Goodbye to 'polycystic ovary': it is now called PMOS, and they were never really cysts

Let's start from the beginning: where did the name come from?

The classic description of the syndrome dates back to 1935, when physicians Irving Stein and Michael Leventhal described women who presented with menstrual irregularities, infertility, and ovaries with a characteristic morphology. For decades, the term 'polycystic ovary syndrome' was used, and the name stuck for 91 years.

But over time we came to understand that the name had two major problems. First, we are not talking about true pathological ovarian cysts. And second, the disease is not limited to the ovary.

So, what do we actually see in the ovary?

To understand this, we first need to understand how a normal ovary works. Each month, multiple follicles begin to develop. A follicle is a small structure that contains an oocyte. Normally, one of these follicles becomes the dominant follicle, continues to grow, matures, and finally releases the oocyte. That is ovulation.

What happens in PMOS?

In many women with PMOS, follicular development does not normally follow this process. Numerous small antral follicles can accumulate which, on an ultrasound, appear as multiple small rounded structures. Historically, these were interpreted and popularised as 'cysts'.

But they are not the pathological cysts we imagine when we talk about, for example, a large functional cyst, an endometrioma, or a cystadenoma. They are follicles. This confusion was precisely one of the main reasons for changing the name: the international consensus expressly states that the term PCOS erroneously implied the existence of pathological ovarian cysts.

And here another fundamental point emerges.

You do not need to have 'polycystic' ovaries to have the syndrome. And having many follicles on an ultrasound does not automatically mean you have PMOS. This confusion has led, for decades, to incorrect diagnoses — women worried about 'cysts' who did not actually have a disease, and other women with genuine disease who could be underdiagnosed because their ultrasound did not look sufficiently 'polycystic'. That is why PMOS is so much more than an ultrasound.

So, what is PMOS really?

It is an endocrine, metabolic, ovarian, and reproductive syndrome, with manifestations that can vary enormously from one woman to another. It affects approximately 1 in 8 women of reproductive age, which amounts to more than 170 million women worldwide. And it is precisely that diversity that explains why, for so many years, it has been so difficult to understand.

What does 'polyendocrine' mean?

It means we are not talking exclusively about the ovary: different hormonal and metabolic systems are involved. These can include the ovaries, the hypothalamus, the pituitary gland, adipose tissue, the pancreas and insulin signalling, the adrenal glands, and hepatic metabolism. It does not mean that all of these organs are 'diseased', but rather that there is an altered hormonal and metabolic network.

The brain is also involved.

Our reproductive system is controlled by an extraordinarily complex axis. The hypothalamus produces a signal called GnRH, which acts on the pituitary gland, and the pituitary gland mainly produces LH and FSH. These hormones regulate follicular growth, hormonal production, and ovulation.

In PMOS, there may be alterations in the dynamics of this neuroendocrine axis, including — in many patients — an increased frequency of GnRH pulses and relative changes in the secretion of LH and FSH. But we must not turn this into yet another oversimplification along the lines of 'PMOS = high LH': that is not necessarily the case.

Now we come to a key player: insulin

Insulin is a hormone produced by the pancreas. Its best-known function is to help regulate glucose, but insulin does much more than that: it is also a metabolic, anabolic, and endocrine signal, and it can interact directly with the ovary.

What is insulin resistance?

Under normal circumstances, insulin sends a signal to certain tissues to facilitate the handling of nutrients and glucose. When insulin resistance is present, certain tissues respond less effectively, and the body attempts to compensate by producing more insulin. This can lead to hyperinsulinemia.

And what does insulin have to do with the ovaries?

A great deal. Insulin can enhance ovarian androgen production, particularly by acting on the theca cells. In addition, hyperinsulinemia can reduce the liver's production of SHBG, the sex hormone-binding globulin; when SHBG decreases, the biologically available fraction of androgens can increase.

We can therefore see a sequence like this: insulin resistance, hyperinsulinemia, a greater androgenic signal, and ultimately, disruption of follicular development and ovulation.

