Polyendocrine metabolic ovarian syndrome management for GPNs and ANPs

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Reference: September-October 2026 | Issue 5 | Vol 19 | Page 43

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Start this Module

People with PMOS frequently report seeing multiple healthcare professionals before receiving an explanation that connects their symptoms

An international consensus statement published in 2026 proposed renaming polycystic ovary syndrome (PCOS) to polyendocrine metabolic ovarian syndrome (PMOS), reflecting broader recognition of its endocrine and metabolic features.^1,2 This evolving terminology reflects increasing recognition that the condition extends beyond ovarian dysfunction alone, and involves complex endocrine, metabolic, reproductive, and cardiometabolic pathways.

Historically, the term PCOS has been criticised as potentially misleading because many affected individuals do not have ovarian cysts in the conventional sense, while others experience substantial metabolic and endocrine dysfunction that is not adequately reflected by the older terminology. The proposed term PMOS aims to better represent the multisystem nature of the condition, including insulin resistance, androgen excess, ovulatory dysfunction, cardiometabolic risk, and broader endocrine involvement.

At the time of writing, much of the published evidence base, guideline literature, and historical research continues to use the term PCOS. In this module, the updated term PMOS is used throughout the main text, while the term PCOS is retained where necessary within guideline titles, published study titles, and reference terminology.

PMOS

PMOS is a common endocrine-metabolic condition characterised by variable combinations of ovulatory dysfunction, hyperandrogenism, and polycystic ovarian morphology.² It is not simply a ‘period problem’ or a cosmetic condition – it is a lifelong syndrome with reproductive, dermatological, metabolic, and psychological implications.³

PMOS affects approximately 8-13 per cent of women and people assigned female at birth of reproductive age, although prevalence varies according to diagnostic criteria, age, ethnicity, and population studied.^2,3 Symptoms may include irregular or absent periods, subfertility, hirsutism, acne, androgenic alopecia, weight gain or weight cycling, insulin resistance, acanthosis nigricans, fatigue, and psychological distress.²

The 2023 International Evidence-based Guideline for the Assessment and Management of PCOS² was developed by the Monash Centre for Health Research and Implementation (MCHRI) alongside international societies like the American Society for Reproductive Medicine and the European Society of Human Reproduction and Embryology, engaging multidisciplinary experts and consumers across over 70 countries. It remains the most important contemporary clinical standard underpinning diagnosis and management of the condition.

In Ireland, there does not currently appear to be a dedicated national clinical practice guideline for PMOS equivalent to the Irish national clinical practice guideline for endometriosis. Irish clinical practice therefore continues to draw on international guidance, HSE patient information, Irish GP and nursing education resources, and local referral pathways.^4,5

General practice nurses (GPNs) are well placed to support early recognition, provide clear education, reduce stigma, screen for metabolic risk, support contraception and fertility planning, and co-ordinate long-term follow-up.

Irish context and patient-facing resources

Irish patients commonly access initial information through the HSE website, which describes PMOS/PCOS as a common condition affecting how the ovaries work, and outlines symptoms including irregular periods, excess facial or body hair, weight gain, thinning hair, acne, and difficulty getting pregnant.⁴

The HSE treatment information emphasises that PMOS cannot currently be ‘cured’, but symptoms and long-term risks can be managed through lifestyle measures, medicines, and, where needed, fertility treatment. This is useful patient-facing language because it avoids unrealistic promises while supporting active management.

In Irish professional education, the Irish College of GPs includes PCOS within its Community Gynaecology Certificate module on abnormal bleeding, oligomenorrhoea, amenorrhoea, and adolescent gynaecology.⁵ This reflects the reality that many patients first present in primary care with symptoms, concerns, or fertility questions.

The evidence base for this CPD module remains the 2023 International Guideline, HSE patient information, Irish professional education resources, and peer-reviewed academic literature.^2,4

GPN practice point: Use HSE pages and credible Irish resources to support understanding after consultation, but base assessment, treatment, and referral on clinical guidelines and local pathways.

Epidemiology and public health impact

PMOS is one of the most common endocrine disorders affecting reproductive-aged individuals. The 2023 International Guideline estimates a prevalence of approximately 8-13 per cent, with many affected individuals remaining undiagnosed.² This means that in a typical general practice population, PMOS is likely to be encountered regularly, although it may not always be coded, named, or managed as a single condition.

Under-recognition is common because PMOS presents across several clinical domains. Menstrual irregularity may be managed as a period issue, acne as a dermatology concern, hirsutism as cosmetic, and infertility as a separate reproductive issue.^2,3 Without a unifying diagnosis, patients may receive fragmented care and miss opportunities for metabolic screening, endometrial protection, and fertility counselling.

There is no national Irish PMOS registry or robust publicly available dataset reporting the exact number of people diagnosed or treated for PMOS in Ireland. The main prevalence estimates used are generally extrapolated from international data.^4,5 A 2024 Irish professional education article reported an Irish prevalence figure of 128 per 100,000 women, but this is likely to reflect recorded or recognised disease rather than true population prevalence, as international population-based estimates are considerably higher.^2,6,7

The absence of strong Irish epidemiological data is itself clinically important. It means that GPNs should not rely solely on coded prevalence or prior diagnosis, but should actively recognise symptom clusters and consider PMOS where irregular cycles, hyperandrogenic symptoms, infertility, or metabolic risk factors occur together.^2,4

Diagnostic delay and fragmented care

People with PMOS frequently report seeing multiple healthcare professionals before receiving an explanation that connects their symptoms.^2,8 Delayed diagnosis can lead to untreated irregular bleeding, prolonged distress about body changes, delayed fertility counselling, and missed opportunities to screen for cardiometabolic risk.^2,9 Diagnostic delay may also contribute to worsening psychological wellbeing, reduced trust in healthcare encounters, and prolonged uncertainty regarding fertility and long-term health risks.^2,8 International literature suggests that up to half of affected individuals may remain undiagnosed, highlighting the importance of proactive recognition in primary care.²

