PCOS, Now Called PMOS: Diagnosis, Treatment and Fertility

Key Takeaways

PMOS (formerly PCOS) is the same clinical condition under a new name selected through a global consensus process. Diagnosis still follows revised Rotterdam criteria after exclusions. AMH may replace ultrasound for polycystic ovarian morphology in adults only — never as a stand-alone test. Glycaemic status should be assessed at diagnosis regardless of BMI, preferably with a 75 g OGTT. Letrozole is first-line for anovulatory infertility when no other major infertility factor is present. IVF, when needed, prioritises OHSS prevention with antagonist protocols, agonist trigger and freeze-all in predicted high responders.

Key evidence: 2023 International Evidence-based Guideline (Teede et al.) · Lancet — PMOS naming consensus (2026) · ASRM — PCOS is now PMOS (May 2026)

PCOS / PMOS: diagnosis, treatment and fertility

PMOS (formerly PCOS) is the new name selected through a May 2026 global consensus process and endorsed by leading international professional organisations — not merely a suggestion. Patients, laboratories and health systems still use PCOS widely. In titles and search-facing text, PCOS / PMOS belong together for now. After first mention, this guide mainly says PMOS.

PMOS is the same clinical picture previously called PCOS; the name has changed, and your diagnosis and treatment remain valid. Diagnostic criteria and care recommendations from the 2023 international guideline did not change with the rename. A roughly three-year transition is planned, with fuller integration into the expected 2028 international guideline. See also ASRM and the Endocrine Society. For a short naming overview: PMOS: the new name for PCOS.

The point of the new name is simple: this is not a disease of “cysts.” It involves reproductive, hormonal and metabolic health together. PMOS is the most common endocrine disorder in women of reproductive age — about 10 to 13% with Rotterdam criteria (WHO) — and the leading cause of anovulatory infertility.

Three practical points from the 2023 guideline still shape care:

• Adult ultrasound thresholds for polycystic ovarian morphology: ≥ 20 antral follicles per ovary (high-frequency probe ≥ 8 MHz) or ovarian volume ≥ 10 mL. In adults, AMH may replace ultrasound for that morphological criterion — not as a stand-alone diagnosis, and not with one universal cut-off.
• Letrozole is preferred for ovulation induction when anovulation is the main infertility problem and no other major factor is present.
• Lifestyle and metabolic health matter at every age — whether or not pregnancy is the immediate goal.

PMOS in numbers

• Prevalence: about 10 to 13% of women of reproductive age.
• Anovulatory infertility: PMOS is the most common cause worldwide.
• Diagnostic delay: many women wait a long time and see several clinicians before recognition (Gibson-Helm et al., 2017).
• Metabolic risk: long-term type 2 diabetes risk is substantially higher — and not only in those with higher BMI.
• Pregnancy: gestational diabetes, hypertensive disorders and preterm birth are more common in many cohorts, so antenatal surveillance should be adapted.

What drives PMOS?

There is no single cause. Three mechanisms often feed each other:

• Brain–ovary signalling: GnRH pulses can raise LH relative to FSH, which pushes ovarian androgen production and can stall normal follicle growth. The LH/FSH ratio is not a diagnostic test.
• Ovarian hyperandrogenism: the ovaries make more testosterone and androstenedione than they should.
• Insulin resistance: common at any body size. Higher insulin fuels ovarian androgen production and lowers SHBG, so more free androgen circulates.

Genetics matter, and so do metabolic and environmental factors. Endocrine disruptors and the intrauterine environment are research questions — not proven single causes.

How diagnosis works

In adults, diagnosis still follows revised Rotterdam criteria: two of three features, after other causes are excluded.

