Polycystic ovary syndrome (PCOS), now referred to as polyendocrine ovarian syndrome (PMOS), is a complex cardiometabolic hormonal disorder prevalent in reproductive-age females. Due to the complexity and variability of its symptoms, the management of this disorder continues to be optimised: including efforts to uncover its pathophysiology, identify better treatment options, and refine terminology. This article seeks to outline what PMOS is, how it is managed, and highlight the recent extensive change in terminology and its rationale. These actions serve to improve the management of PMOS in healthcare, providing the patients with a better tomorrow.

What is Polyendocrine Metabolic Ovarian Syndrome (PMOS)?(#e07d84)

Polyendocrine metabolic ovarian syndrome (PMOS), previously known as polycystic ovary syndrome, is a common cardiometabolic hormonal disorder affecting one in eight women.1 The most prominent symptoms of PMOS include irregular menstrual cycles, infertility, acne vulgaris, androgenetic alopecia, acanthosis nigricans, hirsutism, secondary dysmenorrhoea, and weight gain.2,3 PMOS is also associated with anxiety, depression, sleep apnoea, diabetes, hypertension, dyslipidaemia, and even endometrial cancer.2 As illustrated above, the features of PCOS are often multisystemic, encompassing metabolic, reproductive, psychological, and dermatological manifestations.1 Indeed, the aetiology and pathophysiology of PMOS are complex and unclear. Therefore, it is most important that the proposed mechanisms be examined cautiously.

Evidence shows that genetic and epigenetic factors may be the culprits for PMOS. Contemporary theories point to genes associated with insulin resistance, steroidogenesis, and gonadotrophic dysregulation.4 One of the numerous genes that are strongly associated with PMOS is the DENND1A (Differentially Expressed in Normal and Neoplastic Development isoform A1) gene.4,5 The DENND1A gene codes for 2 protein variants in the cytoplasm and nuclei of theca cells, with the second variant (DENND1A.V2) inducing increased CYP17A1 and CYP11A1 expressions, and driving androgen biosynthesis.6 This coheres with the established understanding of PMOS pathophysiology. Another major contributor to PMOS is epigenetics. Various studies have found that dysregulated methylation in various tissues and peripheral blood may contribute to PMOS. Promoter hypomethylation of the AMH and AMHR2 genes is a crucial epigenetic alteration that causes the chronic overactivation of Anti-Müllerian Hormone signalling, shifting follicle regulation into a state of permanent arrest. Hypermethylation of the INSR gene is a crucial epigenetic mechanism that drives ovarian-specific insulin resistance and metabolic dysfunction.5 These factors are just a small part of the complex aetiology of PMOS. However, they demonstrate the pathways by which PMOS progresses.

The pathophysiology of PMOS is similarly complex. Insulin resistance, as previously discussed, is a major part of PMOS progression as insulin resistance leads to hyperandrogenism in three ways: increasing circulating androgens as the production of sex hormone binding globulin (SHBG) is decreased; increasing androgen production in ovarian tissues, driven by the gonadotropic property of insulin; promoting androgen production via luteinising hormone (LH) sensitisation in theca cells.5,6 It is also suggested that gonadotropin-releasing hormone (GnRH) from the hypothalamic-pituitary-ovarian axis plays a major role.5,6 It has been demonstrated that an increase in GABA innervation and AMH levels leads to increased GnRH neuron firing.7,8 The increased firing of GnRH neurons increases the luteinising hormone to follicle-stimulating hormone ratio (LH/FSH), contributing to ovarian hyperandrogenism.5 These findings not only serve as the underlying mechanisms of PMOS pathophysiology but also represent possible therapeutic targets (Figure 1).

Figure 1. PMOS Pathophysiology5

How Is PMOS Managed?

The complex and multigenic nature of PMOS underscores the importance of holistic management strategies. Pharmacological interventions and lifestyle modifications remain the paradigm for PMOS care. Combined hormonal contraceptives remain the first-line medication for the alleviation of hyperandrogenic symptoms such as hirsutism, acne vulgaris and anovulation in PMOS.2,5 Increased attention has also been given to the use of metformin and glucagon-like-peptide-1 receptor agonists (GLP-1RA) for managing metabolic symptoms by insulin sensitisation, and managing blood glucose to prevent diabetes and dyslipidaemia.2,5 To improve fertility and induce ovulation, letrozole is also often utilised; similarly, GLP-1RA is used to improve reproductive function.2,5 While the importance of pharmacological interventions have been underscored, the effects of lifestyle modifications cannot be undermined. Dietary changes and exercise are key lifestyle interventions for improving PMOS.2 Body fat composition and insulin resistance may be improved with healthy dieting and adequate exercise, with the additional benefits of preventing diabetes and cardiovascular diseases.2,5 It is imperative to understand that PMOS is highly heterogeneous, requiring individualised and holistic management.5

Why Has the Name Changed?

