From Misnomer to Meaning: A Patient-Centered Shift from PCOS to PMOS

Following a thorough, multistep global consensus process, Professor Helena Teede, PhD, MBA, FRACP, an endocrinologist with Monash University in Australia, spearheaded an initiative to rename polycystic ovary syndrome (PCOS) to polyendocrine metabolic ovarian syndrome (PMOS).¹ This change was a long time coming.

For years, medical experts argued that PCOS was a misnomer, contributing to confusion and, ultimately, underdiagnosis.^1,2 Despite what the PCOS name suggested, polycystic ovarian morphology is neither required nor sufficient alone for diagnosis.³ Furthermore, the ovarian “cysts” of PCOS were not cysts at all but rather growth-arrested follicles.^1,4

These misconceptions contributed to delayed diagnoses, with up to 70% of affected people remaining undiagnosed, and poor patient satisfaction.¹ PCOS implied a purely gynecologic condition that ignored the disorder’s endocrine, cardiovascular, and metabolic pathophysiologic dysfunction entirely.

Conversely, PMOS encapsulates its multisystem dysfunction, including its polyendocrine features (hyperandrogenism, gonadotropin dysregulation), metabolic features (obesity, insulin resistance, type 2 diabetes, dyslipidemia, cardiovascular disease, metabolic dysfunction-associated steatotic liver disease, sleep apnea), and ovarian features (ovulatory disturbances, irregular menstrual cycles, infertility, pregnancy complications, endometrial cancer, follicular arrest).¹

In theory, this name change will have positive impact for patients as better understanding of the condition expands throughout the medical community. But what are the practical implications for pharmacists?

An implementation strategy is underway with a focus on evolution rather than disruptive transformation.¹ During this transitional period, consider the following^1,5-7:

• The diagnostic criteria for the syndrome remain the same. Patient still need 2 of the 3 following for diagnosis: hyperandrogenism, oligo-anovulation (ovulatory dysfunction), polycystic ovaries on ultrasound, or elevated Anti-Müllerian hormone.
• All current clinical recommendations for the condition remain the same. As of now, pharmacotherapy for PMOS is entirely off-label and treatment selection is determined by primary symptoms, patient preferences, and reproductive goals (Table 1).
• The current International Classification of Diseases (ICD) code for billing and claims processing remains the same for now. The consensus group is working with international classification bodies for a planned 3-year transition period to a new PMOS ICD code. However, until coding systems update, expect prescriptions, prior authorizations, and insurance documents to continue referencing PCOS/E28.2 (ICD-10) or PCOS/5A80.1 (ICD-11).
• Drug labeling and workflows at the pharmacy remain the same. That said, prior authorization requests and insurance documentation may note either PCOS or PMOS. Understand they are the same condition.

During this transition period, pharmacists likely will play the biggest role in educating others. Start by updating your clinical vocabulary from PCOS to PMOS and encourage the same of your colleagues. Proactively address the name change with patients to mitigate confusion. Advocate for appropriate cardiometabolic screening and evidence-based management. Educate patients and provider colleagues about the metabolic and endocrine components of the condition and the available off-label uses of medications for PMOS.

REFERENCES

1. Teede HJ, Khomami MB, 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

2. Teede HJ, Moran LJ, Morman R, et al. Polycystic ovary syndrome perspectives from patients and health professionals on clinical features, current name, and renaming: a longitudinal international online survey. EClinicalMedicine. 2025;84:103287. doi:10.1016/j.eclinm.2025.103287

3. Joham AE, Norman RJ, Stener-Victorin E, et al. Polycystic ovary syndrome. Lancet Diabetes Endocrinol. 2022;10(9):668-680. doi:10.1016/S2213-8587(22)00163-2

4. Meczekalski B. Polycystic ovary syndrome: past, present and future. J Clin Med. 2023;12(11):3808. doi:10.3390/jcm12113808

5. Teede HJ, Tay CT, Laven J, et al. Recommendations from the 2023 International Evidence-based Guideline for the Assessment and Management of Polycystic Ovary Syndrome. Hum Reprod. 2023;38(9):1655-1679. doi:10.1093/humrep/dead156

6. Chapter IV: Endocrine, nutritional, and metabolic diseases (EOO-E90). ICD. Accessed June 29, 2026. https://icd.who.int/browse10/2019/en#/E28.2

7. 5A80.1: Polycystic ovary syndrome. ICD-11 for Mortality and Morbidity Statistics. Accessed June 29, 2026. https://icd.who.int/browse/2026-01/mms/en#1213633323

8. Williams T, Moore JB, Regehr J. Polycystic ovary syndrome: common questions and answers. Am Fam Physician. 2023;107(3):264-272.

9. 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. Hum Reprod. 2023;38(9):1655-1679. doi:10.1093/humrep/dead156

10. Melin J, Forslund M, Alesi S, et al. Metformin and combined oral contraceptive pills in the management of polycystic ovary syndrome: a systematic review and meta-analysis. J Clin Endocrin Metab. 2024;109(2):e817-e836. doi:10.1210/clinem/dgad465

11. Ma R, Ding X, Wang Y, Deng Y, Sun A. The therapeutic effects of glucagon-like peptide-1 receptor agonists and metformin on polycystic ovary syndrome: a protocol for systematic review and meta-analysis. Medicine (Baltimore). 2021;100(23):e26295. doi:10.1097/MD.000000000026295

12. Lin J, Yang R, Zhuang J, et al. The efficacy and safety of novel antidiabetic agents in polycystic ovary syndrome: a network meta-analysis. J Ovari Res. 2026;19(167). doi:10.1186/s13048-026-02078-x

13. Stewart M, Black K. Choosing a combined oral contraceptive pill. Aust Prescr. 2015;38(1):6-11. doi:10.18773/austprescr.2015.002

14. Yaribeygi H, Sathyapalan T, Maleki M, Jamialahmadi T, Sahebkar A. Molecular mechanisms by which SGLT2 inhibitors can induce insulin sensitivity in diabetic milieu: a mechanistic overview. Life Sci. 2020:240:117090. doi:10.1016/j.Ifs.2019.117090

15. Kaltsas A, Efthimiou A, Roidos C, et al. Letrozole at the crossroads of efficacy and fetal safety in ovulation inducation: a narrative review. Biomedicines. 2025;13(9):2051. doi:10.3390/biomedicines13092051

16. Premji R, Nylen ES, Naser N, Gandhi S, Burman KD, Sen S. Lipid profile changes associated with SGLT-2 inhibitors and GLP-1 agonists in diabetes and metabolic syndrome. Metab Syndr Relat Disord. 2022;20(6):321-328. doi:10.1089/met.2022.0004