The three criteria

1. Oligo- or anovulation, defined by years since menarche (see table below).
2. Clinical or biochemical hyperandrogenism:
   • clinical: hirsutism (Ferriman-Gallwey score ≥ 4–6 depending on population), moderate-to-severe or treatment-resistant acne, androgenic hair loss;
   • biochemical: raised total or free testosterone, or free androgen index.
3. Polycystic ovarian morphology on ultrasound, or — in adults — AMH used instead of ultrasound for that morphological criterion:
   • ultrasound: ≥ 20 antral follicles per ovary (high-frequency probe) or ovarian volume ≥ 10 mL;
   • AMH is an adult alternative to ultrasound for polycystic ovarian morphology only. It is not a stand-alone PMOS test. There is no universal AMH cut-off. Ultrasound and AMH should not both be used to establish the same morphological criterion, because this adds no diagnostic value and may increase the risk of over-diagnosis. AMH is not used to diagnose PMOS in adolescents.

If irregular cycles and hyperandrogenism are already present, neither AMH nor the ultrasound morphology criterion is needed to complete the diagnosis. In adults, diagnosis can rest on ovulatory dysfunction and hyperandrogenism even when polycystic ovarian morphology is absent or has not been assessed. Metabolic features shape health risks and management, but they are not diagnostic criteria.

Menstrual irregularity by years since menarche

What to exclude first

• Pregnancy should be excluded where clinically relevant, particularly with amenorrhoea
• Hyperprolactinaemia — see hyperprolactinaemia
• Thyroid dysfunction
• Non-classic congenital adrenal hyperplasia (17-OH-progesterone)
• Cushing’s syndrome if clinically suspected
• Androgen- or cortisol-secreting tumours

Rapidly progressive hirsutism, deepening of the voice, clitoromegaly or markedly elevated androgen levels require urgent evaluation for causes other than PMOS.

The four phenotypes — useful, not a destiny map

Rotterdam combinations create four phenotypes that describe how different PMOS can look:

• A (complete): anovulation + hyperandrogenism + polycystic morphology — often a more adverse average metabolic profile
• B: anovulation + hyperandrogenism — metabolic picture often similar to A on average
• C (ovulatory): hyperandrogenism + polycystic morphology with preserved cycles — intermediate on average
• D (non-hyperandrogenic): anovulation + polycystic morphology without hyperandrogenism — often a milder average metabolic profile, but individual risk still needs checking

Phenotypes describe patterns. They do not replace individual assessment of weight, glucose, lipids, blood pressure, symptoms and fertility goals.

What patients notice

• Widely spaced periods, amenorrhoea, or irregular cycles since puberty
• Hirsutism, persistent inflammatory acne, or crown/midline hair thinning
• Difficulty conceiving when ovulation is rare or absent
• Acanthosis nigricans — a clinical clue to marked insulin resistance
• Weight that is hard to manage for some, but not for everyone
• Sleep apnoea symptoms more often than expected
• Anxiety, low mood, and body-image strain

Examination usually covers Ferriman-Gallwey score, blood pressure, waist circumference, BMI, and a look for acanthosis nigricans.

Blood tests that actually help

A typical workup includes:

• Total and free testosterone, SHBG (and free androgen index if needed). Validated LC–MS/MS is the preferred method for total testosterone. If it is unavailable, use a high-quality assay shown to perform adequately at the low concentrations seen in women, and interpret results with that method’s limits in mind. Biochemical androgen assessment is unreliable on a combined oral contraceptive; if testing is essential, stopping the pill should be discussed only under medical supervision, with alternative contraception planned.
• 17-OH-progesterone to rule out non-classic CAH
• DHEAS when adrenal contribution is being weighed
• AMH only when used as an adult alternative to ultrasound for morphology
• TSH and prolactin
• Glycaemic assessment at diagnosis, regardless of age or BMI — a 75 g OGTT is the most accurate test. Fasting glucose and HbA1c are lower-accuracy alternatives when OGTT cannot be done. Even a normal HbA1c or fasting glucose can miss post-meal glucose disturbance in PMOS — which is why OGTT is preferred, especially before pregnancy or fertility treatment.
• Full lipid profile

Vitamin D may be checked when deficiency is suspected or local guidance says so. It is not a PMOS diagnostic test.

Insulin resistance is central to the biology, but routine fasting insulin or HOMA-IR is not accurate or standardised enough for diagnosis or follow-up. A high fasting insulin or HOMA-IR alone is not a prescribing threshold.

