Endometriosis and adenomyosis

• Endometriosis is endometrium-like tissue growing outside the uterus, usually in the pelvis, usually with inflammation. Adenomyosis is the same kind of tissue growing inside the muscular wall of the uterus.
• Pain and infertility are the two great problems. Pain can be cyclical, non-cyclical, deep, or present with sex, bowel or bladder symptoms. Heavy menstrual bleeding is more typical of adenomyosis.
• You can diagnose endometriosis clinically from history, examination and imaging; you no longer have to wait for a laparoscopy. Normal examination and normal ultrasound do not exclude endometriosis.
• First-line treatment is analgesia plus hormonal suppression, guided by symptoms, fertility plans and safety. Gonadotrophin-releasing hormone (GnRH) drugs are second-line because they can reduce bone density and need specialist oversight.
• Surgery is usually laparoscopic and is planned around the patient's goals: pain relief, fertility, or both. Adenomyosis is managed with similar medicines first, with surgery held in reserve.

By the end of this page you should be able to:

1. Define endometriosis and adenomyosis and describe the main ways they differ and overlap.
2. Explain, in ordinary language, why pain and infertility happen, without falling back on a memorised list.
3. Build a presumptive clinical diagnosis from symptoms, examination and imaging, and know when imaging helps and when it does not.
4. Offer first-line analgesic and hormonal treatment, with safety limits, and know when to move to second-line GnRH therapy or surgery.
5. Adapt management when fertility is a priority, and know which treatments help conception and which do not.
6. Recognise adenomyosis as a distinct but related condition and manage it with the same staged approach.

Endometriosis is endometrium-like epithelium and stroma sitting outside the uterine cavity and muscle wall, usually with an associated inflammatory process.^[1] The lesions are real living tissue: they can bleed, inflame and stick to nearby organs. That single fact explains almost everything below.

Adenomyosis is similar tissue growing inside the myometrium, the muscle wall of the uterus. It can occur with or without endometriosis, and the two conditions often overlap.^[5]

A simple classification useful in practice is the ESHRE grouping: peritoneal endometriosis on the surface, deep endometriosis infiltrating below the peritoneum (often into ligaments, bowel, bladder or ureter), and endometrioma, the cystic ovarian form.^[1] Adenomyosis is often described as internal endometriosis of the uterus, but it behaves differently enough to keep its own section below.

Two traditional but flawed classification systems sit behind how teams talk. The revised American Society for Reproductive Medicine (rASRM) score is widely used for staging (stages I to IV), but its primary usefulness is as a research descriptor. NICE states that treatment should be offered according to the woman's symptoms, preferences and priorities, rather than the stage of the endometriosis.^[2] The American Association of Gynecologic Laparoscopists systems and the endometriosis fertility index exist to describe operative findings or to predict fertility, and the ACOG 2026 guideline notes that the 2021 World Endometriosis Society consensus concluded that there is still no universal validated staging system that correlates with pain or fertility.^[4] In short: describe the anatomy you see, treat the woman you see.

Measured prevalence depends on the method. Global estimates for endometriosis range from 2% to 10% of women generally, rising to 50% of women with infertility.^[1] About one in 10 women of reproductive age develop endometriosis in ACOG's statement.^[4] In a recent Australian data set, 14% of women are diagnosed by age 48, many more have suspected disease without a diagnosis, and delayed recognition (historically described as roughly 8 years from symptom onset) may be decreasing.^[5]

Adenomyosis is harder to count because many women have no symptoms and imaging has only recently become reliable enough to measure. Approximately 30% of women diagnosed with adenomyosis report no symptoms, and a 2023 meta-analysis found a 19% prevalence among women with subfertility.^[5] Women in their 40s are at highest risk of symptomatic disease.^[5]

Why so many undiagnosed cases? The symptom list is long and non-specific, the pain is often dismissed as bad periods, and the old model required surgery before confirming the diagnosis. ACOG's 2026 diagnosis guidance puts diagnostic delay at an average of four to 11 years from symptom onset to diagnosis, with all the harms that implies.^[4]

No one knows the single cause of either condition, and both are best understood as multifactorial, estrogen-responsive, inflammatory diseases. The recognised risk and associated factors include:

• Retrograde menstruation, where menstrual flow passes backwards through the fallopian tubes into the peritoneum. This is common and only sometimes leads to disease, so something else is required: perhaps altered clearance of the tissue, immune dysfunction, or the molecular state of the tissue that lands.
• Coelomic metaplasia, where peritoneal or mullerian-derived cells change into endometrium-like cells under hormonal or inflammatory signals. This helps explain lesions in women without a uterus and lesions at distant sites.
• Adenomyosis is thought to arise from a different but related mechanism: disruption of the endometrial-myometrial border (the junctional zone), followed by invagination or infiltration of basalis endometrium into the muscle, often after pregnancy or uterine surgery, with local estrogen production and inflammation sustaining it.^[5]
• Genetic and epigenetic susceptibility. Endometriosis is much more likely in first-degree relatives; ask about family history.^[5]
• Immune and inflammatory factors, including peritoneal fluid cytokines and prostaglandins, and neuroangiogenesis that allows lesions to sensitise pain pathways.
• Estrogen dependence: symptoms usually improve after natural menopause and can return if exogenous estrogen is given later.

One practical habit is therefore useful: ask first-degree relatives about endometriosis, and take family history as a real clue, not a footnote.^[2]

Pain is not simply the lesions themselves; it is a conversation between lesions, nerves, muscle and central sensitisation.

1. The tissue can bleed and release inflammatory mediators, including prostaglandins and cytokines, into the peritoneal fluid. That produces dysmenorrhoea that is often worse than normal cramping and can be premenstrual.
2. Lesions can lie on or invade structures that are richly innervated: uterosacral ligaments, the posterior vaginal fornix, the rectovaginal septum, the bowel wall, the bladder. Deep infiltration mechanically stretches and irritates these tissues, and cyclical bleeding inside firm tissue produces pressure pain.
3. Deep lesions can recruit their own nerve fibres; endometriotic tissue is not just silent ectopic endometrium, it can be neuroangiogenic.
4. Repeated inflammation leads to adhesions and fibrosis, which tether organs, reduce their mobility and make deep palpation painful.
5. Over time pain can outlast the lesions. Central and peripheral sensitisation, myofascial pelvic floor spasm and neuropathic pain can become the main drivers, so a woman may still hurt after an operation that removed every visible lesion. That is not imagined pain; it is what chronic pain neurobiology looks like.

This explains NICE's comment that regular opioid use can make endometriosis-related pain more difficult to manage, and why neuropathic pain drugs may be considered even though the evidence is limited.^[5]

Infertility in endometriosis is not about a single blocked tube. Several mechanisms run together:

• Peritoneal inflammation can alter oocyte, sperm and embryo function and can impair fertilisation through macrophage and cytokine activity.
• Adhesions can bury the fimbriae, distort the tubes and trap the ovary, physically preventing egg pick-up.
• Endometriomas can compress ovarian tissue and can alter ovarian reserve; large or multiple cysts are a special case.
• Deep disease can infiltrate the connective tissue between bowel, vagina and ovary and can distort pelvic anatomy.
• Severe disease may be associated with low progesterone effect and altered endometrial receptivity, although that partnership (endometriosis with adenomyosis) is still being worked out.

Important surgical consequence: for women trying to conceive, excision or ablation of endometriosis plus adhesiolysis for disease not involving bowel, bladder or ureter improves the chance of spontaneous pregnancy, and no hormonal treatment should be offered alone or with surgery because hormonal suppression does not improve spontaneous pregnancy rates.^[2]

In adenomyosis the myometrium becomes bulky, with asymmetric thickening and disrupted muscle fibres, and the junctional zone is often thickened and irregular. The resulting uterus cannot contract efficiently; menstrual shedding is heavier because the muscle's normal wringing action is lost, and the junctional zone is disorganised. That is why menorrhagia and dysmenorrhoea are the dominant symptoms, and why heavy menstrual bleeding is an explicit reason to consider hysterectomy when other treatment fails.^[2]

Endometriosis is famously non-specific. Every presentation below is worth recognising.

• Dysmenorrhoea that is severe, progressive, starting in adolescence or young adulthood, or that limits work and sleep.
• Pelvic pain that is cyclical or persistent and may be non-menstrual.
• Deep dyspareunia.
• Cyclical bowel symptoms: painful bowel movements, rectal bleeding with menses.
• Cyclical urinary symptoms: dysuria, haematuria.
• Subfertility or infertility, often as the presenting complaint when pain is minimal.
• Rare but classic referred symptoms: shoulder tip pain with menses (irritation under the diaphragm), cyclical chest pain or cough or haemoptysis from thoracic endometriosis, cyclical scar swelling and pain at a previous surgical incision, catamenial pneumothorax.
• Systemic fatigue and low mood from chronic pain, and rarely a cyclical urinary or gastrointestinal flare pattern.