Ethnicity, symptom diversity, and weight diversity

PMOS expression varies by ethnicity and clinical presentation^2,3,6 Some individuals present predominantly with hyperandrogenic symptoms, while others present mainly with irregular cycles, infertility, or metabolic dysfunction.³ Metabolic risk may occur across body mass index (BMI) categories, and lean PMOS should not be dismissed.^2,9

Conversely, weight stigma can worsen healthcare avoidance, disordered eating, anxiety, and psychological distress.^2,8 The international guideline specifically emphasises the importance of culturally sensitive, person-centred, and weight-stigma-informed care.² Differences in symptom presentation and metabolic risk between ethnic groups may also influence diagnosis, cardiometabolic risk assessment, and treatment priorities.^2,6

Psychological burden

PMOS is associated with higher rates of anxiety, depression, body image distress, reduced quality of life, and disordered eating.^2,8 Hirsutism, acne, scalp hair thinning, fertility concerns, and weight stigma can all affect self-esteem, intimate relationships, and overall quality of life.^2,8 Psychological symptoms should therefore be actively assessed rather than treated as secondary or less important.

Fertility and reproductive impact at population level

PMOS is one of the leading causes of anovulatory infertility worldwide.^2,3 Ovulatory dysfunction may contribute to delayed conception, cycle unpredictability, and fertility-related psychological distress.^2,8 Importantly, PMOS should not be viewed as synonymous with infertility. Many individuals conceive spontaneously, while others conceive following ovulation induction or assisted reproductive treatment.^2,10,11,12 Fertility concerns may significantly affect quality of life, relationships, and emotional wellbeing, highlighting the importance of early recognition, evidence-based counselling, and timely referral, where appropriate.^2,8 

Long-term health burden

PMOS is associated with increased risk of insulin resistance, impaired glucose tolerance, type 2 diabetes, gestational diabetes, hypertensive disorders of pregnancy, dyslipidaemia, obstructive sleep apnoea, and endometrial hyperplasia.^2,9,13,14 It should therefore be understood as a chronic condition requiring long-term health surveillance.

The evolving terminology of PMOS reflects increasing recognition that cardiometabolic dysfunction is not simply a secondary association, but a core component of the condition for many individuals. Contemporary evidence demonstrates important links between insulin resistance, endothelial dysfunction, dyslipidaemia, chronic inflammation, altered glucose metabolism, and increased long-term cardiometabolic risk.^9,13

Large population-based data from the UK demonstrate increasing recorded incidence and prevalence of PMOS over time, alongside higher healthcare utilisation compared with controls.¹⁵ Although UK data cannot be directly applied to Ireland, these findings support the view that PMOS is an important primary-care and public health condition, rather than a niche reproductive diagnosis.

Normal menstrual cycle: Foundation for understanding PMOS

Understanding normal menstrual physiology helps explain why PMOS causes irregular periods, abnormal bleeding patterns, and subfertility.^2,3 The menstrual cycle is regulated by the hypothalamic-pituitary-ovarian (HPO) axis.^2,3 The hypothalamus releases gonadotropin-releasing hormone (GnRH) in pulsatile patterns. GnRH stimulates the pituitary gland to release follicle-stimulating hormone (FSH) and luteinising hormone (LH). FSH supports follicular growth and oestradiol production, while LH stimulates androgen production by ovarian theca cells. Oestradiol and progesterone feed back to the hypothalamus and pituitary to regulate the cycle.^2,3

✽ Follicular phase: In a typical ovulatory cycle, FSH stimulates development of a group of ovarian follicles. One dominant follicle matures and produces rising oestradiol. Oestradiol thickens the endometrium and prepares the reproductive system for ovulation.²
✽ Ovulation: Sustained high oestradiol triggers an LH surge,leading to release of an oocyte from the dominant follicle. Ovulation is the key event supporting predictable menstrual cyclicity and fertility.²
✽ Luteal phase: After ovulation, the corpus luteum produces progesterone. Progesterone stabilises the endometrium and prepares it for potential implantation. If pregnancy does not occur, progesterone levels fall and menstruation follows.^2,14

What changes in PMOS?: In PMOS, many follicles begin development but do not consistently progress to dominant follicle selection and ovulation. Increased LH activity, insulin resistance, and androgen excess contribute to this follicular arrest.^2,3,9 As ovulation becomes irregular or absent, progesterone exposure is reduced or absent for prolonged periods. This may lead to prolonged cycles, unpredictable bleeding or amenorrhoea, and increases endometrial exposure to unopposed oestrogen.^2,14

Patient explanation: “PMOS is not only an ovarian condition, it also affects metabolism and hormone regulation throughout the body. The ovaries may receive mixed hormonal and metabolic signals, meaning eggs can begin developing but may not release regularly, leading to irregular periods. Changes in insulin and androgen hormones can also affect skin, hair growth, weight regulation, energy levels, fertility, and long-term cardiometabolic health. This broader endocrine and metabolic understanding is one of the reasons the terminology changed from PCOS to PMOS.”

Pathophysiology of PMOS

The exact cause of PMOS is not fully understood. Current evidence suggests that genetic predisposition interacts with environmental and metabolic influences to disrupt hormonal signalling pathways. Many patients have a family history of PMOS, type 2 diabetes, or metabolic disease, suggesting inherited susceptibility. However, clinical presentation varies considerably between individuals.^2,3

Insulin resistance and hyperinsulinaemia

In PMOS, elevated insulin levels contribute directly to ovarian androgen production. Insulin acts synergistically with LH on ovarian theca cells, increasing androgen synthesis. High insulin levels also suppress hepatic production of sex hormone-binding globulin (SHBG), resulting in increased free testosterone levels.¹³

This explains why insulin resistance contributes not only to metabolic dysfunction, but also to acne, hirsutism, ovulatory dysfunction, and fertility problems.^2,3,9 Importantly, insulin resistance can occur across all BMI categories. While adiposity may worsen insulin resistance, lean individuals with PMOS can also experience significant metabolic dysfunction.^2,9

Hyperandrogenism

Hyperandrogenism refers to excess androgen activity. Clinically, this may present as hirsutism, acne, scalp hair thinning, or androgenic alopecia. Biochemically, elevated testosterone or free androgen index may be detected.^2,3 Androgens are normally present in all women and are important for physiological function.

