Does Endometriosis Cause Miscarriage? A Surgeon’s Reading of the Evidence

Endometriosis Surgical Specialists International — Reviewed September 2026

In one paragraph: Women with endometriosis miscarry more often than women without it. That is real, it is measured in millions of pregnancies, and it gets stronger with each loss. What is not established — and we will not tell you otherwise — is that endometriosis caused your miscarriage, or that removing it will prevent the next one. This page lays out what is known, what is contested, and what that means for the decision in front of you.

If You Have Had Losses and You Have Endometriosis, You Have Probably Been Given Two Answers

The first is that it was bad luck. The second is that the two things are unrelated — your endometriosis is a pain problem, your miscarriages are a separate problem, and the specialists for each will see you separately.

Neither answer is good enough. The first is a way of ending a conversation. The second is a statement about how medicine is organised, not about how your body works.

There is a third answer, and it is the position we have argued: endometriosis and recurrent pregnancy loss may frequently be two expressions of the same underlying dysfunction rather than two diseases that happen to share a patient. We put it forward in Fertility and Sterility in 2023, as a question and a position rather than a finding, and it is the frame for everything below.

It also has a consequence you should hold on to while you read: if the two are expressions of one process, then treating the lesion is not automatically the same thing as treating the process. That is why this page will tell you, plainly, that surgery has never been shown to reduce miscarriage.

How Much Higher Is the Risk, Really?

Large population studies agree that the risk is elevated. They disagree about how much.

• A meta-analysis of 24 cohort studies covering 1.92 million women found miscarriage odds of 1.75 in endometriosis.

• The Nurses’ Health Study II, following 196,722 pregnancies prospectively, found a relative risk of 1.40.

• A Danish national cohort of 29,563 women with endometriosis against 295,630 matched controls found the association deepening with each loss: 1.37 for one, 1.75 for two, 2.57 for three or more.

• A separate meta-analysis, addressing reproductive and obstetric outcomes in adenomyosis and endometriosis, found a more conservative 1.30.

What Those Numbers Mean for You, in Absolute Terms

This matters more than the odds ratios, and it is where most of the internet misleads people.

A 40% relative increase is not a 40% chance of miscarriage. If a woman’s baseline risk in a given pregnancy is around 15 in 100 — the figure most commonly quoted, with estimates ranging from roughly 10 to 20 in 100 — a 40% relative increase moves it to roughly 21 in 100. The great majority of pregnancies in women with endometriosis continue normally. Both halves of that sentence are true and you are entitled to both.

The Finding That Should Make Everyone Slow Down

Here is the part that rarely makes it into patient-facing writing, and it is the single most important fact on this page.

The signal is strongest in population registries and weakest — or absent — in IVF.

A 2026 meta-analysis of 29 studies covering 93,071 women with endometriosis undergoing assisted reproduction found miscarriage not significantly increased (RR 1.17, 95% CI 0.71–1.94). A matched study of 313 women conceiving through IVF found no increase either (adjusted OR 0.81). And when embryos are screened so that only chromosomally normal ones are transferred, the difference disappears entirely: 11.1% loss with endometriosis versus 13.5% without.

There are two honest readings of that divergence, and nobody has settled which is right. Either a substantial part of the population-level excess reflects age and how women come to be diagnosed in the first place — or IVF populations are selected and monitored in ways that mask a real effect. We do not know. Anyone who tells you they do is selling something.

One thing the IVF data do not show is that IVF cancels out the disease. The same 2026 meta-analysis found live birth lower with endometriosis (RR 0.72, 95% CI 0.56–0.92), and a prospective cohort that scanned every woman before treatment found cumulative live birth over three cycles of 70.0 in 100 with endometriosis and/or adenomyosis against 85.7 in 100 without (adjusted RR 0.85). The miscarriage signal fades in IVF; the lower chance of getting to a baby does not.

The Stage Paradox

Counterintuitively, the studies that looked stage by stage found the highest miscarriage rates in mild disease — 42.1% in rASRM stage I/II, against 30.8% in stage III/IV and 22.0% in controls. One qualifier belongs with those numbers and is almost always left off: the excess was confined to subfertile women — among fertile women in the same study the rates were 24.5% versus 21.5%, not significantly different.

Two explanations compete — that superficial disease is genuinely more disruptive to an early pregnancy than a large, walled-off endometrioma, or that mild disease is disproportionately found by accident in women already being investigated for infertility. Nobody has separated them. We take that apart properly in Can an ultrasound miss endometriosis?

