PMOS - The New Name for PCOS (2026)

What Happened

Why the Name Changed

• Implied the condition is about pathological ovarian cysts (most people with the condition don't actually have true cysts)
• Obscured the condition's true nature as a hormonal and metabolic disorder
• Contributed to diagnostic delays, fragmented care, and stigma
• Limited research framing and policy attention

What PMOS Better Captures

• Polyendocrine - multiple hormonal/endocrine axes are involved (androgens, insulin, LH, AMH)
• Metabolic - insulin resistance, metabolic syndrome, and cardiovascular risk are central features
• Ovarian - retains the ovarian connection (irregular ovulation, reproductive effects)

Key Clinical Changes Under PMOS

• De-emphasis on ultrasound: Diagnosis can now be made on clinical signs of androgen excess (acne, hirsutism) and irregular cycles - no ultrasound required to find "cysts"
• AMH blood test can officially replace ultrasound in diagnosis
• Metabolic focus: Treatment plans now heavily emphasize insulin sensitivity and cardiovascular protection
• Reduced diagnostic delay expected, as patients no longer need to "prove" cysts exist

Transition Timeline

• 2026-2028: Transition period - both PCOS and PMOS names will appear in clinical documentation and research
• 2028: Full integration into the International Evidence-Based Guideline update

Q. Write a detailed note on Polyendocrine Metabolic Ovarian Syndrome (PMOS). [20 marks]

INTRODUCTION (1 mark)

RATIONALE FOR RENAMING (2 marks)

• It implies pathological ovarian cysts - in reality, the follicles seen on ultrasound are small antral follicles due to arrested folliculogenesis, not true cysts
• It obscures the primary metabolic and endocrine pathology (insulin resistance, hyperandrogenism, neuroendocrine dysfunction)
• It caused diagnostic delays (average 2-3 years) when no cysts were found on ultrasound
• It contributed to stigma, particularly around weight
• It limited research framing and underfunded metabolic aspects of care
• 86% of 9,358 surveyed patients wanted a name change vs 70% of healthcare professionals

• Polyendocrine - multiple hormonal axes involved
• Metabolic - insulin resistance and metabolic dysfunction are central
• Ovarian - ovarian dysfunction and reproductive consequences retained

EPIDEMIOLOGY (1 mark)

• Prevalence: 8-13% of women of reproductive age globally (1 in 8)
• Most common cause of anovulatory infertility (accounts for ~80% of anovulatory infertility)
• Average diagnostic delay: 2-3 years (ESHRE 2023)
• ICD-10 code: E28.2 (retained during transition; ICD-11 update expected 2028)

PATHOPHYSIOLOGY (3 marks)

1. Neuroendocrine Dysfunction

• Increased frequency of GnRH pulsatility leads to preferential LH over FSH secretion
• Elevated LH:FSH ratio (>2:1) stimulates excess androgen production from theca cells
• Disrupted negative feedback from progesterone (due to anovulation) perpetuates the cycle

2. Hyperandrogenism

• Excess LH drives theca cell androgen overproduction (testosterone, androstenedione)
• Insulin resistance causes hyperinsulinemia, which directly stimulates ovarian androgen synthesis and suppresses SHBG (sex hormone-binding globulin), increasing free androgen bioavailability
• Adrenal androgen excess (DHEAS) may also contribute in some phenotypes

3. Insulin Resistance and Metabolic Dysfunction

• Affects 85% of women with PMOS (including 75% of lean women with BMI ≤25)
• Compensatory hyperinsulinemia amplifies androgen secretion and disrupts steroidogenesis
• Drives central adiposity, dyslipidemia, glucose intolerance, and cardiovascular risk
• Low-grade chronic inflammation and adipokine signaling dysfunction further worsen metabolic profile

4. Ovarian Dysfunction

• Hyperinsulinemia and hyperandrogenism dysregulate granulosa and theca cell function
• Follicular arrest at the 5-8 mm stage leads to accumulation of small antral follicles
• Elevated AMH (anti-Mullerian hormone) reflects the increased antral follicle pool and is now formally included in diagnostic criteria

CLINICAL FEATURES (2 marks)

Menstrual / Reproductive

• Oligomenorrhea or amenorrhea (cycles >35 days or <8 per year)
• Anovulatory cycles - subfertility/infertility
• Recurrent miscarriage

Hyperandrogenism Features

• Hirsutism (most specific clinical sign - Ferriman-Gallwey score ≥6-8)
• Acne (comedonal/inflammatory)
• Androgenic alopecia (frontoparietal hair thinning)
• Acanthosis nigricans (marker of insulin resistance)

Metabolic Features

• Central obesity (waist circumference >80 cm in Asian women)
• Insulin resistance / impaired glucose tolerance
• Dyslipidemia (elevated triglycerides, low HDL)
• Non-alcoholic fatty liver disease (now: MAFLD)

Psychological

• Depression (3x increased prevalence), anxiety, reduced quality of life
• Body image issues and eating disorders

DIAGNOSIS (3 marks)

Rotterdam Criteria (2003, reaffirmed 2023 and 2026)