ESHRE considers the following cyclical and non-cyclical signs and symptoms as grounds to consider the diagnosis: dysmenorrhoea, deep dyspareunia, dysuria, dyschezia, painful rectal bleeding or haematuria, shoulder tip pain, catamenial pneumothorax, cyclical cough or haemoptysis or chest pain, cyclical scar swelling and pain, fatigue and infertility.^[1]

NICE frames suspicion even more broadly: chronic pelvic pain (defined as pelvic pain lasting 6 months or longer), period-related pain affecting daily activities and quality of life, deep pain during or after intercourse, cyclical gastrointestinal symptoms (especially painful bowel movements), cyclical urinary symptoms (especially blood in the urine or pain passing urine), or infertility with one or more of the above.^[2]

In the Australian general-practice data set, 66.7% of women diagnosed with endometriosis had at least one documented endometriosis-related symptom before diagnosis and 57.6% had 2 or more. The most frequent symptoms were cyclical or persistent pelvic pain (40.8%), dysmenorrhoea (22.1%), fatigue (19.3%), heavy menstrual bleeding (15.0%) and altered bleeding (12.5%). Infertility and non-specific symptoms such as headache, urinary or bowel symptoms, back pain and pain with sex were less common.^[5]

First-degree relatives are at higher risk, so take a family history.^[5] NICE also asks practitioners to take into account that every person's experience of pain is unique and may vary with cultural background, socioeconomic status and neurodiverse conditions, and to offer a pain and symptom diary because it aids discussion.^[2]

On pelvic examination you may see visible vaginal endometriotic lesions, tenderness, reduced organ mobility, enlargement of pelvic structures, or tender nodularity in the posterior vaginal fornix.^[2] A normal examination does not rule out endometriosis.^[5] General practice data confirm that on pelvic examination the useful signs are pelvic and vaginal tenderness, nodularity of the posterior vaginal wall and enlarged pelvic organs with reduced mobility.^[5]

Women in their 40s are at highest risk of symptomatic adenomyosis; about 30% are asymptomatic.^[5] The commonest symptoms are dysmenorrhoea, heavy menstrual bleeding, pelvic pain, subfertility and bladder or gastrointestinal symptoms.^[5] The uterus is often enlarged, tender, globular and mobile, with menstrual cramps that are deep and aching rather than sharp.

A 24-year-old student has had dysmenorrhoea since menarche, now bad enough to make her miss lectures. She also has deep dyspareunia and penile pain with sex, and constipation only around her periods. Her partner and she have been trying to conceive for 8 months without success. Examination is uncomfortable but reveals nodularity behind the cervix. Transvaginal ultrasound is normal. The presumptive diagnosis is endometriosis, and empiric hormonal treatment plus analgesia is a reasonable first step without surgery. This is the everyday pattern ACOG's 2026 guidance and NICE 2024 are written for.^[2][4]

The differential is broad because the symptoms are non-specific and chronic pelvic pain has many causes. Always think in categories: gynaecological, gastrointestinal, urinary, musculoskeletal and neuropathic.

A thorough history should ask when the pain starts relative to menses, what relieves or worsens it, pain with sex in what position, bowel and bladder symptoms, bleeding, and fertility goals. NICE recommends offering an abdominal and pelvic examination to identify masses and pelvic signs, and an abdominal examination if a pelvic examination is declined or unsuitable.^[2]

ESHRE strongly recommends not using biomarkers in endometrial tissue, blood, menstrual or uterine fluids to diagnose endometriosis, because none has adequate accuracy.^[1] NICE adds: do not use serum CA-125 to diagnose endometriosis.^[2] If you are used to ordering CA-125 "just in case", stop. It is a source of false reassurance and false alarm, and it is not a screening or diagnostic tool here.