Either way, the clinical consequence is the same: a clear scan is a statement about the scan, not about your risk.

Why It Might Happen: Mechanism, Honestly Labelled

Everything in this section is biologically real and none of it is clinically actionable yet. We are telling you what is plausible, not what is proven about you.

• Inflammation That Doesn’t Stay Local: Endometriosis is an inflammatory disease of the whole pelvic environment, not a collection of isolated implants. Plasma IL-17A is substantially higher in women with endometriosis than in women without it, and surgical removal of lesions significantly reduces it. A separate study that sampled a broad cytokine panel before surgery, at two weeks and at three months found several inflammatory markers — GM-CSF, IL-2, IL-8 and IL-10 — significantly lower by two weeks, and beginning to rise again by three months. Neither study measured pregnancy outcome. What they establish is that the inflammatory milieu is not fixed. What they do not establish is that changing it changes anything that matters to you. That is a biomarker moving. It is not evidence of a fertility benefit, and we will not present it as one.

• Progesterone Resistance: Endometriotic tissue shows a disturbed progesterone receptor profile, and the endometrium in endometriosis responds abnormally to progesterone signalling. This is tissue-level and in-vitro evidence. No test for it predicts an individual woman’s outcome, and no assay for HOXA10 or decidualisation is clinically validated. It is the mechanism we think most likely to connect endometriosis with loss, and the main thread in the “two manifestations” argument above. That is our hypothesis, not a demonstrated cause, and the IVF and euploid-transfer findings earlier on this page are a reason for caution about it.

• The Junctional Zone and How the Placenta Takes Hold: The inner myometrium behaves abnormally in endometriosis and adenomyosis, and the “great obstetrical syndromes” — pre-eclampsia, abruption, preterm birth, some stillbirth — share a signature of defective deep placentation. Junctional-zone thickening appears in a large proportion of women with endometriosis. Whether that abnormality precedes the disease or follows it has never been established.

• What Mechanism Does Not Support: It does not support the claim that endometriosis makes your embryos chromosomally abnormal and that is why you miscarry. When investigators actually examined the chromosomes of miscarried pregnancies after IVF, they found no difference in the rate of chromosomal abnormality between women with and without endometriosis (35.3% vs 43.5%). If follicular-fluid oxidative stress translated into meaningfully worse embryo genetics, that is exactly where it would have shown up. It didn’t. The precise statement is quantity, not quality: endometriosis more consistently affects the number of eggs and ovarian reserve than the chromosomal normality of the embryos those eggs make.

Adenomyosis: The Confounder Nobody Has Untangled

This is the most important unresolved question in the field, and it is not usually disclosed to patients.

Adenomyosis carries a miscarriage signal that looks larger than endometriosis — roughly double, in a meta-analysis of nine IVF studies (RR 2.12, 95% CI 1.20–3.75). The most-quoted figure, a threefold increase, rests on two studies with a confidence interval running from 1.41 to 8.65. Treat it as “roughly double, with wide uncertainty,” not as a fact.

In some small studies the signal persists when the embryo is a less likely explanation. In a retrospective study of 171 pregnancies after a single euploid frozen embryo transfer, miscarriage was 53% in the 34 women with adenomyosis against 19.7% in those without, most of it at the very early, biochemical stage. In a prospective study of 228 women receiving donor eggs, miscarriage was 35.4% with adenomyosis against 18.1% without, although live birth did not differ significantly (36.8% against 43.9%). Donor eggs remove the effect of the recipient’s own egg age, but they do not guarantee a chromosomally normal embryo.

Not all studies agree. A prospective study of 648 women having a single euploid transfer found no link between adenomyosis on 3D ultrasound and live birth, although the scan readers often disagreed about who had it. And a 2024 conference abstract of 282 single euploid transfers found that mild adenomyosis made no significant difference to miscarriage or live birth. Our reading is our hypothesis, not a finding: when a chromosomally normal pregnancy is lost, the uterus becomes the leading remaining candidate to map. Mapping it does not prove that it caused the loss.

The two conditions coexist constantly. And the older endometriosis cohorts — the ones generating the headline miscarriage numbers — did not image for adenomyosis at all. The only prospective cohorts to phenotype both by standardised ultrasound had just 21 women with isolated adenomyosis.