But here I need to make a very important clarification

PMOS does not automatically mean insulin resistance. Insulin resistance is a very important and common pathophysiological feature of the syndrome, but not all women with PMOS present to the same degree: there are slim, athletic women without diabetes and without obesity who can also have PMOS.

International guidelines recognize insulin resistance as an important pathophysiological factor, but they also note that the standard clinically available insulin tests have limitations and do not recommend routinely measuring insulin to diagnose the syndrome. Insulin is therefore part of the story — but it is not the whole story.

And this is precisely what the new name attempts to explain

We used to say 'polycystic ovary'. Now we say polyendocrine, metabolic, and ovarian. Three dimensions, much closer to the true nature of the disease.

Why do androgens increase?

In many patients, hyperandrogenism is present — that is, excessive activity of androgenic hormones. It may be biochemical, when it appears in laboratory tests, or clinical, when we observe its effects on the body.

And here the dermatologist has a great deal to say

Because some of the earliest manifestations of PMOS appear precisely in the skin and hair.

Acne

Androgens can stimulate the sebaceous glands, increase sebum production, and contribute to an environment favorable to the development of acne. What particularly catches our attention is persistent acne in an adult woman, mandibular acne, acne accompanied by menstrual irregularities, or acne associated with hirsutism or hair loss. But a word of caution: having acne does not mean having PMOS. Acne is extremely common and has many other causes.

Hirsutism

Excess androgenic signaling can transform certain fine hairs into thicker, more pigmented terminal hairs. These may appear especially on the upper lip, chin, jaw, chest, abdomen, and back. This is called hirsutism, and it is one of the most characteristic clinical manifestations of hyperandrogenism.

Hair loss

We may also find female-pattern alopecia. Hair can lose density especially in the central and upper region of the scalp, and the follicles sensitive to androgens may progressively miniaturize. But, once again, hair loss does not automatically mean PMOS: we must differentiate telogen effluvium, iron deficiency, thyroid disease, independent androgenetic alopecia, alopecia areata, inflammatory conditions, cicatricial alopecias, certain medications, and many other causes.

And what about dark patches?

There is another particularly interesting dermatological manifestation: acanthosis nigricans. It appears as darker, thickened, velvety skin, especially on the neck, armpits, groin, and skin folds. It can be a clinical sign of hyperinsulinemia and insulin resistance. Not all patients with PMOS have it, but when it is present it can be an important metabolic clue.

And what about rosacea?

Here I want to correct a common misconception. Although a woman with PMOS may have rosacea, we do not currently consider rosacea a classic diagnostic manifestation of the syndrome. It may coexist, but we should not place it on the same level as hirsutism, acne, ovulatory disturbances, or hyperandrogenism.

Why is ovulation disrupted?

Because the follicle requires a very precise hormonal sequence in order to grow, be selected, mature, and ovulate. When androgenic, neuroendocrine, or metabolic disturbances are present, that process can be interrupted. This is when oligoovulation or anovulation occurs.

What does the patient notice?

She may present with irregular periods, very long cycles, absence of menstruation, infrequent ovulation, or difficulty becoming pregnant. However, some women with PMOS may have cycles that appear relatively regular. That is why, once again, no single symptom in isolation defines the entire syndrome.

Does PMOS mean infertility?

No, and this is very important. Many women with PMOS become pregnant spontaneously. Others may need help to restore ovulation or to induce it. PMOS is an important cause of anovulatory infertility, but PMOS does not mean sterility.

And what about weight?

Another major source of stigma. For years, many women have been told: 'Lose weight and it will sort itself out.' That is an unfair and medically incomplete oversimplification. Excess adiposity can worsen insulin resistance, increase hiperinsulinemia, alter hormonal production, and aggravate certain manifestations. But obesity does not cause PMOS on its own, and there are women with PMOS who have a normal weight. The relationship is bidirectional and complex.

So why do we talk about 'metabolic'?