However, excess androgen activity affects hair follicles, sebaceous glands, and ovarian follicle development. Increased androgen exposure can disrupt normal ovulation and perpetuate the hormonal cycle underlying PMOS.^2,3

Ovulatory dysfunction and follicular arrest

In a normal ovulatory cycle, one dominant follicle matures and releases an oocyte following the LH surge. In PMOS, follicles often begin development but fail to reach full maturation.^2,3 This follicular arrest results in accumulation of multiple small follicles within the ovaries. Importantly, these are not true ovarian cysts in the conventional sense.

The historical term PCOS can therefore be misleading and contributed to the rationale for the updated terminology PMOS.^2,3 Ovulatory dysfunction results in irregular cycles, oligo-ovulation, or anovulation. Reduced ovulation also means reduced progesterone exposure, leading to prolonged endometrial exposure to oestrogen without regular shedding.^2,14

Diagnosis of PMOS

The modified Rotterdam criteria remain the most widely used international diagnostic framework for PMOS and are supported by the 2023 guideline.² Diagnosis requires the presence of two of the following three features, after exclusion of alternative causes:
✽ Clinical or biochemical hyperandrogenism
✽ Ovulatory dysfunction
✽ Polycystic ovarian morphology on ultrasound.²

Importantly, PMOS remains a clinical diagnosis rather than a diagnosis based solely on ultrasound or laboratory findings. Symptoms, metabolic profile, menstrual history, and broader endocrine assessment should always be interpreted together.^2,3

PMOS phenotypes

The modified Rotterdam criteria recognise four main phenotypes of PMOS.² These phenotypes help explain why clinical presentation varies substantially between individuals and why some patients present primarily with reproductive symptoms while others demonstrate more prominent metabolic, dermatological, or psychological features.⁶ Recognition of phenotypic variation is clinically important because PMOS is a heterogeneous condition rather than a single uniform disorder.² Some individuals experience significant insulin resistance and cardiometabolic dysfunction, while others may present predominantly with infertility, acne, hirsutism or menstrual irregularity, despite relatively limited metabolic features.^2,6,9

Phenotype A (classic PMOS): This phenotype includes hyperandrogenism, ovulatory dysfunction, and polycystic ovarian morphology.² Individuals with this phenotype may demonstrate more significant metabolic dysfunction, insulin resistance, and reproductive symptoms.^6,9 Hirsutism, acne, irregular cycles, and infertility concerns are often prominent.

Phenotype B: This phenotype includes hyperandrogenism and ovulatory dysfunction without polycystic ovarian morphology on ultrasound.² Patients may still experience significant endocrine and fertility symptoms despite normal ovarian imaging.

Phenotype C: This phenotype includes hyperandrogenism and polycystic ovarian morphology with apparently preserved ovulation.² Menstrual cycles may appear relatively regular, which can delay diagnosis and contribute to under-recognition of androgen-related symptoms like acne, hirsutism, or scalp hair thinning.

Phenotype D: This phenotype includes ovulatory dysfunction and polycystic ovarian morphology without clear hyperandrogenism.² Patients may present primarily with irregular periods, subfertility, or abnormal bleeding patterns rather than acne or excess hair growth.

Biochemical assessment

Biochemical assessment in PMOS has two important aims: Supporting diagnosis of hyperandrogenism and ovulatory dysfunction, and excluding alternative endocrine or metabolic conditions which may mimic PMOS.^2,3 Common investigations may include:
✽ Total testosterone and calculated free testosterone or free androgen index
✽ SHBG
✽ DHEAS (dehydroepiandrosterone sulphate)
✽ Androstenedione
✽ LH and FSH
✽ Oestradiol
✽ Thyroid function tests
✽ Prolactin
✽ 17-hydroxyprogesterone
✽ HbA1c (glycated haemoglobin) and/or oral glucose tolerance testing
✽ Fasting glucose and lipid profile
✽ Fasting insulin in selected cases.^2,9

Markedly elevated testosterone, rapidly progressive virilisation, or very high DHEAS levels should prompt consideration of androgen-secreting ovarian or adrenal tumours.^2,3

Ultrasound and AMH

Ultrasound may identify polycystic ovarian morphology, typically characterised by increased follicle number and/or increased ovarian volume.² However, ultrasound findings alone are not diagnostic of PMOS and must be interpreted within the wider clinical context. In adults, transvaginal ultrasound is generally preferred, where appropriate and acceptable, because it provides superior assessment of ovarian morphology and follicle number compared with transabdominal imaging.²

Anti-Müllerian hormone (AMH) levels are often elevated in PMOS because of increased small follicle number. However, AMH should not be used as a standalone diagnostic test for PMOS in routine clinical practice.²

Diagnosis in adolescents

Diagnosis in adolescence requires particular caution because irregular cycles, acne, and multi-follicular ovarian appearance may occur during normal pubertal maturation.² The international guideline recommends that adolescent diagnosis requires both persistent ovulatory dysfunction and evidence of hyperandrogenism after exclusion of other causes.² Ultrasound is not recommended for diagnosis in adolescents because ovarian morphology may overlap substantially with normal puberty.²

Differential diagnoses

Important differential diagnoses include pregnancy, thyroid dysfunction, hyperprolactinaemia, non-classic congenital adrenal hyperplasia, Cushing syndrome, androgen-secreting ovarian or adrenal tumours, hypothalamic amenorrhoea, primary ovarian insufficiency, and medication-related hyperandrogenism.^2,3

Routine cortisol testing is not recommended in all individuals with suspected PMOS. Investigation for Cushing syndrome should be reserved for patients with clinical features suggestive of hypercortisolism, such as proximal muscle weakness, facial plethora, wide purple striae, dorsocervical fat pad, easy bruising, or rapid central weight gain.^2,3