Key 2026 Update - AMH

• Elevated AMH can now formally replace ultrasound as the third criterion in adult women
• AMH thresholds vary by assay (typically >3.4-5 ng/mL depending on age)
• Ultrasound-based PFOM criterion not used in adolescents (< 3 years post-menarche)

Investigations

• Free testosterone (most sensitive biochemical marker - ESHRE 2023 priority)
• Total testosterone, SHBG
• DHEAS, 17-OH progesterone (to exclude CAH)
• LH, FSH (LH:FSH >2:1 in ~60%)
• AMH (elevated; now diagnostic)
• Prolactin, TSH (to exclude differentials)

• Fasting glucose + 2-hour OGTT (preferred over HbA1c alone)
• Fasting insulin, HOMA-IR
• Fasting lipid profile
• Liver function tests (screen for MAFLD)

• Pelvic USS (transvaginal preferred; transabdominal if not sexually active)
• Now optional in adults if AMH is elevated and other criteria met

Exclusion of Differentials (mandatory before diagnosis)

• Thyroid disorders (TSH)
• Hyperprolactinemia (prolactin)
• Congenital adrenal hyperplasia - late onset (17-OHP)
• Cushing's syndrome (24-hr urinary free cortisol if suspected)
• Androgen-secreting tumors (testosterone >5 nmol/L - rapid virilization)
• Premature ovarian insufficiency

MANAGEMENT (5 marks)

A. Lifestyle Modification (First-line for ALL phenotypes)

• Even 5-10% weight loss restores ovulation in 55-85% of women with obesity
• Calorie-restricted diet, aerobic + resistance exercise (150 min/week moderate intensity)
• Addresses insulin resistance, improves menstrual regularity, reduces androgen levels, improves fertility outcomes

B. Pharmacological Management

• Combined Oral Contraceptive Pill (COCP) - first-line pharmacological agent
  • Reduces LH-driven androgen production
  • Increases SHBG → reduces free testosterone
  • Regulates cycles
  • Preferred: 30-35 mcg EE with anti-androgenic progestogen (cyproterone acetate, drospirenone, or desogestrel)
• Cyclical progestogens - if COC contraindicated; induces withdrawal bleed every 3-4 months minimum (prevents endometrial hyperplasia)

• Spironolactone (75-200 mg/day) - anti-androgen of choice
• Cyproterone acetate - in combination with estrogen (Diane-35)
• Topical eflornithine for facial hirsutism
• Laser/IPL hair removal for established hirsutism

• Metformin - improves insulin sensitivity; second-line after lifestyle
  • Dose: 500 mg BD to 2000 mg/day (titrate for GI tolerance)
  • Benefits: lowers androgens, restores ovulation, reduces T2DM risk
  • Preferred in adolescents and women with dysglycemia
• GLP-1/GIP receptor agonists (emerging):
  • Tirzepatide (SURMOUNT-PCOS trial, NEJM 2024): significant weight loss, improved hormonal profile
  • Currently off-label for PMOS specifically; approved for obesity management

• Myo-inositol (2000 mg BD) - improves insulin sensitivity and ovulation; safe adjunct

C. Fertility Management

• Indicated after failure of OI methods or in severe cases/tubal/male factor coexistence
• PMOS women are at high risk for Ovarian Hyperstimulation Syndrome (OHSS)
• GnRH antagonist protocol preferred; GnRH agonist trigger instead of hCG to prevent OHSS
• Freeze-all strategy (frozen embryo transfer) recommended to minimize OHSS risk

D. Surgical Management

• Laparoscopic Ovarian Drilling (LOD) - as above for ovulation induction
• Bariatric surgery - for morbidly obese women with PMOS; can achieve remission of metabolic features and restore ovulation

LONG-TERM COMPLICATIONS (2 marks)

SCREENING AND MONITORING (1 mark)

• OGTT every 1-3 years (screen for T2DM progression)
• Lipid profile annually
• Blood pressure at every visit
• Endometrial biopsy if amenorrheic >1 year or abnormal uterine bleeding (exclude hyperplasia)
• Mental health screening at diagnosis and follow-up (PHQ-9, GAD-7)

CONCLUSION (As summary points)

• Diagnosis by Rotterdam criteria (2 of 3: dysovulation, hyperandrogenism, PFOM/elevated AMH)
• Treatment individualized by phenotype - lifestyle first, then targeted pharmacotherapy
• Fertility management with letrozole as first-line, escalating to LOD or IVF as needed
• Long-term surveillance for metabolic, cardiovascular, endometrial, and psychological complications
• The 2026 Lancet renaming to PMOS marks a paradigm shift from a gynecological to a systemic metabolic framework, expected to reduce diagnostic delay and improve holistic care

Exam tip: This is a 20-mark answer. Write all sections with subheadings. The examiner will look for: correct Rotterdam criteria with AMH update, pathophysiology (insulin resistance axis), letrozole as first-line OI, LOD indications, endometrial cancer risk, and the 2026 name change rationale. Draw a table for OI drugs if time permits - it scores well.