Because women with PMOS have a higher risk of conditions such as glucose intolerance, type 2 diabetes, dyslipidemia, hypertension, obstructive sleep apnea, and other cardiometabolic risk factors. International guidelines specifically emphasize that the evaluation should not be limited to menstruation and fertility, but should also incorporate metabolic, cardiovascular, dermatological, psychological, and sleep health.

The liver matters too

Insulin resistance and metabolic alterations can be associated with metabolic steatotic liver disease. This does not mean that every woman with PMOS has fatty liver disease, but it forms part of the metabolic context that we must assess when risk factors are present.

And we must also talk about the endometrium

When a woman goes through long periods without ovulating, she does not produce progesterone in the normal cyclical way, and the endometrium may remain exposed for prolonged periods to oestrogenic stimulation without adequate opposition. This increases the risk of endometrial hyperplasia and also of endometrial cancer. International guidelines acknowledge an increased risk, while noting that the absolute risk remains low. That is why we must not normalize months and months without menstruation.

And PMOS also affects psychological health

This dimension was overlooked for far too long. Women with the syndrome show a higher prevalence of anxiety, depression, body image disturbances, eating disorders, and impaired quality of life. International guidelines recommend actively evaluating symptoms of anxiety and depression. And this also explains why changing the name matters: a disease is not just an ultrasound scan — it affects a whole person.

So, how do we diagnose PMOS?

During the transition period you will still constantly encounter PCOS, PCO, and 'polycystic ovary syndrome.' The new term PMOS will be incorporated progressively and is expected to become fully part of the 2028 update of the international guidelines. The name change does not mean that we have suddenly invented a new disease: it is the same clinical entity, better understood and better named.

Diagnosis is not made with an ultrasound scan alone

In adult women, evaluation is based on characteristics such as ovulatory dysfunction, clinical or biochemical hyperandrogenism, and characteristic ovarian morphology, after excluding other conditions that may produce a similar picture. In certain current contexts, anti-Müllerian hormone (AMH) may also be used as an alternative to ultrasound to define ovarian morphology in adult women, but it should not be used as a standalone test to diagnose PMOS.

What must we rule out?

Because not every case of hyperandrogenism is PMOS. Depending on the case, we may need to exclude thyroid disease, hyperprolactinemia, non-classic congenital adrenal hyperplasia, Cushing's syndrome, androgen-secreting tumors, certain medications, and other endocrine disorders. Especially when symptoms appear very rapidly or significant virilization is present, we must look for other causes.

Which tests can be useful?

It depends entirely on the patient. We may evaluate total testosterone, calculated free testosterone or free androgen indices, SHBG, DHEAS, and, depending on the context, androstenedione. TSH, prolactin, 17-hydroxyprogesterone, blood glucose, HbA1c, lipid profile, and other parameters may also be assessed according to symptoms. Metabolic evaluation is essential. But we do not need to order fifty hormones for every woman: a good set of labs is one that answers a clinical question.

What about insulin and HOMA?

Here we must be especially careful. It can be tempting to reduce PMOS to 'your HOMA is high,' but international recommendations are clear: insulin resistance has pathophysiological importance, although available insulin measurements have limited clinical utility and are not routinely recommended for diagnosing or managing PMOS. This does not mean insulin does not matter; it means we should not confuse pathophysiology with a perfect diagnostic test.

How is PMOS treated?

Here comes another consequence of the new name: there is no single treatment, because there is no single manifestation. We treat the woman, not simply 'the polycystic ovary.'

When metabolic dysfunction predominates

Lifestyle is a fundamental part of treatment: physical activity, good-quality nutrition, sleep, maintaining or improving body composition when necessary, reducing sedentary behavior, and preventing excessive weight gain. But this must be done without stigmatizing: a slender woman with PMOS also needs physical activity, healthy eating, and metabolic follow-up.

Metformin?

Metformin can be useful particularly for certain metabolic goals and in selected patients. It can improve insulin sensitivity, certain metabolic parameters, and, in some women, contribute to improving menstrual regularity. However, not all women with PMOS need metformin: the indication depends on phenotype, metabolic risk, BMI, tolerability, reproductive goals, and individual circumstances.