So it is entirely possible that some of the miscarriage risk attributed to endometriosis actually belongs to adenomyosis travelling alongside it. No study has separated them adequately. ESHRE’s recurrent-loss guideline now suggests that all women with recurrent loss could have ultrasound to look for adenomyosis — currently the only guideline-level endorsement of doing so.

Practically: if you have had recurrent losses and nobody has looked at your junctional zone, that is a gap worth closing.

What Surgery Does — and What It Has Never Been Shown to Do

We are excision surgeons. This is the section where we have the most to gain by overstating, so read it with that in mind.

• What Surgery Can Do: Relieve pain, and in early-stage disease improve the chance of natural conception. The randomised evidence here compared operative laparoscopy — excision or ablation — with diagnostic laparoscopy alone, and pooled data give odds of 1.89 for a viable intrauterine pregnancy.

• What It Has Never Been Shown to Do: Reduce miscarriage. No randomised trial has been designed to test it. The Cochrane review of 14 randomised trials in 1,563 women reports that no live-birth data exist at all. The two randomised trials that recorded miscarriage at all — Marcoux 1997 and Gad 2012 — are pooled in that same review: 112 women, no clear difference in miscarriage, and low-certainty evidence. There is no benefit to argue about here.

And the guidelines go further. The ASRM committee opinion on recurrent pregnancy loss published in 2026 — the first update since 2012 — explicitly lists “treatment of endometriosis and adenomyosis” among interventions without evidence of benefit for recurrent loss. ESHRE recommends against routine surgery before assisted reproduction for stage I/II disease, and against routine endometrioma surgery.

Our own commentary on the ASRM opinion (manuscript in preparation) accepts that bottom line and adds three qualifications. First, ASRM’s heading for these treatments — “proven ineffective or with no evidence of benefit” — puts treatments that were tested and failed in the same list as questions that have simply never been answered; surgery for endometriosis or adenomyosis as a way of preventing loss belongs to the second group: untested, not disproven. Second, the opinion makes no diagnostic recommendation on adenomyosis at all, whereas ESHRE’s recurrent-loss guideline suggests ultrasound to look for it. Third, its reassuring figure — 50 to 80 in 100 patients with recurrent loss going on to a successful pregnancy without treatment — is population context, not a probability for you, and it fits least well after repeated losses of chromosomally normal pregnancies. None of that turns surgery into a treatment for miscarriage.

That is not the end of the conversation about surgery, and we will say why in a moment. But it is where the conversation has to start, and a practice that hides it from you is not being straight.

The Endometrioma Decision, with the Cost Attached

Removing an endometrioma has a measured, durable price. Pooled data from 14 prospective studies of 650 women show AMH falling by 35–54% after cystectomy, still down at 9 to 18 months. Those are pooled averages, not a forecast for your ovary. Antral follicle count frequently fails to detect this, which is why AMH is the better marker of surgical impact.

That does not make endometrioma surgery wrong. It makes it a trade, and you are the one who should be told the terms.

So Why Operate at All, in a Woman Who Has Miscarried?

Because pregnancy loss is rarely the only thing happening. The honest indications are pain, disease burden and organ involvement: symptoms that have shaped a decade of someone’s life, and disease on bowel, bladder or ureter with its own trajectory.

For some patients the illness starts before, reaches beyond and outlasts the pelvic disease eventually found. For that pattern we have proposed a name, Pelvic Overlap Spectrum Syndrome (POSS): endometriosis and/or adenomyosis, confirmed or strongly suspected, plus features in other body systems — autonomic, vascular, immune, connective-tissue, nerve sensitisation, gut motility, bladder and pelvic floor, and mood. Reproductive outcomes are recorded but deliberately do not count toward the definition, and POSS is a proposal with provisional research criteria, not a validated diagnosis; it describes conditions that occur together and is not a claim that they share one biology. One practical consequence is that surgery is aimed at structural disease and is not offered as treatment of the whole illness.

What it does not do is come with a promise about your next pregnancy. We would rather operate on the honest indication than manufacture a false one. If a transfer is the reason surgery has been suggested to you, read Surgery before your next transfer: questions to ask before you consent first. That page also explains the one situation we weigh differently, recurrent loss with endometriosis and an otherwise empty evaluation, where we treat surgery before the next transfer as a strong consideration, decided case by case. That is phenotype-matched reasoning, not a proven benefit.

The Other Risk Nobody Mentions: The Pregnancy Itself

If you do conceive, this is the evidence that is actually strong — and it is the part most often left out of the conversation entirely.

