Feature|Articles|July 6, 2026

Polyendocrine metabolic ovarian syndrome: looking past the reproductive system to the eye

Fact checked by: Katherine Talcott, MD
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Key Takeaways

  • Insulin resistance (up to 70%), hyperinsulinemia-driven androgen excess, genetic susceptibility, and inflammation create a self-reinforcing endocrine–metabolic milieu that worsens obesity-related diabetes and vascular risk.
  • Large cross-sectional EHR data (~500,000 women) show increased ocular disease prevalence in PMOS versus general and high-BMI controls, including dry eye, glaucoma, papilledema/IIH, and diabetic retinopathy.
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Patients with polyendocrine metabolic ovarian syndrome have higher ocular disease prevalence.

Polycystic ovarian syndrome (PCOS), recently renamed polyendocrine metabolic ovarian syndrome (PMOS),1is the most common endocrine disorder among females of reproductive age worldwide,2 affecting from 4% to 20% of women.3

The disease’s effects are not limited to the reproductive system. “It affects the whole body, driving multi-organ dysfunction, particularly in the liver, heart, and pancreas, primarily fueled by chronic low-grade inflammation, insulin resistance, and excess androgens,”4 according to Singh and colleagues.

The disease manifestations include menstrual dysfunction, infertility, hirsutism, acne, and obesity.5 By definition, at least one ovary has an ovarian volume exceeding 10 mL and at least one ovary has about 10 small cysts, with diameters ranging from 2 to 9 mm.6 PMOS generally is diagnosed once those complications develop and result in significant alterations in the quality of life.7

PMOS causes

The precise cause of PMOS remains undetermined, but it is primarily driven by a combination of genetic predisposition, hormonal imbalances, and metabolic dysfunction. These factors create a cycle that disrupts ovulation and triggers symptoms.8

The main drivers of PMOS development include the following.

• Research has indicated that insulin resistance is present in up to 70% of women with PMOS. The cellular responses to insulin are ineffective, which results in excessive amounts produced by the pancreas. The elevated levels of insulin then stimulate the ovarian production of excess androgens.9

• The high androgen levels prevent release of eggs from the ovaries, which results in leading to irregular periods, acne, and excess facial or body hair.10

• PMOS tends to have a genetic component. If a mother or sister has PMOS, a patient’s risk of developing it is significantly higher. Researchers have identified several gene variants linked to the condition.9

• Chronic, low-grade inflammation can be present in women with PMOS and can stimulate ovarian production of more androgens, which can contribute to cardiovascular and metabolic issues.11

• Women’s with PMOS have up to a three-fold increased risk of developing type 2 diabetes. This metabolic risk is heavily compounded by obesity. While the syndrome has intrinsic insulin resistance, obesity severely exacerbates these metabolic defects, making weight management a critical preventive measure.12

Katherine Talcott, MD, a retina specialist at the Cole Eye Institute, Cleveland Clinic, Cleveland, spoke with Ophthalmology Times to explain the disease’s effects on the eye. “This is an area that we are learning more about. Researchers are trying to understand the associations between ocular disease and PMOS. This is not normally something that ophthalmologists think about when evaluating patients,” she said.

However, ophthalmologists should be aware of the disease and the wide age range of patients with PMOS, ie, from the teens to elderly patients, she mentioned.

In clinic, many of her patients have diabetic retinopathy or retinal vein occlusion, diseases that develop in younger patients who may have risk factors for PMOS, such as obesity.

“In these patients, I think about their systemic health overall while I treat them. In addition, PNOS will impact subspecialties in ophthalmology other than retina,” she explained.

During dilated examinations and on optical coherence tomography images, Talcott looks for retinal bleeding, new blood vessels, swelling, or fluid.

Studies of ocular impact

In a recent study13 published in the European Journal of Ophthalmology, Talcott and colleagues conducted a large cross-sectional investigation in which they wanted to determine the prevalence and odds of the development of ocular diseases other than retinal diseases in patients with PMOS. The health records of almost 500,000 women aged 15 to 50 years were included and compared to two controls, ie, a total female population of over 32 million and body mass index (BMI) of 30 or over in almost 5 million.

They reported, “Patients with PMOS had higher ocular disease prevalence than both the total female (11/17) and high BMI (12/17) groups, and higher prevalence odds ratios. Dry eye (245.63 vs. 129.99 and 105.99 per 10,000) and glaucoma (117.86 vs. 80.39 and 56.44 per 10,000) were significantly more prevalent (p < 0.001). Idiopathic intracranial hypertension, papilledema, diabetic retinopathy (p < 0.001), and several posterior segment diseases also had increased prevalence rates among patients with PMOS (p < 0.05).”

The conclusion reached was that PMOS is associated with an increasedodds ofocular disease independent of the BMI. Hormonal and metabolic factors may underlie this relationshipand should be further explored.13

These results correlated findings from previous studies. Sumer and colleagues14 and Acet and Sarikaya15 reported that dry eye disease and meibomian gland dysfunction were linked to PMOS, which are driven by hormonal imbalances (such as excess androgens) and systemic inflammation.

In addition to the marked prevalence of dry eye in women with PMOS, Zong and colleagues16 also found that abnormalities of the anterior segment, optic nerve, and retina were seen that were not observed in controls (p = 0.0002).

Other research has suggested that patients with PMOS may have a higher prevalence of conditions like glaucoma and idiopathic intracranial hypertension (pseudotumor cerebri that require medical management and routine monitoring.13,17,18

A Turkish study19 reported that the mean central corneal thickness values were significantly higher in the PMOS group (p = 0.001).

