PMOS (Formerly PCOS): Hormones, Ovulation and Metabolism
Polyendocrine metabolic ovarian syndrome (PMOS) is the new name for the condition long known as polycystic ovary syndrome (PCOS). The change in terminology reflects something clinicians have understood for years: this is not simply a condition of ovarian “cysts”. It is a reproductive, endocrine and metabolic syndrome in which ovulation, androgen production and insulin signalling can all be altered.
That combination explains why two people with PMOS can look very different clinically. One may present because their periods have become widely spaced. Another may be struggling with hirsutism or acne. Someone else may first come to attention during fertility assessment or after abnormal glucose testing. The ovaries are involved, but they are only one part of the picture.
From normal ovulation to PMOS
During a typical menstrual cycle, gonadotrophin-releasing hormone from the hypothalamus stimulates the pituitary to release follicle-stimulating hormone (FSH) and luteinising hormone (LH). Within the ovary, LH acts mainly on theca cells, which produce androgen precursors. FSH acts mainly on granulosa cells, where aromatase converts much of that androgen substrate into oestrogens.
Several follicles may begin developing early in the cycle, but usually one becomes dominant. That follicle continues to mature until ovulation. After ovulation, the remaining follicular tissue forms the corpus luteum and produces progesterone. If pregnancy does not occur, progesterone falls and menstruation follows.
PMOS alters this process at several points. Ovarian theca cells can produce excess androgen, gonadotrophin signalling can become dysregulated, and insulin can amplify androgen production. At the same time, follicles may begin to develop but fail to progress normally towards dominant follicle selection and ovulation.
The ovary may therefore contain many small pre-antral and antral follicles. These are the structures that created the “polycystic” description in the old name, but they are follicles rather than pathological ovarian cysts.
When dominant follicle development and ovulation happen less often, menstrual cycles become longer or unpredictable. Some people develop oligomenorrhoea, while others have periods of amenorrhoea.
The hormonal consequences continue beyond the ovary. If ovulation does not occur, a corpus luteum does not form in the usual way and there is no normal cyclical progesterone phase. The endometrium can therefore remain exposed to oestrogenic stimulation for prolonged periods without regular progesterone opposition.
Over time, prolonged untreated amenorrhoea can increase the risk of endometrial hyperplasia and endometrial cancer. The relative risk is increased, although the overall chance of an individual developing endometrial cancer remains low. Routine endometrial screening is not recommended solely because someone has PMOS, but very infrequent bleeding often needs active management to provide endometrial protection.
Androgens and insulin connect many of the symptoms
Androgens are normal hormones. They contribute to reproductive physiology, bone, muscle, libido and other functions in all sexes. In PMOS, the problem is excessive androgen production or activity.
Higher androgen activity can affect the skin and hair follicles. Fine vellus hairs may become thicker terminal hairs in androgen-sensitive areas, producing hirsutism. Sebaceous gland activity can increase, contributing to acne, and some people develop scalp hair thinning in an androgen-pattern distribution.
Not everyone with biochemical hyperandrogenism develops the same visible features. Some people have marked hirsutism with only modest biochemical changes, while others have raised androgen concentrations with relatively little change in hair or skin. Rapidly progressive hirsutism, virilisation or very high androgen concentrations are not typical of uncomplicated PMOS and need investigation for other causes of androgen excess.
Insulin is closely connected to this endocrine picture. When tissues such as muscle and liver respond less effectively to insulin, the pancreas may compensate by producing more. The resulting hyperinsulinaemia can stimulate ovarian androgen production and reduce hepatic production of sex hormone-binding globulin (SHBG). Lower SHBG leaves a greater proportion of circulating testosterone biologically available.
The relationship is not purely one-way. Hyperandrogenism can also contribute to metabolic dysfunction and insulin resistance. This helps explain why reproductive and metabolic features often appear together rather than behaving as two separate conditions.
Anti-Müllerian hormone (AMH) is also frequently higher in PMOS because of the increased number of small developing follicles. AMH is involved in follicle recruitment and development, and its concentration can be used in adult diagnostic pathways as an alternative marker of polycystic ovarian morphology. It should not be treated as a stand-alone diagnostic test.
How the diagnosis is made
There is no single blood test or scan that diagnoses PMOS in every patient. In adults, diagnosis is based on a pattern of findings after other relevant causes have been excluded.
Current international recommendations generally require at least two of three features:
- clinical or biochemical hyperandrogenism
- ovulatory dysfunction, usually reflected in irregular or infrequent menstrual cycles
- polycystic ovarian morphology, assessed by ultrasound or, in adults, by an elevated AMH concentration used within an appropriate diagnostic pathway
If irregular cycles and hyperandrogenism are already present, ultrasound or AMH is not required simply to provide a third feature. Equally, an ultrasound showing polycystic ovarian morphology does not diagnose PMOS by itself.
Other conditions can produce similar features. Depending on the presentation, assessment may include thyroid function, prolactin, 17-hydroxyprogesterone and other endocrine investigations. Pregnancy should also be considered when periods are absent or delayed.
Adolescents are approached differently because normal puberty can resemble PMOS. Menstrual cycles may be irregular for some time after menarche, acne is common, and androgen concentrations are changing. Current recommendations therefore require both persistent menstrual irregularity, interpreted according to time since menarche, and clinical or biochemical hyperandrogenism after other causes have been excluded.
Ultrasound morphology and AMH should not be used to diagnose PMOS during adolescence. Multifollicular ovaries are common in healthy adolescents, so ovarian appearance can be misleading. Where only one diagnostic feature is present, follow-up over time may be more appropriate than assigning a diagnosis too early.