Transvaginal ultrasound is the first-line investigation in suspected endometriosis according to both the recent Australian living evidence guideline summarised by Crawford and NICE. It detects endometriomas and deep pelvic disease well, especially in specialist hands, and it rules in or out other pathology. It does not rule out endometriosis, especially superficial peritoneal disease, and normal findings should not be treated as reassuring.^[2][5]

If deep endometriosis is suspected, or transvaginal ultrasound is unavailable or unacceptable, pelvic MRI is the next step and can both diagnose and map the extent of deep disease.^[2] ESHRE reminds clinicians that a negative imaging finding does not exclude endometriosis.^[1]

For adenomyosis, ultrasound is first-line and MRI second-line; ultrasound is more accessible and cheaper.^[5]

Imaging is not just "is there a disease?" It is preoperative planning. Before operating on suspected deep disease, specialist transvaginal ultrasound or MRI defines whether bowel, bladder or ureter is involved, and whether the case belongs in a specialist endometriosis centre rather than a general gynaecology list.

Laparoscopy remains the only definitive visual diagnosis with histological confirmation, but the modern approach is to make a presumptive clinical diagnosis and start treatment, reserving laparoscopy for when it is needed. ACOG's 2026 guideline, summarised in its news release, argues that avoiding routine reliance on surgical diagnosis helps cut the four to 11 year diagnostic delay, and that a presumptive diagnosis lets clinicians offer empiric medical treatment while evaluation with imaging continues.^[4]

NICE recommends considering laparoscopy to diagnose endometriosis even if ultrasound or MRI is normal; contrariwise, there is no evidence that diagnostic laparoscopy does better than imaging plus empiric treatment, so the two approaches can both be considered with the patient.^[2] ESHRE recommends laparoscopy after negative imaging or after failed or inappropriate empiric treatment.^[1] NICE also says that if a systematic laparoscopy with recorded findings is normal, the woman should be told endometriosis is unlikely and offered other management.^[2] During laparoscopy, if present, treat peritoneal disease not involving bowel, bladder or ureter, and treat uncomplicated endometriomas.^[2]

Histology matters: laparoscopic identification of lesions should be confirmed histologically, but negative histology does not entirely rule out disease.^[1] Suspected lesions on endometrioma that are not excised should be biopsied to exclude malignancy.^[2]

There is no blood test or imaging test that diagnoses all endometriosis. The diagnosis is made from the clinical picture and is strengthened by imaging and, when needed, laparoscopy and histology.

Staging exists, but treat the patient rather than the label. NICE says offer treatment according to symptoms, preferences and priorities, rather than stage.^[2] rASRM stages I to IV are useful for describing disease extent in studies; they do not track pain well. ESHRE's guideline also focuses on symptom-based management because evidence for a fixed long-term monitoring schedule is lacking.^[1]

Monitoring has specific hooks: after a laparoscopic finding, NICE suggests outpatient follow-up with or without imaging for women who choose not to have surgery, particularly if they have deep endometriosis involving bowel, bladder or ureter, or endometrioma over 3 cm.^[2]

Before writing a prescription, ask two questions and document them. First: is the patient's main problem pain, infertility, or both? Second: what is her priority right now? The same anatomy can support several different plans. NICE, ESHRE and every real clinic converge on this point, even if the wording differs.

A chronic disease deserves chronic disease management. Crawford's review of the current Australian guideline offers conditional recommendations for pelvic physiotherapy, dietary modification, acupuncture, counselling and mindfulness, with low certainty of evidence, mainly for pain. A chronic condition management plan and a mental health care plan are useful supports. There is very little evidence to guide non-pharmacological management of adenomyosis.^[5] Opioids should be reserved for postoperative or other acute pain, short-term, at the minimum effective dose, and regular use can make endometriosis-related pain harder to manage.^[5]

NSAIDs are the analgesic mainstay. NICE suggests considering a short trial, for example 3 months, of paracetamol or an NSAID, alone or together, as first-line management of endometriosis-related pain.^[2] ESHRE offers NSAIDs or other analgesics weakly as an option to reduce pain.^[1] The Australian living evidence guideline summarised by Crawford offers NSAIDs, with or without paracetamol, for cyclical pain, by trial of intermittent NSAIDs for up to 7 days over 3 months, followed by review.^[5] These two durations are not a contradiction: one is a trial of a strategy, the other a pattern of intermittent use; both say "try, review, and do not escalate blindly". Guidelines differ on exactly how to run the trial, so follow your local guideline. Use local formulary cautions, renal status, gastrointestinal risk and interactions.