Treatment of ocular symptoms of PMOS

Dry eye syndrome and meibomian gland dysfunction can be treated usingregular instillation of preservative-free artificial tears, application of warm compresses, lid hygiene (eg, baby shampoo or specialized wipes), and omega-3 supplementation to restore tear homeostasis and reduce discomfort.18

For patients with increased central corneal thickness, that women with PMOS should undergo complete hormonal regulation via medical therapy before planning corneal or refractive (e.g., LASIK) surgeries to avoid poor outcomes.19

For patients with increased retinal thickness changes, standard treatment focuses on managing systemic insulin resistance and dyslipidemia, which are thought to impact the structural integrity of the retina.20

Take-away for ophthalmologists and optometrists

“PMOS is increasing in incidence, with our patient populations facing obesity and other medical conditions. It is helpful to keep PMOS in mind as a potential risk factor that hormonal dysregulation in these patients beyond just obesity might be increasing the risk of retinal disease. When examining patients with PMOS, eye care clinicians might want to take an extra look to screen them for any of these other findings,” Talcott suggested.

References
1. Endocrine Society. Polyendocrine Metabolic Ovarian Syndrome: new name to improve diagnosis and care of condition affecting 170 million women worldwide. Press release May 12, 2026. http://www.endocrine.org/news-and-advocacy/news-room/2026/pcos-name-change
2. Shukla A, Rasqyub KI, Anastasopoulos C. Polyendocrine metabolic ovarian syndrome. StatPearls [Internet]. 2025; updated July
3. Ghafari A, Maftoohi M, Samarin ME, Barani S, Banimohammad M, Samie R. The last update on polycystic ovarian syndrome (PCOS), diagnosis criteria, and novel treatment. Endocr Metab Sci. 2025;17:100228. https://doi.org/10.1016j.endmts.2025.100228
4. Singh S, Pal N, Shubham S, et al. Polycystic ovary syndrome; etiology, current management, and future therapeutics. J Clin Med. 2023;12:1454. doi:10.3390/jcm12041454
5. Motlagh Asghari K, Nejadghaderi SA, Alizadeh M, et al. Burden of polycystic ovary syndrome in the Middle East and North Africa region, 1990-2019. Sci Rep. 2022;12:7039. doi:10.1038/s41598-022-11006-0.
6. Balen AH, Tan SL, MacDougall J, Jacobs HS. Miscarriage rates following in-vitro fertilization are increased in women with polycystic ovaries and reduced by pituitary desensitization with buserelin. Hum Reprod. 1993;8:959–64.
7. Azziz R, Woods KS, Reyna R, Key TJ, Knochenhauer ES, Yildiz BO. The prevalence and features of the polycystic ovary syndrome in an unselected population. J Clin Endocrinol Metab. 2004;89:2745–9.
8. US Department of Health and Human Services, National Institutes of Health. PCOS. https://www.nichd.nih.gov/health/topics/pcos/conditioninfo/causes
9. National Health Services. Causes. Polycystic ovarian syndrome. https://www.nhs.uk/conditions/polycystic-ovary-syndrome-pcos/causes/
10. FDA Office of Women’s Health. Polycystic ovary syndrome (PCOS). https://www.fda.gov/consumers/womens-health-topics/polycystic-ovary-syndrome-pcos
11. University of Pittsburgh Medical Center. Polycystic ovary syndrome (PCOS). https://www.upmc.com/conditions/p/polycystic-ovary-syndrome
12. Sam S. Obesity and polycystic ovary syndrome. Obes Manag. 2007;3:69-73. doi: 10.1089/obe.2007.0019
13. Lopez A, Zhang A, Kaelber DC, Talcott KE, Singh RP, Shaia J. The impact of polycystic ovarian syndrome on ocular health. Eur J Ophthalmol. 2026; 10:11206721261436102. doi: 10.1177/11206721261436102.
14. Sumer F, Gurlek B, Yildiz E, et al. Alterations in tear function and meibomian gland dysfunction across various phenotypes of polycystic ovary syndrome. Sci Rep. 2025;15:12680. https://doi.org/10.1038/s41598-025-94890-6
15. Acet Y, Sarikaya S. Another etiological factor of meibomian gland loss in patients with polycystic ovary syndrome: inflammation. J Ocul Pharmacol Ther. 2022;38:626-34. doi: 10.1089/jop.2022.0097.
16. Zong Z, Kalyan S, Andres C, Akkor S, Prior JC, Patel MS. Prevalence of ocular anomalies is increased in women with polycystic ovary syndrome—exploration of association with PAX6 genotype. Ophthalmic Genet. 2022;43:340–3. https://doi.org/10.1080/13816810.2022.2025605
17. RzewuskaN, Jacek KunickiJ, Katarzyna PieniakK, et al. A systematic review on idiopathic intracranial hypertension comorbid with polycystic ovarian syndrome and its consequences.Eur J Obstet Gynecol Reprod Biol. 2024:292:1-7.doi: 10.1016/j.ejogrb.2023.11.005.
18. Sandhu JK, Singh S, Basu S. Severe meibomian gland loss in polycystic ovarian syndrome patients on estrogen-progesterone therapy: a case series. F100Res. 2024;12:1154. doi: 10.12688/f1000research.139229.2
19. Adıyeke SK, Karaca I, Yıldırım S, AdıyekeM,Uyar I, Türe G. Anterior segment findings in women with polycystic ovary syndrome. Turk J Ophthalmol. 2017;47:24–7. doi: 10.4274/tjo.73659
20. Puthiyedath R, Kakkanatt CVA, Mathai MT, Ramachandran L, Sunny A, Arun S. A comparative study on ocular manifestations in patients with polycystic ovary syndrome and healthy volunteers. Kerala J Ophthalmol. 2022;34:250-5.doi: 10.4103/kjo.kjo_111_21


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