Red flags requiring urgent or specialist referral

Although most patients with PMOS present with gradual symptom progression over time, certain clinical features require urgent assessment because they may indicate alternative endocrine or malignant pathology.^2,3 Rapid onset androgenic symptoms are particularly important because uncomplicated PMOS typically develops gradually across adolescence or early adulthood. Sudden or severe virilisation raises concern for androgen-secreting tumours or significant endocrine pathology.^2,3

Persistent abnormal uterine bleeding or prolonged amenorrhoea with heavy bleeding may also indicate endometrial hyperplasia or malignancy associated with chronic anovulation and prolonged unopposed oestrogen exposure.^2,14 The following features should prompt urgent investigation or specialist referral:
✽ Rapid onset hirsutism or virilisation
✽ Deepening voice, clitoromegaly, or rapidly progressive androgenic alopecia
✽ Very high testosterone or DHEAS
✽ Pelvic mass
✽ Postmenopausal androgen excess
✽ Prolonged amenorrhoea with abnormal bleeding or suspected endometrial pathology.^2,3,14

Non-pharmacological management

Lifestyle and behavioural interventions are considered first-line management for many individuals with PMOS. However, modern PMOS care emphasises that lifestyle support should be collaborative, realistic, evidence-based and non-stigmatising.^2,16 Historically, consultations often focused narrowly on weight loss. This approach can be harmful, particularly for individuals who have experienced repeated dieting, body shame, weight stigma, or disordered eating.

For GPNs, non-pharmacological management represents one of the most important aspects of PMOS care. Nurses are often central to continuity of care, behaviour-change support, psychological assessment, metabolic screening, education, and long-term follow-up.

EDUCATION AND VALIDATION
Many individuals with PMOS report years of feeling dismissed, misunderstood, or blamed for symptoms such as weight gain, acne, irregular periods, fatigue, or infertility. Some patients describe previous consultations focused solely on body weight without broader discussion of endocrine or metabolic health. Others report being told that symptoms are simply part of being female or that fertility problems are inevitable.^1,8

Providing a clear explanation of the condition can reduce shame, improve health literacy, and support engagement with treatment plans. The international guideline emphasises person-centred care, shared decision-making, and awareness of the psychological impact of PMOS.² Education should therefore emphasise that PMOS is a hormone-metabolic condition influenced by genetics, insulin resistance, and ovarian signalling, rather than a failure of willpower or lifestyle.^2,3

Many patients experience relief when symptoms are finally linked together within a coherent diagnosis. Explaining how insulin resistance, androgen excess, ovulatory dysfunction, and metabolic changes interact may help individuals understand why symptoms such as fatigue, hunger changes, weight fluctuation, acne, irregular cycles, and fertility difficulties often occur together.

Consultation language nurses can use: “PMOS affects metabolism as well as hormones, so fatigue, hunger changes, and weight fluctuation are not simply about willpower.

“The goal is not perfection or rapid weight loss. Small sustainable changes in sleep, movement, nutrition, and stress can significantly improve symptoms and long-term health.

“Even modest improvements in insulin sensitivity can positively affect periods, ovulation, energy levels, and long-term cardiometabolic health.”

Many individuals with PMOS have already attempted multiple lifestyle interventions before presentation. Previous negative experiences with dieting, shame-based messaging, unrealistic goals, or repeated weight cycling may affect confidence and engagement with healthcare.^2,8

GPNs are well placed to support realistic goal setting, self-management, and sustainable behavioural change. Motivational interviewing techniques, collaborative planning, and non-judgemental communication may improve long-term adherence and therapeutic relationships.

Importantly, behaviour-change conversations should avoid framing the patient as non-compliant or unmotivated. PMOS involves biological drivers affecting appetite regulation, satiety, insulin signalling, fatigue, and energy regulation.⁹ This means lifestyle change may feel considerably more difficult for some individuals than simplistic public health messaging often suggests.

Helpful consultation approaches may include exploring what has or has not worked previously, identifying barriers to change, discussing emotional responses to food and movement, and recognising social or financial factors affecting health behaviours. Useful approaches may include:
✽ Collaborative goal setting
✽ Exploring barriers to change
✽ Identifying achievable behavioural targets
✽ Focusing on health outcomes rather than appearance
✽ Encouraging gradual habit formation
✽ Recognising relapse as part of long-term behaviour change rather than ‘failure’.

Long-term consistency is generally more clinically meaningful than short periods of highly restrictive behaviour.

NUTRITION
There is no single PMOS diet. Current evidence supports healthy eating principles tailored to individual preferences, culture, metabolic risk, and eating behaviours.^2,16 Reducing highly processed foods and improving dietary quality may support insulin sensitivity, satiety, glycaemic control, and energy regulation.^2,9,16

Some individuals find lower glycaemic-load approaches helpful, particularly where insulin resistance or prediabetes are present.^2,9 However, excessively restrictive diets may increase risk of disordered eating behaviours, food preoccupation, and psychological distress.^2,8 General dietary strategies may include:
✽ Increasing fibre intake
✽ Prioritising protein intake
✽ Reducing ultra-processed foods
✽ Supporting stable blood glucose patterns
✽ Encouraging regular meal patterns
✽ Limiting sugar-sweetened beverages
✽ Supporting realistic and culturally appropriate food choices.

Referral to a dietitian may be particularly useful where complex metabolic dysfunction, obesity, disordered eating, fertility planning, or diabetes risk are present.

PHYSICAL ACTIVITY
Exercise improves insulin sensitivity, cardiovascular health, mood, and body composition independent of major weight loss.^2,16 Both aerobic and resistance exercise are beneficial. Movement should be framed positively as supporting energy, strength, metabolic health, and wellbeing rather than solely weight reduction. Sustainable and enjoyable activity is more likely to be maintained long-term and may reduce shame-based relationships with exercise.²

Practical advice may include:
✽ Encouraging gradual increases in movement
✽ Promoting enjoyable and sustainable activity
✽ Combining aerobic and resistance exercise where possible
✽ Reducing prolonged sedentary time
✽ Supporting realistic activity goals in individuals with fatigue or obesity
✽ Recognising barriers such as pain, body image concerns, caring responsibilities, or financial limitations.