The metabolic side belongs in the same condition
PMOS is associated with increased risk of impaired glucose regulation and type 2 diabetes, and this risk is not confined to people who are overweight. Insulin resistance can occur across the weight spectrum.
The international guideline recommends assessment of glycaemic status at diagnosis in adults and adolescents with PMOS, with repeat assessment every one to three years according to additional risk factors. A 75 g oral glucose tolerance test is considered the most accurate method for identifying dysglycaemia in PMOS. Fasting glucose and HbA1c can also be used in some settings, although they are less sensitive for detecting impaired glucose tolerance and type 2 diabetes in this population.
Blood pressure and lipid status are also relevant because PMOS is associated with several cardiovascular risk factors. An individual person's long-term cardiovascular risk still depends on the wider clinical picture, including age, smoking, family history, blood pressure, lipids and glycaemia.
Weight can influence metabolic and reproductive features in some people, but it does not define the condition. Reducing PMOS to “a weight problem” misses people in smaller bodies, oversimplifies the biology and can contribute to weight stigma. Lifestyle support is more useful when it focuses on sustainable health behaviours rather than assuming one diet or exercise programme suits everyone.
Psychological health sits alongside the physical effects. Depression, anxiety, body-image distress, eating difficulties and infertility-related distress are more common in people with PMOS. Symptoms such as hirsutism, acne and unpredictable bleeding can affect confidence and quality of life even when they are not medically dangerous.
Treatment follows the patient's priorities
PMOS does not have one standard treatment because the clinical problems are not the same for everyone. Management is shaped by menstrual pattern, androgen-related symptoms, metabolic risk, fertility plans and the person's own priorities.
For someone troubled by irregular cycles or hirsutism and who is not trying to conceive, a combined oral contraceptive pill may be considered when clinically appropriate. Progestogen-containing treatment may also be used to provide endometrial protection when bleeding is very infrequent.
Metformin is used particularly when metabolic features are prominent and can improve insulin sensitivity and some reproductive features. Anti-androgen treatment may be considered for persistent hirsutism in selected patients when response to other treatment is inadequate, with effective contraception where the medicine could affect fetal development.
Fertility management is different because creating a withdrawal bleed is not the same as restoring ovulation. PMOS is a common cause of anovulatory infertility, although many people with the condition conceive spontaneously.
When ovulation is infrequent or absent and there are no other infertility factors, the international evidence-based guideline recommends letrozole as first-line pharmacological ovulation induction. Clomifene, metformin, gonadotrophins and other fertility treatments may be used in selected circumstances. Local NHS pathways and commissioning arrangements can differ, so fertility treatment is guided by specialist assessment.
For nurses, the useful clinical picture is broader than the old image of “polycystic ovaries”. A patient may need support with long gaps between periods, endometrial protection, hirsutism, acne, fertility, glucose risk, weight stigma or psychological distress. Those problems come from different parts of the same syndrome and should not be treated as unrelated complaints.
Summary
Polyendocrine metabolic ovarian syndrome is the 2026 name for the condition previously called polycystic ovary syndrome.
PMOS involves interacting ovarian, endocrine and metabolic abnormalities. Hyperandrogenism, disturbed follicle development and ovulation, and altered insulin action are central features, but the pattern varies between individuals.
The small structures seen in a polycystic ovary are follicles rather than pathological ovarian cysts. In adults, diagnosis is based on at least two of hyperandrogenism, ovulatory dysfunction and polycystic ovarian morphology after other causes have been excluded. AMH may be used as an alternative marker of ovarian morphology in adults within the diagnostic pathway.
Adolescents are diagnosed more cautiously because normal pubertal development can resemble PMOS. The condition also extends beyond reproduction, with implications for glucose regulation, cardiovascular risk, endometrial health and psychological wellbeing.
Management is therefore individualised. The treatment chosen for irregular bleeding may be very different from the treatment chosen for hirsutism, metabolic risk or anovulatory infertility.
References
Monash University (2026) International evidence-based guideline for the assessment and management of polyendocrine metabolic ovarian syndrome. Available at: https://www.monash.edu/medicine/mchri/pcos/guideline
NHS (2026) Polyendocrine metabolic ovarian syndrome (PMOS). Available at: https://www.nhs.uk/conditions/polyendocrine-metabolic-ovarian-syndrome-pmos/
Royal College of Obstetricians and Gynaecologists (2023) International Evidence-based Guideline for the assessment and management of polycystic ovary syndrome. Available at: https://www.rcog.org.uk/guidance/browse-all-guidance/other-guidelines-and-reports/international-evidence-based-guideline-on-polycystic-ovary-syndrome/
Teede, H.J. et al. (2023) ‘Recommendations from the 2023 International Evidence-based Guideline for the Assessment and Management of Polycystic Ovary Syndrome’, Human Reproduction, 38(9), pp. 1655–1679. Available at: https://pubmed.ncbi.nlm.nih.gov/37580037/
Teede, H.J. et al. (2026) ‘Polyendocrine metabolic ovarian syndrome, the new name for polycystic ovary syndrome: a multistep global consensus process’, The Lancet, 407(10545), pp. 2329–2339. Available at: https://pubmed.ncbi.nlm.nih.gov/42119588/
Peña, A.S. et al. (2025) ‘International evidence-based recommendations for polycystic ovary syndrome in adolescents’, BMC Medicine, 23. Available at: https://pubmed.ncbi.nlm.nih.gov/40069730/
Rosenfield, R.L. and Ehrmann, D.A. (2016) ‘The Pathogenesis of Polycystic Ovary Syndrome: The Hypothesis of PCOS as Functional Ovarian Hyperandrogenism Revisited’, Endocrine Reviews, 37(5), pp. 467–520. Available at: https://pubmed.ncbi.nlm.nih.gov/27459230/