Hormonal treatment works by suppressing ovulation and menstruation and by lowering systemic and local estrogen stimulation of lesions. It can reduce pain and does not permanently harm later fertility.^[2] Hormonal treatment for endometriosis does not treat infertility, so do not give it to someone actively trying to conceive.^[2]

First-line options for women with endometriosis who are not trying to conceive include the combined oral contraceptive pill, the contraceptive vaginal ring, progestogen-only options (oral, depot injection, implant, intrauterine system), and oral dienogest.^[5] ESHRE's strong recommendation is to offer hormone treatment (combined hormonal contraceptives, progestogens, GnRH agonists or GnRH antagonists) as one of several options to reduce pain.^[1] NICE offers hormonal treatment (for example, the combined pill or a progestogen) for suspected, confirmed or recurrent endometriosis.^[2] Choice is guided by preference, symptoms, previous contraceptive use, adverse effect profiles and contraindications. Review response within 3 to 6 months, including pain, bleeding, adverse effects and suitability; if the response is unsatisfactory, an alternative first-line hormonal method can be tried.^[5]

For adenomyosis, first-line hormonal treatment options are oral dienogest, oral contraceptives, the levonorgestrel intrauterine system and the etonogestrel implant, with review after 3 months and escalation or referral if there is no improvement.^[5]

The levonorgestrel intrauterine system deserves a special mention: it reduces menstrual loss and local prostaglandins, works for both conditions, and is first-line contraceptive option for women of all ages including young women who have not had children.^[5] A short course of a GnRH agonist can be used as an adjunct before deep-devive surgery (below) and sometimes as a test of whether pain is hormonally driven.

When first-line hormonal treatment does not work, GnRH analogues are second-line for both endometriosis and adenomyosis, and should be initiated and overseen by a gynaecologist.^[5] They suppress systemic estrogen to near-menopausal levels, producing a reversible medical pseudo-menopause. That is exactly what reduces bleeding and lesion activity, and exactly why adverse effects occur: hot flushes, vaginal dryness, mood change, headache and reduced bone mineral density. For this reason:

• GnRH agonists (goserelin or nafarelin by implant or nasal spray) are limited to 6 months without add-back, or to 2 years if combined with menopausal hormone therapy add-back.^[5]
• GnRH antagonists are oral. Relugolix is available as a daily combination tablet with estradiol and norethisterone (add-back) to limit hot flushes and bone loss; NICE's technology appraisal TA1057 allows it for adults of reproductive age who have had medical or surgical treatment for endometriosis.^[3] NICE NG73 also signposts linzagolix with hormonal add-back under TA1067.^[2]
• The 6 month bone-density caution applies to younger patients in particular, who have not yet achieved peak bone mass.

A word about add-back: the aim is to add back just enough estrogen to protect bone and relieve vasomotor symptoms, while keeping the patient hypoestrogenic enough to keep the disease suppressed. That tension is why these drugs are second-line and specialist-directed.

Surgery for endometriosis is usually laparoscopic, should be performed by a gynaecologist with appropriate laparoscopic skill, and has clear goals: diagnosis plus treatment, relief of pain, restoration of fertility, or management of complications such as bowel obstruction. Perform surgery laparoscopically unless there are contraindications, and record findings with intra-operative imaging.^[2]

• For peritoneal disease not involving bowel, bladder or ureter, and for uncomplicated endometriomas, laparoscopic treatment can be considered during a diagnostic laparoscopy.^[2]
• Excision and ablation offer equivalent benefit for pain in most peritoneal disease; excision is more expensive in operating time and bleeding risk. For endometriomas, excision (stripping the cyst wall) is preferred to ablation, balanced against fertility wishes and ovarian reserve.^[2][5]
• For deep disease involving bowel, bladder or pelvic side wall, surgery should be performed by specialists with appropriate expertise, often in a multidisciplinary centre with colorectal and urological support.^[5] NICE suggests considering 3 months of a GnRH agonist before surgery for deep disease involving bowel, bladder or ureter.^[2]
• Hysterectomy rarely helps pain on its own. NICE notes there is little evidence that hysterectomy improves outcomes including pain, and hysterectomy for endometriosis is usually combined with excision of all visible lesions.^[5] Hysterectomy is more clearly indicated when there is adenomyosis or heavy menstrual bleeding that has not responded to other treatments.^[2]
• Careful patient selection is essential. Repeat laparoscopy carries real harms (adhesions, tubal damage) and little or no added benefit in pain for many patients, so NICE and Crawford both stress discussing the possible benefits and risks and the possible need for further surgery.^[2][5]
• After laparoscopic excision or ablation, consider hormonal treatment (for example the combined pill) to prolong benefit and manage symptoms.^[2]