Resistance exercise may be particularly beneficial for insulin sensitivity, metabolic health, and preservation of lean muscle mass.

WEIGHT STIGMA AND WEIGHT-NEUTRAL CARE
Weight stigma is increasingly recognised as a major issue within PMOS care. Repeated exposure to shame-based healthcare interactions may worsen anxiety, disordered eating, healthcare avoidance, and low self-esteem.^2,8 Clinicians should therefore use respectful, person-centred and weight-stigma-informed communication. Weight should not be treated as a measure of personal worth, motivation, or compliance.

Practical approaches include:
✽ Asking permission before discussing weight
✽ Using neutral terminology
✽ Avoiding moralising language around food or body size
✽ Focusing on health behaviours rather than appearance
✽ Recognising that metabolic dysfunction occurs across BMI categories
✽ Avoiding assumptions regarding lifestyle habits.

Lean individuals with PMOS should not be falsely reassured that metabolic risk is absent simply because BMI is within normal range.^2,9

PSYCHOLOGICAL SUPPORT
Anxiety, depression, body image distress, and eating disorders occur more frequently in PMOS.^2,8 Psychological symptoms may be amplified by infertility, hirsutism, acne, weight stigma, social isolation, or repeated unsuccessful dieting attempts.^2,8 For some individuals, PMOS symptoms affect identity, confidence, sexuality, intimate relationships, and social participation. Visible symptoms such as facial hair growth, scalp hair thinning, or severe acne may lead to embarrassment, avoidance behaviours, or reduced self-esteem.

Psychological distress may also be worsened by delayed diagnosis or previous healthcare encounters in which symptoms were minimised or attributed solely to weight.^2,8 Psychological assessment should therefore form part of routine PMOS care rather than being treated as a secondary issue.

GPNs should consider:
✽ Mood assessment
✽ Anxiety screening
✽ Eating disorder awareness
✽ Assessment of emotional eating patterns
✽ Body image concerns
✽ Social isolation and relationship impact
✽ Fertility-related distress
✽ Impact on self-esteem and quality of life.

Cognitive behavioural therapy (CBT) and psychological support may improve coping, self-esteem, emotional eating patterns, anxiety, and adherence to treatment plans.^2,8

SLEEP AND CIRCADIAN HEALTH
Sleep disturbance and obstructive sleep apnoea are more common in PMOS, particularly where metabolic dysfunction and higher BMI are present.² Poor sleep may worsen insulin resistance, appetite regulation, fatigue, and daytime function.^2,9  Shift work, chronic stress, and circadian disruption may also negatively affect metabolic health and hormonal regulation. Assessment should therefore include:
✽ Sleep quality
✽ Snoring or witnessed apnoea
✽ Daytime sleepiness
✽ Shift work patterns
✽ Fatigue
✽ Sleep duration
✽ Sleep hygiene practices.

Sleep optimisation strategies may include regular sleep routines, reduction of evening screen exposure, stress management, and referral for sleep assessment where indicated.

STRESS MANAGEMENT AND SELF-MANAGEMENT SUPPORT
Stress may contribute to hormonal and metabolic dysregulation through neuroendocrine and behavioural pathways. Chronic stress may also worsen emotional eating, sleep disturbance, fatigue, and psychological distress.

Nurses can support stress reduction through:
✽ Relaxation strategies
✽ Mindfulness approaches
✽ Breathing exercises
✽ Encouraging restorative activities
✽ Signposting psychological supports
✽ Supporting realistic self-management expectations.

Self-monitoring tools such as symptom tracking, cycle monitoring, wearable devices, or health apps may help some individuals recognise progress and improve engagement with care.

Peer support and long-term engagement: Many individuals with PMOS feel isolated or misunderstood. Peer support groups, reputable educational resources, and ongoing nurse follow-up may improve confidence and long-term self-management.

TABLE 1: Non-pharmacological approaches

Pharmacological management

Treatment should be individualised according to symptoms, fertility goals, metabolic risk, contraindications, and patient preference.²

COMBINED HORMONAL CONTRACEPTION
Combined hormonal contraception is commonly used for menstrual regulation, endometrial protection, and hyperandrogenic symptoms. It suppresses LH-driven ovarian androgen production and increases SHBG, reducing free testosterone.² Choice of formulation may be influenced by the patient’s predominant symptoms, cardiovascular risk profile, tolerability, metabolic profile, and contraceptive needs.

Examples commonly used in practice include:
✽ Ethinylestradiol with drospirenone, which may be particularly helpful where acne, fluid retention, or mild hirsutism are prominent because drospirenone has anti-androgenic activity.²
✽ Ethinylestradiol with cyproterone acetate may be considered for more significant hirsutism or acne, although thromboembolic risk profile should be considered carefully.²
✽ Ethinylestradiol with desogestrel or norgestimate, which may be useful where acne predominates and a lower androgenic progestogen is preferred.²
✽ Levonorgestrel-containing combined oral contraceptives, which may provide effective menstrual regulation and endometrial protection, but may be less beneficial for androgenic symptoms in some individuals.²

Patients should be counselled that improvement in acne and hirsutism may take several months because androgen-sensitive hair follicles and sebaceous glands respond gradually to hormonal change.²

Newer formulations such as estetrol/drospirenone (Drovelis) may be considered in selected patients with PMOS. Drospirenone has anti-androgenic properties which may support improvement in acne, fluid retention, and mild hirsutism. Emerging evidence suggests estetrol-containing combined pills may offer favourable cycle control and tolerability, although long-term comparative data in PMOS populations remain limited.^2,17

PROGESTERONE-BASED MANAGEMENT AND ENDOMETRIAL PROTECTION
Individuals with infrequent periods may require progesterone therapy or other forms of endometrial protection to reduce the risk of endometrial hyperplasia associated with prolonged unopposed oestrogen exposure.^2,14 This is particularly important where menstrual cycles are prolonged, highly irregular, or amenorrhoea persists.