Glucose status is usually rechecked every 1 to 3 years, depending on results and risk.

Metabolic and heart health

Cardiometabolic risk in PMOS is not limited to higher BMI:

• Type 2 diabetes risk is substantially higher long term — screen at diagnosis and every 1–3 years as risk dictates (OGTT preferred)
• Gestational diabetes risk is higher — offer OGTT before conception or fertility treatment when possible
• Triglycerides often rise and HDL often falls
• Metabolic syndrome is common when other risk factors cluster
• Fatty liver is more common with metabolic risk factors; normal ALT or AST does not exclude fatty liver
• Screen for sleep apnoea when snoring, unrefreshing sleep or daytime sleepiness appear

How often to reassess

Managing symptoms when fertility is not the only goal

Lifestyle first

Nutrition, movement, sleep and stress care come first for everyone. In women with overweight, a 5 to 10% weight loss often improves cycles, spontaneous fertility and metabolic markers. Counselling should avoid blame. Benefits can occur even without weight loss.

No single diet has clear superiority. Mediterranean, lower-glycaemic and DASH-style patterns are all reasonable. Aim for about 150 minutes of moderate activity a week, or 75 minutes vigorous, plus some strength work when feasible.

Cycles and skin

Combined oral contraceptives can regulate cycles and help clinical hyperandrogenism. No pill is “the PMOS pill.” Lower oestrogen doses and lower-risk preparations are generally preferred first. Preparations with 35 µg ethinylestradiol plus cyproterone acetate remain second-line: for marked hyperandrogenic symptoms not controlled with safer options, after careful review of venous thromboembolism risk.

Laser, electrolysis or topical eflornithine can help hair. Anti-androgens such as spironolactone are second-line in selected cases — always with reliable contraception.

Protecting the endometrium

The goal is not simply to produce a bleed. It is to protect an endometrium exposed for long periods to unopposed oestrogen.

PMOS raises the relative risk of endometrial hyperplasia and endometrial cancer, but the absolute risk stays low, so routine screening ultrasound or biopsy is not recommended for everyone. Bleeding-free intervals longer than 90 days warrant clinical review and discussion of endometrial protection, usually through cycle regulation or regular progestogen exposure.

Choice depends on the aim:

• contraception, cycle control, acne or hirsutism also needed, and no contraindication → combined oral contraceptive often appropriate
• endometrial protection alone, or oestrogen unwanted or contraindicated → cyclic progestogen
• pregnancy desired → ovulation-induction planning rather than a contraceptive pill

Metformin

In adults with BMI ≥ 25 kg/m², metformin should be considered for metabolic outcomes, alongside active lifestyle intervention. It is not automatic: glycaemic status, gastrointestinal tolerance, contraindications and patient preference still matter. Evidence at BMI < 25 kg/m² is more limited; in that group metformin is discussed mainly with impaired glucose tolerance or prediabetes, clear central metabolic risk, or when cycle regulation is needed and a combined pill cannot be used. A single fasting insulin or HOMA-IR result is not a prescribing threshold.

Gastrointestinal effects are common early; dose escalation should be gradual. Long-term use can lower vitamin B12 in some people. Metformin should not be presented as a general improver of pregnancy outcomes apart from its role in selected ovulation-induction settings.

Inositols

Benefits remain uncertain. No type, dose or myo- to D-chiro-inositol ratio can currently be recommended. For infertility, inositol stays experimental. Product quality varies.

Ovulation induction

Before treatment, check the basics: semen analysis, tubal testing when it would change the plan, age and infertility duration, and preconception metabolic preparation — including OGTT when pregnancy or fertility treatment is planned.

Letrozole

Letrozole is the preferred first-line pharmacological option for women with PMOS who have anovulatory infertility and no other major infertility factor. Starting dose and any escalation are individualised under fertility-specialist supervision, guided by previous response, ovulation and ultrasound monitoring — not by a self-directed schedule.