This is a different conversation with different endpoints. The key points:

• Excision or ablation of endometriosis plus adhesiolysis for disease not involving bowel, bladder or ureter improves the chance of spontaneous pregnancy.^[2]
• For endometriomas, laparoscopic cystectomy with cyst-wall excision or drainage and ablation both improve the chance of spontaneous pregnancy; balance cystectomy against possible reduction in ovarian reserve, because ablation and drainage may preserve ovarian reserve more than cystectomy.^[2]
• Do not offer hormonal treatment alone or combined with surgery to women with endometriosis who are trying to conceive, because hormonal suppression does not improve spontaneous pregnancy rates.^[2]
• Do not suppress the cycle for fertility. If a woman requests, or cannot access, conception right away, superovulation and intrauterine insemination or in vitro fertilisation may be appropriate, guided by age and ovarian reserve.
• For deep disease in women trying to conceive, surgery is not automatic. Discuss the possible impact of disease on pregnancy, whether surgery could alter the chance of future pregnancy, risks if complications arise, alternatives, and other fertility factors before deciding.^[2]
• NICE reminds clinicians that the management of endometriosis-related subfertility should involve a multidisciplinary team with a fertility specialist, diagnostic fertility tests, and access to fertility services.^[2]

The same staged approach applies, with menorrhagia as a bigger part of the picture.

• Definition: endometrial tissue within the muscular wall of the uterus, often with a thickened junctional zone. It can occur with or without endometriosis.^[5]
• Epidemiology: about 30% of diagnosed women are asymptomatic; women in their 40s are most often symptomatic; 19% prevalence among women with subfertility in one meta-analysis.^[5]
• Clinical picture: heavy menstrual bleeding, dysmenorrhoea, pelvic pain, subfertility, bladder or gastrointestinal symptoms, an enlarged globular tender uterus, no proven association between stage and symptom severity.^[5]
• Imaging: ultrasound first-line, MRI second-line.^[5]
• First-line medical: oral dienogest, oral contraceptives, levonorgestrel intrauterine system or etonogestrel implant; review after 3 months.^[5]
• Second-line: GnRH agonist or antagonist, specialist-directed, duration-limited.
• Surgery: usually conservative. Endometrial ablation may relieve heavy menstrual bleeding. Hysterectomy ends bleeding and recurrence, but chronic pain sensitisation means pain can persist afterwards, and there is no good evidence for or against hysterectomy relieving adenomyosis-associated pain.^[5] Hysterectomy with excision of any visible endometriosis is also the NICE solution where adenomyosis or heavy menstrual bleeding has not responded to other treatment and surgery is indicated.^[2]

A practical pearl: when a woman in her 40s with menorrhagia and dysmenorrhoea does not respond to hormonal first-line and ultrasound is equivocal, MRI and gynaecological referral should not be delayed simply because symptoms seem "normal for age".

• Chronic pelvic pain, dyspareunia and neuropathic pain; central sensitisation.
• Infertility and recurrent implantation or pregnancy loss, especially with adenomyosis.
• Endometrioma-related risks: rupture, torsion, infection, and reduced ovarian reserve when large or multiple.
• Deep disease: ureteric obstruction and hydronephrosis, bowel stricture, bladder or rectal involvement, and the significant operative challenges these create.
• Adenomyosis: menorrhagia with iron-deficiency anaemia, an enlarged uterus that can complicate any future pregnancy.
• Postmenopausal or exogenous estrogen-related recurrence or persistence (rare) and, on the far side of the differential, the need to remember malignant transformation is extremely rare but must not be dismissed in postmenopausal women with a new mass.
• Surgical complications: adhesions, ureteric or bowel injury, reduced ovarian reserve after cystectomy, recurrence of disease and pain, and the disappointment that can follow when pain outlives surgery.

Endometriosis and adenomyosis are chronic conditions with no cure, but management is effective in most women when it is persistent and personalised. Pain and quality of life improve substantially with the staged approach above, and recurrence after good laparoscopic management combined with postoperative hormonal treatment is much lower than after surgery alone. Fertility improves for many women with appropriate surgery, particularly less advanced disease, but not for all. Natural menopause usually brings relief for estrogen-dependent disease; earlier surgical menopause (oophorectomy) is sometimes chosen but carries significant long-term health risks, so it is never a casual option. The key prognostic factors are the woman's goals, the presence of deep disease, ovarian reserve and the degree of central sensitisation.