• Placenta Previa: Elevated in every major meta-analysis, with odds between 2.2 and 3.3, reaching 5.82 in a 2026 prospective cohort where every woman was scanned before treatment. It is the most consistent obstetric finding in endometriosis.

• Preterm Birth: Consistently raised, roughly 25–70% in relative terms.

• Caesarean Delivery: Elevated in most analyses, though that is heavily influenced by clinician behaviour rather than biology alone.

What is not established: Pre-eclampsia as a specific diagnosis, postpartum haemorrhage and small-for-gestational-age babies are inconsistent across the major analyses — significant in some, null in others. We are not going to tell you they are proven risks, because they are not. The broader composite of hypertensive disorders of pregnancy is a different and more consistent story — raised in the Nurses’ Health Study II (RR 1.30, 95% CI 1.16–1.45) and in the 2026 assisted-reproduction meta-analysis (RR 1.16, 1.10–1.23) — and that is worth your obstetric team knowing, even though pre-eclampsia on its own is unsettled.

The practical point: a pregnancy in a woman with endometriosis is not automatically high-risk, but it warrants early placental localisation and an obstetric team that knows the history. That is a conversation to have at booking, not at 28 weeks.

Immune Testing and NK Cells: What the Results Can Tell You

Many women arrive having already been tested — NK cells, cytokine ratios, Th1:Th2, HLA or KIR genotyping — often at considerable cost. Here is what those results can and cannot tell you.

Uterine natural killer cells do behave differently in women with recurrent miscarriage. The largest systematic review to date, covering 1,100 women, found them modestly elevated. Three things follow from that same review, and all three matter:

1. There is no established normal range.

2. Uterine NK level does not predict whether a given pregnancy continues.

3. Blood NK levels showed no significant correlation with uterine NK levels.

That third point is not a matter of interpretation. A blood NK test does not tell you what is happening in your uterus.

Both ESHRE (2023) and ASRM (2026) recommend against routine immune testing in recurrent loss. ASRM lists IVIG, intralipids and prednisone among treatments proven ineffective or without evidence of benefit — the same heading that, as noted above, mixes tested-and-failed with not-yet-answered. ESHRE finds insufficient evidence to recommend intralipid and recommends against glucocorticoids, both as Strong recommendations — with one narrow Conditional exception: repeated high doses of IVIG very early in pregnancy may improve live birth in women with four or more unexplained losses. The American Society for Reproductive Immunology published recommendations in 2025 taking a more permissive, biomarker-guided position. Those bodies are in open disagreement, and you deserve to know that before anyone bills you.

We do offer immune evaluation, selectively: in the context of endometriosis, and after recurrent loss or implantation failure where a complete standard evaluation has found nothing. Where that evaluation finds a defined immune abnormality, we may also treat it, with one drug at a time and never a combination. Neither ASRM nor ESHRE carves out those groups, and apart from aspirin and heparin for antiphospholipid syndrome and ESHRE’s narrow IVIG recommendation, they do not support those treatments. That makes our approach phenotype-matched reasoning, not established treatment, and we tell patients so before anything is ordered. Our evaluation includes a Th1/Th2 profile even though ESHRE recommends against cytokine testing as a Strong recommendation. We use it as one input and never on its own, because “no evidence of benefit” is not the same as “proven ineffective”. It has no validated cut-off, and we say so. What we test, what we may treat, what we never use and what the trials show are set out on the NK page linked below.

Disclosure: Dr. Vidali directs this practice’s reproductive-immunology program, which offers clinical evaluation and treatment of immunologic reproductive failure, and he founded and has an ownership interest in Pregmune, a reproductive immunology testing company. Weigh what we say about immune testing with that in mind.

In endometriosis specifically, the consistent NK finding runs the opposite way to the one patients are sold. It is not too many NK cells attacking a pregnancy. It is NK cells in the pelvis and the blood that work less well, while the uterine lining shows no consistent change. That has not been shown to cause miscarriage, and it is not a reason to test or treat. We set out that evidence, with its sources, in NK cells in endometriosis: why the problem is weakness, not attack.

Diagnosis: You Do Not Need Surgery to Be Believed

ACOG’s 2026 clinical practice guideline recommends transvaginal ultrasound as the first imaging test, and no longer requires surgical confirmation — endometriosis may be diagnosed, and treatment begun, on symptoms, history and examination. NICE has moved in the same direction on imaging, recommending early transvaginal ultrasound in everyone with suspected endometriosis even when the pelvic examination is normal; it does not go on to endorse diagnosis without surgical confirmation.