What about contraceptives?

Combined hormonal contraceptives can be used in certain women to regulate cycles, control hyperandrogenism, improve acne and hirsutism, and protect the endometrium. But, again, they are not 'the treatment for PMOS': they are a tool for specific objectives.

What about hirsutism?

We can combine different strategies: hormonal treatment, antiandrogens in selected situations with appropriate contraception, laser, and cosmetic treatments. Antiandrogens require special caution due to the fetal risk if pregnancy occurs.

What about acne?

It is treated as acne, but if there is a significant hormonal component we must also address the endocrine context. Depending on severity, we can use topical treatments, retinoids, antibiotics when indicated, hormonal treatment, and isotretinoin in selected situations.

What about hair loss?

First, diagnosis. Because a woman with PMOS can also have iron deficiency, telogen effluvium, alopecia areata, thyroid problems, or cicatricial alopecia. If female-pattern alopecia is present, we can use strategies such as minoxidil and, in selected cases, antiandrogen treatment. But we must never assume that all hair loss in PMOS is 'the hormones'.

What if the woman wants to become pregnant?

Then our objective changes completely: we want to achieve ovulation, optimise metabolic health, prepare for pregnancy, and minimise risks. Currently, letrozol is the first-line pharmacological treatment for inducing ovulation in many women with PMOS and anovulation without other significant infertility factors.

A woman can present different 'faces' of the same syndrome

One patient may consult primarily for infertility; another for acne; another for hirsutism; another for hair loss; another for irregular cycles; another because she develops metabolic alterations; and another may present several things simultaneously. This explains why the old name was so inadequate.

There is no 'typical woman with PMOS'

She may be slim or overweight; have very irregular or relatively regular cycles; have acne or not; have hirsutism or not; have significant insulin resistance or much more subtle metabolic alterations. That is why we speak of a syndrome, not of a single disease that is identical in every person.

Why change the name after 91 years?

Because words matter. The name 'polycystic ovary' led patients to think 'I have cysts on my ovaries', and all too easily led the healthcare system to think 'this is a gynaecological problem'. But PMOS may require the involvement of gynaecology, endocrinology, internal medicine, dermatology, nutrition, reproductive medicine, and mental health. That is precisely what multisystemic disease means.

And the name change was not decided overnight

The international process took years and involved patients, physicians, researchers, scientific societies, and patient organizations. The consensus published in The Lancet involved 56 international organizations and 14,360 formal responses from affected individuals and healthcare professionals from different regions of the world. Delphi processes, workshops, and implementation analyses were used before arriving at the term Polyendocrine Metabolic Ovarian Syndrome.

That is why PMOS is not simply a marketing change

The goal is that when a physician hears PMOS, they immediately think endocrine, metabolic, and ovarian — and not just 'cysts.'

What I want you to remember

For 91 years we spoke of polycystic ovary syndrome, but the famous 'cysts' are not true pathological cysts: they are fundamentally follicles. And the condition was never solely ovarian. In 2026, a broad international consensus adopted a new name: PMOS, Polyendocrine Metabolic Ovarian Syndrome.

Insulin can play a fundamental role. Androgens can cause acne, hirsutism, and hair loss. Ovulatory dysfunction can lead to irregular cycles and reproductive difficulty. And the metabolic component can increase the risk of type 2 diabetes, lipid abnormalities, and other cardiometabolic problems. But none of these features is necessarily present in every woman.

I am Dr. Florian Vallecillo, and if there is one single idea I want to leave you with today, it is this: they were never simply cysts, and it was never simply a disease of the ovaries. The ovary is one part of a much broader network in which the brain, hormones, metabolism, insulin, adipose tissue, skin, hair, and the reproductive system all interact. That is why shifting from PCOS to PMOS is not simply a matter of changing four letters, but of leaving behind an overly narrow view of a condition that affects approximately one in eight women. The name changes, and so does the way we understand the disease — because when we understand a disease better, we can also diagnose it earlier, explain it more clearly, and treat the person in a far more complete way.