There is no proven prevention. Sensible emphasis is on early recognition: severe dysmenorrhoea, chronic pelvic pain and cyclical bowel or urinary symptoms in adolescents and young women should be taken seriously, not normalised, because endometriosis can begin early and ACOG's 2026 guidance applies its diagnosis recommendations to adolescents as well as adults.^[4] NICE's 2024 referral pathway asks clinicians to refer young women aged 17 and under with suspected or confirmed endometriosis to a paediatric and adolescent gynaecology service or to a specialist endometriosis service.^[2]

Screening programmes for the general population are not recommended; there is no test accurate enough. NICE explicitly says do not use serum CA-125 to diagnose endometriosis, and ESHRE does not recommend biomarker testing at all.^[1][2] The best "screening" we have is clinical: listen to the history, and believe it.

• Adolescents. Endometriosis can present with severe dysmenorrhoea and school absence. ACOG's 2026 guidance applies to adolescents, and NICE refers young women to paediatric, adolescent and specialist services. Start with NSAIDs and hormonal suppression where safe; diagnostic laparoscopy should not be the default.^[2][4]
• Women trying to conceive. Avoid hormonal suppression, consider surgery when anatomy is distorted, and use fertility services early, guided by age and ovarian reserve.
• Pregnancy. Endometrioma management and any bowel involvement needs specialist planning. Many women have improvement during pregnancy; complications are uncommon but real.
• Older adults and menopause. New or persistent symptoms after menopause warrant assessment for other pathology, including malignancy, before blaming residual endometriosis.
• Women in pain with a normal ultrasound. This is the commonest scenario; it does not exclude disease and is an indication for empiric treatment or referral.

• Transvaginal ultrasound and clinical diagnosis are available in most settings and are enough to start treatment.
• Pelvic MRI, specialist sonographers, deep-disease surgery, IVF and specialist physiotherapy are scarce. Refer the deep (rectal, bladder, ureter) and extrapelvic cases to centres that can treat them safely.
• When imaging is normal but the history is convincing, avoid rushing to diagnostic laparoscopy solely for confirmation; expensive theatre time and possible morbidity buy little for a woman who could have been treated medically first.
• GnRH agonists, dienogest and other hormonal options may be expensive or unavailable; oral combined pills and progestogens are usually cheaper and near-equivalent first-line options.
• Do not forget iron status, pain and mental health support, and a documented plan for chronic care. These are cheap and effective.

• Endometriosis is endometrium-like tissue outside the uterus, with inflammation; adenomyosis is the same kind of tissue inside the uterine muscle.
• Global prevalence is 2% to 10% generally and up to 50% among women with infertility; one in 10 women of reproductive age are affected in ACOG's statement.
• Pelvic pain and infertility are the dominant problems; adenomyosis adds heavy menstrual bleeding.
• Diagnosis is clinical. Biomarkers (including CA-125) should not be used. Normal ultrasound and normal examination do not exclude endometriosis.
• Ultrasound is first-line imaging; MRI is added for suspected deep disease or adenomyosis.
• NSAIDs and hormonal suppression are first-line for pain; hormonal options include the combined pill, progestogens, dienogest and levonorgestrel intrauterine system.
• GnRH agonists and antagonists are second-line, specialist-directed, and duration-limited because of bone effects.
• Surgery is laparoscopic; excision beats ablation for endometriomas, deep disease needs specialist surgeons, and hysterectomy rarely helps pain unless adenomyosis is present.
• When fertility is a priority, avoid hormonal suppression, and excise or ablate disease plus adhesions; hormonal treatment with surgery does not improve spontaneous conception.
• Adenomyosis shares first-line hormones and second-line GnRH drugs; hysterectomy ends bleeding and recurrence but may not end pain.

Endometriosis and adenomyosis sit at the junction of gynaecology, fertility medicine, pain medicine and general practice. Useful near neighbours for your reading list include dysmenorrhea, chronic pelvic pain, ovarian cysts and endometrioma, infertility, contraception and uterine fibroids. These links are provided as plain text because planned topic files are being added alongside this one.