvic pain that is disabling and treatment-resistant. Not all patients with radical surgery will become pain-free.

Semi-conservative therapy preserves a healthy appearing ovary, and yet, it also increases the risk of recurrence.[31]

For patients with extreme pain, a presacral neurectomy may be indicated where the nerves to the uterus are cut. However, strong clinical evidence showed that presacral neurectomy is more effective in pain relief if the pelvic pain is midline concentrated, and not as effective if the pain extends to the left and right lower quadrants of the abdomen.[3] This is due to the fact that the nerves to be transected in the procedure are innervating the central or the midline region in the female pelvis. Furthermore, women who had presacral neurectomy have higher prevalence of chronic constipation not responding well to medication treatment because of the potential injury to the parasympathetic nerve in the vicinity during the procedure.

Comparison of medicinal and surgical interventions

Efficacy studies show that both medicinal and surgical interventions produce roughly equivalent pain-relief benefits. Recurrence of pain was found to be 44 and 53 percent with medicinal and surgical interventions, respectively.[5] However, each approach has its own advantages and disadvantages.[1]

Advantages of medicinal interventions

  1. Decrease initial cost
  2. Empirical therapy (i.e. Can be easily modified as needed)
  3. Effective for pain control

Disadvantages of medicinal interventions

  1. Adverse effects are common
  2. Not likely to improve fertility
  3. Some can only be used for limited periods of time[citation needed]

Advantages of surgery

  1. Has significant efficacy for pain control.[32]
  2. Has increased efficacy over medicinal intervention for infertility treatment
  3. Combined with biopsy, it is the only way to achieve a definitive diagnosis

Disadvantages of surgery

  1. Cost
  2. Risks are "poorly defined... and probably underestimated." In one study, 3-10% experienced major complications from surgery.[33]
  3. Efficacy is questionable. In the same study, substantial short-term pain relief was experienced by approximately 70-80% of the subjects. However, at 1 year follow-up, approximately 50% of the subjects needed analgesics or hormonal treatments.[33]

Treatment of infertility

While roughly similar to medicinal interventions in treating pain, the efficacy of surgery is especially significant in treating infertility. One study has shown that surgical treatment of endometriosis approximately doubles the fecundity (pregnancy rate).[34] The use of medical suppression after surgery for minimal/mild endometriosis has not shown benefits for patients with infertility.[4] Use of fertility medication that stimulates ovulation (clomiphene citrate, gonadotropins) combined with intrauterine insemination (IUI) enhances fertility in these patients.[4]

In-vitro fertilization (IVF) procedures are effective in improving fertility in many women with endometriosis. IVF makes it possible to combine sperm and eggs in a laboratory and then place the resulting embryos into the woman's uterus. The decision when to apply IVF in endometriosis-associated infertility takes into account the age of the patient, the severity of the endometriosis, the presence of other infertility factors, and the results and duration of past treatments.

Other treatments

  • Eating foods high in indole-3-carbinol, such as cruciferous vegetables appears to be helpful in balancing hormones and managing pain,[35] as do omega 3 fatty acids, particularly EPA.[36] The use of soy has been reported to both alleviate pain and to aggravate symptoms, making its use questionable.[37]
  • Physical therapy for pain management in endometriosis has been investigated in a pilot study suggesting possible benefit.[38] Physical exertion such as lifting, prolonged standing or running does exacerbate pelvic pain. Use of heating pads on the lower back area, may provide some temporary relief.


Proper counseling of patients with endometriosis requires attention to several aspects of the disorder. Of primary importance is the initial operative staging of the disease to obtain adequate information on which to base future decisions about therapy. The patient's symptoms and desire for childbearing dictate appropriate therapy. Not all therapy works for all patients. Some patients have reoccurrences after surgery or pseudo-menopause. In most cases, treatment will give patients significant relief from pelvic pain and assist them in achieving pregnancy.[39] It is important for patients to be continually in contact with their physician and keep an open dialog throughout treatment. This is a disease without a cure but with the proper communication, one with endometriosis can attempt to live a normal, functioning life.


The underlying process that causes endometriosis may not cease after surgical or medical intervention, and the annual recurrence rate is given as 5–20 % per year reaching eventually about 40% unless hysterectomy is performed or menopause reached.[3] Monitoring of patients consists of periodic clinical examinations and sonography. Also, the CA 125 serum antigen levels have been used to follow patients with endometriosis.