The PPCOS II trial (Legro et al., 2014) compared letrozole and clomiphene in 750 women:

• Live birth: 27.5% with letrozole vs 19.1% with clomiphene in that trial
• Cumulative ovulation: 61.7% vs 48.3%
• Overall side-effect profile was comparable; letrozole generally has less anti-oestrogenic effect on the endometrium than clomiphene

In many countries, letrozole for ovulation induction is still off-label. That should be said openly.

Clomiphene — an alternative oral option

If letrozole is unsuitable, unavailable or unsuccessful, clomiphene can be an alternative. Because of multiple-pregnancy risk, ultrasound monitoring is needed in some cycles.

Gonadotrophins and drilling

If oral agents fail, low-dose gonadotrophin stimulation with close monitoring may follow. Watch multiples and hyperstimulation carefully — see ovarian stimulation in IVF.

Ovarian drilling is for selected resistant cases or when surgery is already needed for another reason. It is no longer routine care.

When IVF makes sense

Without an absolute IVF indication, IVF generally comes after ovulation-induction options have not worked. Earlier IVF may be appropriate with:

• severe male factor, tubal blockage, older age, or long infertility duration
• repeated genuinely ovulatory induction cycles without pregnancy
• oral-agent resistance and inability to achieve a safe monofollicular response with gonadotrophins
• clearly reduced ovarian reserve, or expected rapid reserve loss
• advanced endometriosis or another coexisting infertility factor
• need for PGT-M or PGT-SR
• previous cycles where uncontrolled multifollicular response made IUI unsafe to continue

A high AMH or a high follicle count alone is not an indication for earlier IVF. See IVF for ovulation disorders.

IVF when ovaries respond strongly

High follicle counts and ovarian sensitivity raise OHSS risk. The protocol has to respect that.

Safety framework

In a predicted high responder, an antagonist protocol with GnRH-agonist trigger and freeze-all is the most effective first-line way to reduce OHSS risk — including late OHSS when a fresh transfer is deferred (ASRM OHSS prevention guideline, 2023).

Also:

• start gonadotrophins conservatively and individually (age, BMI, AMH, antral follicle count, previous response)
• freeze-all when the whole response — follicles, estradiol, egg yield, symptoms and trigger choice — points to real OHSS risk; there is no single universal follicle-count cut-off (frozen embryos in IVF)
• optimise weight, glucose and blood pressure before stimulation when needed

Women with PMOS often retrieve many eggs. More eggs do not automatically mean a higher live-birth chance. Age, embryo quality, metabolic health, the endometrium and safe transfer planning all matter. IVF should be managed by a team experienced in individualised stimulation and OHSS prevention.

Cabergoline and other add-ons

Cabergoline is not limited to hCG-trigger cycles alone — but routine additional cabergoline is generally not required when an effective GnRH-agonist trigger and freeze-all strategy has already been used. It may be considered when residual OHSS risk remains — for example after an hCG or dual trigger, an extreme response, or other clear risk factors. Practice varies according to the trigger, ovarian response and guideline followed (ASRM OHSS prevention guideline, 2023; ESHRE ovarian stimulation update, 2025). Cabergoline never replaces antagonist protocols, agonist trigger or freeze-all when those are indicated.

Pregnancy

• Offer a 75 g OGTT before conception or fertility treatment when possible. If missed, offer it at the first antenatal visit and again at 24–28 weeks. Early HbA1c or fasting glucose alone can miss cases.
• Watch blood pressure and proteinuria for pre-eclampsia risk.
• Preconception care: folic acid, medication review, smoking and alcohol advice, and a realistic plan for weight, blood pressure and glucose. Vitamin D or iodine should follow documented need and local pregnancy guidance.
• PMOS alone is not a reason to continue metformin throughout pregnancy. It has not been shown to prevent gestational diabetes, late miscarriage, pre-eclampsia or macrosomia as routine care. In selected higher-risk situations — for example concern about preterm birth or excessive gestational weight gain — continuation may be discussed jointly with obstetrics and endocrinology. If prediabetes or diabetes is present, the decision is glycaemic management in pregnancy, not “PMOS treatment” alone. Uncertainty about longer-term childhood outcomes should be shared.