The 2023 guideline recommends consideration of regular withdrawal bleeding, combined hormonal contraception, or cyclical progestogen therapy where menstrual cycles are infrequent.² The aim is to ensure adequate endometrial protection and reduce prolonged endometrial proliferation.^2,14 Commonly used approaches in clinical practice may include:
✽ Micronised progesterone 200mg nightly for 12-14 days in cyclical regimens
✽ Medroxyprogesterone acetate 10mg daily for 10-14 days every one to three months
✽ Levonorgestrel intrauterine system
✽ Progesterone-only oral contraceptives
✽ Combined hormonal contraception where appropriate.²

Micronised progesterone may be preferred by some clinicians because of its more physiological profile and favourable tolerability for some patients, although treatment choice should remain individualised.² Continuous progestogenic methods may also provide effective endometrial protection through suppression and stabilisation of the endometrium and do not necessarily require scheduled withdrawal bleeding.²

Progesterone-only contraception may be particularly appropriate for individuals who cannot use oestrogen-containing contraception because of migraine with aura, hypertension, venous thromboembolism risk, smoking history, obesity-related cardiovascular risk, or intolerance of combined hormonal contraception.²

Traditional progesterone-only pills are generally less effective for androgenic symptoms because they do not increase SHBG to the same extent as combined hormonal contraception. However, the drospirenone-only pill (Slynd) may offer additional benefits in selected patients because drospirenone has anti-androgenic and anti-mineralocorticoid activity.^2,18

Slynd uses a 24/4 regimen, which may provide more predictable bleeding patterns than traditional progesterone-only pills, and may improve acceptability for some individuals.^2,18 Slynd may therefore provide contraception and endometrial protection while also offering some improvement in acne, bloating, or mild hirsutism in selected individuals.^2,18

Although evidence remains more limited than for combined anti-androgenic contraceptive formulations, Slynd may be particularly useful where oestrogen is contraindicated or poorly tolerated. Patients should also be advised that prolonged amenorrhoea should not simply be ignored because persistent endometrial proliferation may increase long-term risk of endometrial hyperplasia and malignancy.^2,18

METFORMIN
Metformin reduces hepatic glucose production and improves peripheral insulin sensitivity, helping lower circulating insulin levels.^2,9 Because hyperinsulinaemia contributes directly to ovarian androgen production, metformin may also indirectly reduce androgen excess and support improved ovulatory function.^2,9 Metformin may support:
✽ Improvement in insulin resistance and hyperinsulinaemia
✽ Reduction in impaired glucose tolerance and type 2 diabetes risk
✽ Improvement in menstrual regularity and ovulation in some individuals
✽ Cardiometabolic risk reduction
✽ Modest support for weight management, particularly when combined with lifestyle interventions.^2,9,16

Although metformin is not primarily a weight-loss medication, some individuals experience modest reductions in weight, appetite, or weight regain patterns, particularly where insulin resistance contributes to metabolic dysfunction.^2,9,16 Expectations should remain realistic and treatment should not be framed solely around weight reduction.

Metformin may be particularly useful where impaired glucose tolerance, prediabetes, insulin resistance, higher metabolic risk, or features of metabolic syndrome are present.² It may also be considered in selected patients with menstrual irregularity who cannot tolerate or do not wish to use hormonal contraception.² Gastrointestinal side effects such as nausea, bloating, abdominal discomfort, and diarrhoea are common, particularly during initiation. Gradual dose titration and use of modified-release preparations may improve tolerability.² Long-term treatment may also be associated with vitamin B12 deficiency and periodic review should therefore be considered.²

SPIRONOLACTONE AND ANTI-ANDROGEN THERAPY
Spironolactone is an anti-androgen medication commonly used to reduce hirsutism, acne, and androgen-related scalp hair thinning in PMOS.² It works primarily by blocking androgen receptor activity and reducing androgen effects at the hair follicle and sebaceous gland.² Spironolactone is generally considered when hyperandrogenic symptoms persist despite combined hormonal contraception, or where combined hormonal contraception is contraindicated or declined.²

Improvement in hirsutism is gradual and patients should be counselled that several months of treatment may be required before meaningful clinical improvement becomes apparent because terminal hairs must complete their growth cycle before reduction is visible.²

Potential adverse effects may include dizziness, breast tenderness, menstrual irregularity, fatigue, and hyperkalaemia.² Because spironolactone may affect foetal development, effective contraception is recommended during treatment.² Monitoring may include renal function, potassium levels where clinically indicated, blood pressure assessment, and review of treatment tolerability and adherence.

DERMATOLOGICAL TREATMENTS
Topical acne therapies, oral antibiotics, isotretinoin pathways, and hair removal strategies may be relevant depending on symptom severity and patient preference.^2,8 Cosmetic concerns should not be minimised. Some patients may experience substantial psychological distress despite relatively mild clinical findings.⁸ Hair reduction approaches such as laser therapy, electrolysis, and cosmetic hair removal may therefore form an important part of holistic management.²

GLP-1 RECEPTOR AGONISTS
Glucagon-like peptide-1 (GLP-1) receptor agonists may support weight and metabolic management in selected patients with PMOS, particularly where insulin resistance, obesity, or broader cardiometabolic dysfunction are significant contributors.² These medications work by mimicking the GLP-1 hormone, helping the body release insulin only when glucose levels are elevated, slowing gastric emptying and reducing appetite signals. In PMOS, this may support weight management, insulin resistance and broader metabolic health. Treatment requires individualised prescribing, contraception counselling, side effect discussion, and awareness of licensing and local prescribing policy.

Patient explanation: “These medicines can help regulate appetite and improve how the body handles blood sugar and energy signals. For some people with PMOS, this may reduce food noise, improve fullness, and support healthier metabolic signalling. Improvements in insulin resistance and weight regulation may also positively affect ovulation, energy levels, and long-term cardiometabolic health.”