There are two major reasons for the change in name: improved clarity, and reduced stigmatisation.

The new name PMOS is more medically accurate and clear, facilitating diagnosis and fostering patient awareness. Prior to the renaming, PMOS was known as polycystic ovary syndrome (PCOS). However, PCOS fails to encapsulate the clinical features of the disorder: namely, it over-emphasises the gynaecological aspects of the disorder whilst neglecting the aforementioned neuroendocrine and metabolic aspects.1,9 In fact, “polycystic ovary” is now known to be inaccurate, as ovarian cysts are not specific to the disorder and may not be present in all cases.1,9 This inaccuracy may confuse healthcare professionals and patients, resulting in delayed diagnosis, ineffective communication, and ultimately dissatisfactory healthcare.1 PMOS improves clarity by incorporating the polygenic, endocrinal and metabolic nature of the disorder, making the name much clearer.

The renaming may also help reduce stigma surrounding women’s reproductive health and fertility. In certain cultures, fertility is highly emphasised and linked to sociocultural values.1 One such example would be Chinese culture, where a statistically significant relationship between women’s fertility, and socioeconomic standing has been demonstrated.10 In such cases, PCOS diagnoses may contribute to undesirable distress and pressure on the patients.1 This may even contribute to or even exacerbate existing psychological conditions such as anxiety or depression in patients. Although PMOS retains the term ‘ovary’, it shifts the focus towards the disorder’s endocrine and metabolic features, helping to reduce stigmatisation. It is, therefore, hoped that such change will bring about improved clinical outcomes for patients suffering from PMOS (Figure 2).11

Figure 2. Why PCOS Has Been Renamed PMOS11

How Is the Change Implemented?

To optimise the change in terminology, the global implementation is planned as a staged, progressive transition1:

• Stage 1: Publish the health policy for academic dissemination.

• Stage 2: Develop healthcare resources reflecting the change in terminology.

• Stage 3: Apply the change through structured communication strategies.

• Stage 4: Integrate the new terminology into existing medical systems.

• Stage 5: Foster alignment among policymakers, publishers, and the healthcare industry to support the adoption of the updated terminology.

• Stage 6: Seek formal classification by international bodies such as the WHO (World Health Organization).

• Stage 7: Monitor and evaluate the transition over three years.

• Stage 8: Incorporate the change into international guidelines.

Staged implementation allows for smooth adaptation by all stakeholders, ensuring clarity and efficacy.

Conclusion

PMOS, previously known as PCOS, is a common cardiometabolic hormonal disorder with complex aetiology and pathophysiology warranting further investigation to develop better treatments. Current management of PMOS focuses on pharmacological interventions and lifestyle modifications to alleviate symptoms. While research regarding its aetiology and possible therapeutic strategies continues, a change in terminology is advocated in hopes of improving clarity and reducing stigmatisation. Indeed, there is still much to be done to improve the clinical outcomes and quality of life for PMOS patients. This change serves as a reminder that improvements, no matter the scale, can be made to improve the lives of patients — “in the pursuit of excellence”.

References:

1. Teede HJ, et al. The Lancet. 2026;407:2329–39. 2. Polycystic Ovary Syndrome (PCOS). FDA. 2026. https://www.fda.gov/consumers/womens-health-topics/polycystic-ovary-syndrome-pcos#Symptoms%20of%20PCOS. [Accessed 13 July 2026]. 3. Romeo P, et al. Journal of Endometriosis and Uterine Disorders. 2025;12:100131. 4. Shukla A, et al. Polyendocrine Metabolic Ovarian Syndrome. StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2026 Jan-. https://www.ncbi.nlm.nih.gov/books/NBK459251/. [Accessed 14 July 2026]. 5. Chan JL, et al. J Clin Invest. 2026;136(12):e202824. 6. Crespo RP, et al. Arch Endocrinol Metab. 2018;62:352–61. 7. Herbison AE, Moenter SM. J Neuroendocrinol. 2011;23:557–69. 8. Cimino I, et al. Nature Communications. 2016;7(1):10055. 9. Norman RJ, Morman R, Teede HJ. Fertil Steril. 2023;120:249–50. 10. Zhang C, Li T. China Economic Review. 2017;45:279–88. 11. Goswami S. PCOS Name Changed To PMOS: How This Impacts Women Globally And In India. 2026. https://www.ndtv.com/health/pcos-name-changed-to-pmos-how-this-impacts-women-globally-and-in-india-11487651. [Accessed 14 July 2026].