Adolescents

Mild cycle irregularity and mild acne are common early after menarche. Severe or treatment-resistant acne — and especially hirsutism — carry more weight.

Adolescent diagnosis needs both persistent irregularity (by years since menarche) and clinical or biochemical hyperandrogenism, after exclusions.

Within eight years of menarche, ultrasound should not be used to diagnose PMOS by showing polycystic ovarian morphology. Ultrasound may still be done when another pelvic pathology is suspected. AMH should not be used to diagnose PMOS in adolescents. The exception pathway is not “make an early diagnostic exception” — it is to label the patient at increased risk, treat symptoms, and reassess by full reproductive maturity (around eight years after menarche).

Mental health

Screen adults and adolescents for depression and anxiety with validated tools, and assess self-harm risk when indicated. Think about eating disorders and disordered eating before pushing weight-loss programmes. Lifestyle advice should not shame.

Care in Türkiye

For most patients, diagnostic and medical management in Türkiye follows the same international evidence-based principles. Legal restrictions matter especially when donor gametes or other regulated reproductive options are considered: oocyte, sperm and embryo donation, and surrogacy, are not permitted. When ovarian reserve is preserved, care usually stays within own-oocyte ovulation induction or IVF.

Dr. Aksoy’s approach

I treat PMOS as a reproductive and metabolic condition — not a cyst hunt. I use AMH as an adult morphology alternative, never as a solo diagnostic test, and I do not order ultrasound and AMH together for the same criterion. I prefer OGTT at diagnosis and before pregnancy planning, because a normal fasting glucose or HbA1c can still miss post-meal disturbance. In adults with BMI ≥ 25, I consider metformin for metabolic outcomes alongside lifestyle — it is not automatic from BMI or from one insulin number. Letrozole dosing stays under specialist supervision. In predicted high responders, antagonist protocol with agonist trigger and freeze-all comes first; extra cabergoline is selective when residual OHSS risk remains. And bleeding-free intervals beyond 90 days warrant review of endometrial protection — not a shrug.

In practice

• PMOS (formerly PCOS) is the same diagnosis under a new consensus name; criteria and treatment principles from 2023 still apply
• Adults: Rotterdam 2 of 3 after exclusions; AMH only as adult ultrasound alternative; never both for the same morphology criterion
• Adolescents: irregularity by years since menarche plus hyperandrogenism; no ultrasound/AMH for PCOM diagnosis within 8 years of menarche
• Glucose at diagnosis regardless of BMI; prefer 75 g OGTT
• Protect the endometrium if bleeds are rare (> 90 days without bleeding warrants review)
• Metformin: should be considered in adults with BMI ≥ 25 for metabolic outcomes, alongside lifestyle — not automatic; not driven by HOMA-IR
• Letrozole first for anovulatory infertility without other major factors; dose individualised by a specialist
• IVF usually after failed ovulation induction, unless a clear earlier indication; OHSS prevention built in

FAQ

Can PMOS (PCOS) be cured?

No. It is chronic. Cycles, skin and metabolism are often manageable. Many women notice cycle changes later in reproductive life.

Does PMOS mean I cannot get pregnant?

No. Many women conceive naturally once ovulation returns, with ovulation induction, or with IVF. A high follicle count does not guarantee higher IVF live-birth rates.

Why letrozole rather than clomiphene?

In PPCOS II, live birth was higher with letrozole than clomiphene in that population. The 2023 guideline ranks it as the preferred first oral option when anovulation is the main problem. If letrozole is unsuitable, unavailable or unsuccessful, clomiphene can be an alternative — with ultrasound monitoring in some cycles because of multiple-pregnancy risk.

Should everyone take metformin?

No. In adults with BMI ≥ 25 kg/m² it should be considered for metabolic outcomes alongside lifestyle, but it is not automatic — glycaemic status, tolerance, contraindications and preference still matter. It should not continue through pregnancy solely because of PMOS.

Do inositols work?

Evidence is mixed. No specific type, dose or 40:1 ratio can be recommended. For infertility, treat them as experimental.

How real is OHSS risk in IVF?