PMOS and fertility

PMOS is one of the leading causes of anovulatory infertility worldwide.^2,3 Ovulation may occur unpredictably or not at all, making cycle timing difficult and contributing to delayed conception.^2,3 Importantly, patients with PMOS are sometimes incorrectly told that they are ‘infertile’, which can cause significant psychological distress. In reality, many individuals with PMOS can conceive spontaneously or with relatively simple ovulation induction strategies.^2,10,11,12 

A large Swedish population-based study involving 45,395 women with PMOS and 217,049 controls found the cumulative probability of childbirth after spontaneous conception was approximately 55 per cent in women with PMOS.¹¹ The same study found the overall cumulative probability of childbirth, including assisted conception, was 80.2 per cent in women with PMOS compared with 78.2 per cent in women without PMOS.¹¹

Another longitudinal cohort study involving 291 women with PMOS reported that 73.6 per cent conceived spontaneously.¹² These findings are important in helping clinicians provide realistic reassurance and avoid catastrophic or inaccurate language regarding fertility potential.

Subfertility in PMOS is multifactorial. Ovulatory dysfunction is central, but insulin resistance, obesity, inflammation, and metabolic dysfunction may also affect reproductive outcomes and pregnancy risk.^2,9,13,14

FERTILITY COUNSELLING IN PRIMARY CARE
GPNs should ask routinely about reproductive goals because management priorities differ significantly depending on whether or not pregnancy is desired. If pregnancy is desired, management should shift from ovulation suppression and contraception towards ovulation optimisation, metabolic assessment, preconception counselling, and timely referral where appropriate.² Preconception counselling should include:
✽ Folic acid supplementation
✽ Medication review
✽ Smoking cessation support where relevant
✽ Optimisation of metabolic health
✽ HbA1c or glucose assessment where indicated
✽ Weight-stigma-informed lifestyle support
✽ Discussion of cycle tracking and ovulation awareness.²

TABLE 2: Treatment options

OVULATION INDUCTION AND FERTILITY MEDICATIONS
The 2023 guideline recommends letrozole as first-line pharmacological ovulation induction for anovulatory infertility associated with PMOS where no other infertility factors are present.^2,10 Letrozole is an aromatase inhibitor which transiently lowers oestrogen levels, increasing pituitary FSH secretion and promoting follicular development and ovulation.^2,10

Compared with clomiphene citrate, letrozole is associated with higher ovulation rates, higher live birth rates, and a lower risk of multiple pregnancy.^2,10  In the landmark New England Journal of Medicine trial, cumulative ovulation rates were approximately 62 per cent with letrozole compared with 48 per cent with clomiphene citrate, while live birth occurred in approximately 28 per cent versus 19 per cent respectively.¹⁰

Clomiphene citrate was historically first-line therapy for ovulation induction in PMOS and may still be used in some fertility pathways. It acts as a selective oestrogen receptor modulator, increasing endogenous gonadotropin release and stimulating ovulation.^2,10 However, clomiphene is associated with a higher risk of multiple pregnancy compared with letrozole and may be less effective in some patients with insulin resistance or obesity.^2,10 

METFORMIN AND FERTILITY
Metformin may improve ovulatory function in some individuals with PMOS, particularly where insulin resistance and metabolic dysfunction are significant contributors.^2,9 It may occasionally be used alone or alongside ovulation induction therapy depending on metabolic profile and fertility pathway.

GONADOTROPINS AND ASSISTED REPRODUCTION
Some individuals may require gonadotropin therapy or assisted reproductive technologies such as in vitro fertilisation (IVF), particularly where additional infertility factors are present or first-line ovulation induction is unsuccessful.² Patients with PMOS may have increased risk of ovarian hyperstimulation syndrome during assisted reproduction because of high follicle sensitivity. Fertility management should therefore remain individualised and carefully monitored.

PREGNANCY RISKS IN PMOS
PMOS is associated with increased risk of gestational diabetes, hypertensive disorders of pregnancy, pre-eclampsia, miscarriage, preterm birth, and adverse metabolic outcomes during pregnancy.^2,9,13 Insulin resistance and metabolic dysfunction likely contribute significantly to these risks.^9,13 Preconception care should therefore include folic acid supplementation, medication review, diabetes screening where appropriate, blood pressure assessment, and realistic lifestyle support delivered in a non-stigmatising manner.²

PSYCHOLOGICAL ASPECTS OF FERTILITY IN PMOS
Fertility concerns may significantly affect self-esteem, relationships, and mental wellbeing in individuals with PMOS.^2,8 Patients may experience shame, anxiety, grief, uncertainty, or fear regarding future fertility potential. Repeated exposure to messages suggesting inevitable infertility may further worsen psychological distress and hopelessness. Many patients report significant emotional burden associated with cycle unpredictability, delayed conception, or fear of needing fertility treatment.⁸

The international guideline highlights the importance of psychological assessment and person-centred communication within PMOS care.² GPNs can therefore play an important role in providing realistic reassurance, avoiding catastrophic language, supporting emotional wellbeing, and ensuring timely fertility referral where appropriate.

Glucose metabolism and diabetes risk

Insulin resistance is highly prevalent in PMOS and contributes to increased risk of impaired glucose tolerance and type 2 diabetes.^2,9 Hyperinsulinaemia may precede overt hyperglycaemia for many years.⁹ The 2023 guideline recommends ongoing metabolic surveillance because diabetes risk may increase across the reproductive lifespan.²

This is particularly important where additional risk factors are present, including family history of diabetes, previous gestational diabetes, higher BMI, sedentary lifestyle, or ethnic backgrounds associated with increased diabetes prevalence.²

HbA1c may be useful in ongoing monitoring, but oral glucose tolerance testing may be more sensitive in selected high-risk groups, particularly preconception or during fertility assessment.² GPNs play an important role in reinforcing long-term metabolic follow-up, supporting lifestyle interventions and recognising progression toward impaired glucose tolerance or type 2 diabetes.