In expert hands, ultrasound is very good at deep disease: around 89% sensitivity for rectal involvement. It is much weaker elsewhere — about 60% for uterosacral ligaments, and parametrial disease is the hardest compartment for both ultrasound and MRI. Those are referral-centre numbers with trained operators, not community-ultrasound numbers.

And a normal scan does not exclude endometriosis — particularly superficial peritoneal disease, for which no imaging method has an established sensitivity. The international consensus statement on non-invasive imaging covers deep endometriosis only; superficial disease is explicitly outside its scope. That is precisely the phenotype associated with the highest miscarriage rate. Emerging biomarker and AI-assisted platforms show promising preliminary performance but lack external validation and are not ready for clinical use.

Time from first symptom to diagnosis is still measured in years: commonly six to ten in Europe, with NICE citing eight to ten. An umbrella review of 52 systematic reviews published in 2026 found that this has not meaningfully improved in twenty years.

A normal scan does not mean you do not have endometriosis. It means the scan was normal.

What We Will and Won’t Tell You

We can tell you that endometriosis is associated with a higher rate of miscarriage, that the association strengthens with each loss, and that the obstetric risks in an established pregnancy are real and manageable. ESHRE’s endometriosis guideline says as much in its own careful words — clinicians “should be aware that there may be an increased risk of first trimester miscarriage and ectopic pregnancy” — and that is a Strong recommendation with the hedge written into the middle of it.

We cannot tell you that endometriosis caused your losses, that treating it will prevent the next one, or that any test currently available will identify which women are at risk.

Those are the limits of the 2026 evidence. We would rather state them than sell certainty we do not have — and if a clinic has offered you certainty, that is the thing to ask them about.

How ESSI Approaches This

Most practices see one half of this problem. A fertility clinic sees the losses. A gynaecologist sees the pain. We were built to see both at once. Dr. Vidali is a reproductive endocrinologist, a reproductive immunologist and an excision surgeon, so the same person reads your transfers, your immune results and your scans.

That changes what we can offer you:

• One map before any decision: The surgeon performs your pelvic ultrasound and Doppler himself, with no technician in between. It covers the ovaries, the deep compartments and the junctional zone of the uterus, where adenomyosis sits.

• Complete excision as the foundation, when there is an indication for it: Where disease is structural, painful or involving the organs, we remove it completely, robotically or laparoscopically, in one coordinated operation with colorectal or urologic colleagues when needed.

• Uterus-sparing treatment of adenomyosis: For women who want to keep the uterus, we use microwave ablation to treat the adenomyotic tissue while leaving the lining and cavity in place. Evidence on pregnancy after microwave ablation is still limited, and we plan conception timing with you.

• Protecting the ovaries: For selected endometriomas, we use the argon beam coagulator on the cyst wall instead of stripping it. This technique is designed to limit the loss of healthy ovarian tissue. Where the ovary is at risk, we also discuss banking eggs or embryos first.

• Immune evaluation only where it belongs: With every treatment labelled for what it is: evidence-based, or our clinical reasoning.

None of this comes with a promise about your next pregnancy. It comes with a complete picture, and a plan you can understand.

What a First Consultation Actually Involves

Not a surgical booking. A diagnostic conversation.

• A full reproductive and surgical history, including every loss, every cycle, and what was and wasn’t tested.

• Review of outside imaging, operative reports and pathology — read, not skimmed.

• Where indicated, detailed pelvic ultrasound with attention to the junctional zone, ovarian mobility and deep disease, performed by the surgeon.

• An honest statement of what we think is going on, what we don’t know, and whether surgery has anything to offer you.

The first time you meet your surgeon should never be the day of your surgery.

Keep Reading

• Can an ultrasound miss endometriosis? — why a clear scan excludes almost nothing, and what a proper evaluation would do differently.

• Miscarriage after a euploid embryo: what to check next — what PGT-A tests, what it does not, and the question to ask about your miscarriage tissue.

• Surgery before your next transfer: questions to ask before you consent — the case against reflexive operating, and the AMH cost of endometrioma surgery.

• Pregnant with endometriosis: why your placenta needs an early look — obstetric risk after endometriosis, and the one thing worth asking for at booking.

• NK cells in endometriosis: why the problem is weakness, not attack — why the NK problem in endometriosis is reduced function, not attack, and what that does and does not mean.

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Endometriosis Surgical Specialists International (ESSI)