Real — and largely controllable with antagonist protocols, agonist trigger, individualised dosing and freeze-all in predicted high responders. Routine extra cabergoline is generally not required once that pathway is effective, but it may be considered when residual OHSS risk remains.

What weight should I aim for?

There is no universal target. A 5 to 10% loss in women with overweight often helps cycles and insulin sensitivity. The conversation should not be shaming.

My teenager has irregular cycles and acne. Is it PMOS?

Maybe, maybe not. Firm diagnosis needs persistent irregularity defined by years since menarche plus hyperandrogenism, after exclusions. Ultrasound and AMH are not used to diagnose PMOS by morphology within eight years of menarche; ultrasound may still be done if another pelvic problem is suspected. “At increased risk” follow-up is often wiser than a lifelong label.

What should I bring to the visit?

If available, bring recent relevant laboratory results (androgens, TSH, prolactin, glucose/OGTT or HbA1c, lipids; AMH only if already done for adult morphology). Ultrasound reports help if you have them, along with a cycle diary, weight history, family history of diabetes, and your medication list. You do not need to complete every test before the first visit.

Sources

1. Teede HJ, Tay CT, Laven JJE, et al. Recommendations from the 2023 International Evidence-based Guideline for the Assessment and Management of Polycystic Ovary Syndrome. Fertil Steril 2023;120(4):767–793. doi:10.1016/j.fertnstert.2023.07.025. PMID: 37589624. Also: Hum Reprod open-access version.
2. ASRM. Recommendations from the 2023 International Evidence-based Guideline for the Assessment and Management of Polyendocrine Metabolic Ovarian Syndrome (2023).
3. Teede HJ, Bahri Khomami M, Morman R, et al. Polyendocrine metabolic ovarian syndrome, the new name for polycystic ovary syndrome: a multistep global consensus process. Lancet. 2026;407(10545):2329–2339. doi:10.1016/S0140-6736(26)00717-8. PMID: 42119588.
4. ASRM. PCOS is now PMOS: understanding the name change. May 27, 2026.
5. Endocrine Society. PCOS name change. 2026.
6. ASRM Practice Committee. Prevention of moderate and severe ovarian hyperstimulation syndrome: a guideline. 2023.
7. ESHRE Guideline Group on Ovarian Stimulation, Ata B, Bosch E, Broer S, et al. ESHRE guideline: ovarian stimulation for IVF/ICSI: an update in 2025. Hum Reprod. 2026;41(4):498–514. doi:10.1093/humrep/deag018. PMID: 41732035. Also: ESHRE guideline page.
8. Legro RS, Brzyski RG, Diamond MP, et al. Letrozole versus clomiphene for infertility in the polycystic ovary syndrome. N Engl J Med 2014;371(2):119–129. doi:10.1056/NEJMoa1313517.
9. Gibson-Helm M, Teede H, Dunaif A, Dokras A. Delayed diagnosis and a lack of information associated with dissatisfaction in women with polycystic ovary syndrome. J Clin Endocrinol Metab 2017;102(2):604–612. doi:10.1210/jc.2016-2963.
10. Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome. Hum Reprod 2004;19(1):41–47. doi:10.1093/humrep/deh098.
11. WHO. Polycystic ovary syndrome fact sheet.
12. Monash University. Evidence-Based Guidelines for the Assessment and Management of Polycystic Ovary Syndrome 2023 (full PDF).
13. Azziz R, Carmina E, Chen Z, et al. Polycystic ovary syndrome. Nat Rev Dis Primers 2016;2:16057 — background pathophysiology; treatment follows the 2023 guideline above.

Dr. Senai Aksoy

Dr. Senai Aksoy studied and trained in France before returning to Turkey, where he was a founding member of the ICSI team at Sevgi Hospital, Ankara — the country's first ICSI centre (1994-95) — and a co-author on the first Turkish ICSI publications produced in collaboration with the Brussels Van Steirteghem group (Human Reproduction, 1996; PMID 8671323). He helped build the IVF programme at the American Hospital Istanbul and has been running his own fertility practice since 1998.

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The content has been created by Dr. Senai Aksoy and medically approved.