Long-term cardiometabolic risk

PMOS should be understood as a long-term endocrine-metabolic condition rather than solely a reproductive disorder. Contemporary evidence demonstrates increased prevalence of insulin resistance, impaired glucose tolerance, type 2 diabetes, dyslipidaemia, and cardiovascular risk factors in individuals with PMOS.^2,9,13

Metabolic risk is not confined to individuals with obesity. Lean individuals with PMOS may also demonstrate impaired glucose metabolism and increased cardiovascular risk markers.^2,9 Patients may also experience increased central adiposity, elevated triglycerides, and reduced HDL cholesterol.^2,9,13

Chronic inflammation, insulin resistance, and adverse metabolic signalling likely contribute to long-term cardiovascular risk in PMOS.^9,13 The international guideline therefore recommends regular assessment of blood pressure, glucose metabolism, and lipid profile as part of ongoing care.²

NAFLD

Non-alcoholic fatty liver disease (NAFLD) appears more common in individuals with PMOS, particularly where insulin resistance, obesity, and metabolic syndrome are present.⁹ Chronic hyperinsulinaemia and adverse metabolic signalling are thought to contribute to hepatic fat accumulation and metabolic dysfunction.⁹ Patients may present with abnormal liver function tests, fatigue or incidental imaging findings, although many remain asymptomatic in early disease stages.

Recognition of NAFLD is clinically important because progression may contribute to steatohepatitis, fibrosis, and broader cardiometabolic risk over time.⁹ GPNs should therefore remain aware of liver health within long-term metabolic surveillance, particularly in individuals with obesity, impaired glucose tolerance, dyslipidaemia, or other features of metabolic syndrome.

Obstructive sleep apnoea

Obstructive sleep apnoea is more common in PMOS, particularly in the context of obesity and insulin resistance.² Symptoms may include snoring, witnessed apnoea, morning headaches, poor concentration, and excessive daytime sleepiness.² Sleep disruption may further worsen insulin resistance, appetite regulation, fatigue, and metabolic dysfunction through neuroendocrine and inflammatory pathways.^2,9 This can contribute to a cyclical pattern of worsening metabolic health and daytime functioning.

Endometrial health and cancer risk

PMOS is associated with increased risk of endometrial hyperplasia and endometrial cancer, primarily because chronic anovulation may expose the endometrium to prolonged unopposed oestrogen stimulation without regular progesterone-mediated shedding.^2,14 In ovulatory menstrual cycles, progesterone stabilises the endometrium after ovulation and supports organised shedding during menstruation.²

In PMOS, irregular or absent ovulation means that progesterone exposure may be reduced or absent for prolonged periods.^2,14 This can result in persistent endometrial proliferation and unpredictable bleeding patterns.²^,¹² Patients may therefore present with prolonged amenorrhoea followed by heavy, prolonged, or irregular bleeding.^2,14

Clinical implications for practice

Individuals with infrequent periods should not simply be reassured that irregular cycles are ‘normal for PMOS’ without consideration of endometrial protection.^2,14 The 2023 guideline recommends consideration of regular withdrawal bleeding, combined hormonal contraception, or cyclical progestogen, where appropriate, to reduce the risk of endometrial hyperplasia.² GPNs should therefore:
✽ Assess menstrual frequency and bleeding pattern regularly
✽ Identify prolonged amenorrhoea
✽ Reinforce the importance of endometrial protection
✽ Support adherence to prescribed hormonal treatment
✽ Recognise abnormal bleeding patterns requiring further investigation.

Further assessment or referral should be considered in individuals with:
✽ Persistent abnormal uterine bleeding
✽ Prolonged amenorrhoea followed by heavy bleeding
✽ Intermenstrual bleeding
✽ Failure to respond to treatment
✽ Additional endometrial cancer risk factors.^2,14

Timely recognition is important because prolonged unopposed oestrogen exposure may increase long-term endometrial risk if left untreated.^2,14

Monitoring and follow-up

PMOS is a lifelong condition requiring ongoing monitoring rather than episodic treatment alone. Follow-up should be individualised according to symptoms, metabolic risk, fertility goals, age, and treatment type.² Monitoring should extend beyond menstrual regulation and include psychological wellbeing, metabolic health, cardiovascular risk, and quality of life.

Role of the GPN

GPNs are central to continuity of care in PMOS. They are often the healthcare professionals who have the most regular contact with patients over time and are therefore well placed to identify changing symptoms, reinforce education, and support long-term engagement with care. GPNs can support education, metabolic screening, behaviour change, contraception counselling, fertility discussions, medication monitoring, and psychological support.

Nurse-led consultations may also provide opportunities to identify concerns that patients do not initially disclose during brief medical appointments, including body image distress, emotional eating, fertility anxiety, sexual wellbeing concerns, or previous negative healthcare experiences.

The therapeutic relationship is particularly important because many patients report previous experiences of dismissal, stigma, or fragmented care.^2,8 A validating, non-judgemental, and evidence-based approach can significantly improve engagement and long-term outcomes. GPNs may also play an important role in:
✽ Coordinating referrals to dietetics, fertility services, endocrinology, or psychology
✽ Reinforcing metabolic monitoring and cardiovascular prevention
✽ Supporting adherence to hormonal therapy and endometrial protection
✽ Providing culturally sensitive and weight-stigma-informed care
✽ Encouraging sustainable long-term self-management rather than short-term restrictive approaches
✽ Supporting transition between reproductive, fertility, and later-life health stages.

Conclusion

The terminology shift from PCOS to PMOS reflects a broader contemporary understanding of the condition as a multisystem endocrine-metabolic syndrome rather than a predominantly ovarian disorder alone. Insulin resistance, metabolic dysfunction, and cardiometabolic risk are now recognised as central components of the condition for many individuals, alongside reproductive and androgenic features.

By combining evidence-based pharmacological management with realistic lifestyle support, validation, and long-term follow-up, general practice nurses can help improve both short- and long-term outcomes for people living with PMOS.

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