Endometriosis in the male

Endometriosis has been described in men receiving a very high estrogen medication (TACE) as part of treatment for prostatic cancer.[40]

Additional images

See also


  1. ^ a b c Diagnosis and Treatment of Endometriosis - October 15, 1999 - American Academy of Family Physicians
  2. ^ Endometriosis;NIH Pub. No. 02-2413; September 2002
  3. ^ a b c d Speroff L, Glass RH, Kase NG (1999). Clinical Gynecologic Endocrinology and Infertility (6th ed.). Lippincott Willimas Wilkins. p. 1057. ISBN 0-683-30379-1. 
  4. ^ a b c Buyalos RP, Agarwal SK (October 2000). "Endometriosis-associated infertility". Current Opinion in Obstetrics & Gynecology 12 (5): 377–81. doi:10.1097/00001703-200010000-00006. ISSN 1040-872X. PMID 11111879. 
  5. ^ a b c Dharmesh Kapoor and Willy Davila, 'Endometriosis', eMedicine (2005).
  6. ^ "Endometriosis - Hysterectomy". Retrieved 2009-08-19. 
  7. ^ Bulun SE, Zeitoun K, Sasano H, Simpson ER (1999). "Aromatase in aging women". Seminars in Reproductive Endocrinology 17 (4): 349–58. ISSN 0734-8630. PMID 10851574. 
  8. ^ Batt RE, Mitwally MF (December 2003). "Endometriosis from thelarche to midteens: pathogenesis and prognosis, prevention and pedagogy". Journal of Pediatric and Adolescent Gynecology 16 (6): 337–47. doi:10.1016/j.jpag.2003.09.008. ISSN 1083-3188. PMID 14642954. 
  9. ^ Marsh EE, Laufer MR (March 2005). "Endometriosis in premenarcheal girls who do not have an associated obstructive anomaly". Fertility and Sterility 83 (3): 758–60. doi:10.1016/j.fertnstert.2004.08.025. ISSN 0015-0282. PMID 15749511. 
  10. ^ "Endometriosis cancer risk". 5 July 2003. Retrieved 2007-07-03. 
  11. ^ Roberts, Michelle (3 July 2007). "Endometriosis 'ups cancer risk'". BBC News. BBC / Retrieved 2007-07-03. 
  12. ^ Audebert A (April 2005). "La femme endométriosique est-elle différente ? [Women with endometriosis: are they different from others?]" (in French). Gynécologie, Obstétrique & Fertilité 33 (4): 239–46. doi:10.1016/j.gyobfe.2005.03.010. ISSN 1297-9589. PMID 15894210. 
  13. ^ Sinaii N, Cleary SD, Ballweg ML, Nieman LK, Stratton P (October 2002). "High rates of autoimmune and endocrine disorders, fibromyalgia, chronic fatigue syndrome and atopic diseases among women with endometriosis: a survey analysis" (Free full text). Human Reproduction 17 (10): 2715–24. doi:10.1093/humrep/17.10.2715. ISSN 0268-1161. PMID 12351553. 
  14. ^ Nisolle M, Paindaveine B, Bourdon A, Berlière M, Casanas-Roux F, Donnez J (June 1990). "Histologic study of peritoneal endometriosis in infertile women". Fertility and Sterility 53 (6): 984–8. ISSN 0015-0282. PMID 2351237. 
  15. ^ Shawn Daly, MD, Consulting Staff, Catalina Radiology, Tucson, Arizona (October 18 2004). "Endometrioma/Endometriosis". WebMD. Retrieved 2006-12-19. 
  16. ^ Lone Hummelshoj. "Adhesions in Endometriosis". Retrieved 2009-04-25. 
  17. ^ Warren Volker, OB/GYN MD Endometriosis Diagnosis and Cure
  18. ^ American Society For Reproductive M, (May 1997). "Revised American Society for Reproductive Medicine classification of endometriosis: 1996". Fertility and Sterility 67 (5): 817–21. doi:10.1016/S0015-0282(97)81391-X. ISSN 0015-0282. PMID 9130884. 
  19. ^ Amaral VF, Ferriani RA, Sá MF, et al. (July 2006). "Positive correlation between serum and peritoneal fluid CA-125 levels in women with pelvic endometriosis". São Paulo Medical Journal 124 (4): 223–7. ISSN 1516-3180. PMID 17086305. 
  20. ^ [1]
  21. ^ Redwine DB (October 2002). "Was Sampson wrong?". Fertility and Sterility 78 (4): 686–93. doi:10.1016/S0015-0282(02)03329-0. ISSN 0015-0282. PMID 12372441. 
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