Behind the Renaming of PCOS to PMOS: A Common Hormonal Disorder Being Redefined as a Systemic Disease
For a long time, Polycystic Ovary Syndrome has been commonly understood by the public as a gynecological issue primarily affecting menstruation and fertility. However, the latest medical reviews indicate that this understanding is changing. Growing evidence shows that what was traditionally called PCOS is not just an ovarian disease, but a systemic condition involving reproduction, endocrinology, metabolism, cardiovascular risk, and mental health. To more accurately reflect the nature of the disease, the international academic community has proposed in recent years to rename it PMOS, or Polyendocrine Metabolic Ovarian Syndrome.
Recently, a comprehensive review published in the *Journal of Clinical Investigation* systematically summarized the diagnostic criteria, pathogenesis, long-term health impacts, and future treatment trends of PCOS/PMOS. The article points out that PCOS/PMOS is one of the most common endocrine disorders among women of reproductive age. Depending on the diagnostic criteria used, the global prevalence rate in women is estimated to be approximately 5% to 20%. However, due to its complex symptoms, highly variable presentations, and long-standing lack of unified diagnostic criteria, many patients may remain unidentified for extended periods or receive treatment only for a single symptom.
In the past, PCOS was widely regarded as a "fertility problem," mainly associated with irregular menstrual cycles, ovulatory dysfunction, and polycystic ovarian morphology. Many patients were diagnosed only during evaluations for difficulty conceiving or infertility. However, modern clinical research shows that the core of this disease is not limited to the ovaries but is related to multiple mechanisms, including elevated androgens, insulin resistance, neuroendocrine abnormalities, genetic susceptibility, environmental factors, and inflammatory states. In other words, the ovarian manifestation is just one part of the disease's presentation, behind which lies an imbalance in the systemic endocrine and metabolic network.
This is also a key reason why the name PMOS has garnered attention. PMOS stands for Polyendocrine Metabolic Ovarian Syndrome. Compared to "Polycystic Ovary Syndrome," this name de-emphasizes the central role of "ovarian cystic changes" in diagnosis, highlighting that the disease involves multiple endocrine organs and metabolic systems. Researchers point out that pathological ovarian cysts are not a necessary condition for diagnosing the disease; focusing the disease name on "polycystic ovaries" can easily lead to cognitive biases among the public and clinicians.
According to the 2023 International Evidence-Based Guideline, the diagnosis of adult PCOS/PMOS still recommends using the Rotterdam criteria. After excluding other hormonal diseases, patients must meet two of three main features: ovulatory dysfunction, clinical or biochemical hyperandrogenism, and ultrasound indicating polycystic ovarian morphology. Ovulatory dysfunction often manifests as menstrual cycles that are too short, too long, or irregular. Hyperandrogenism can include hirsutism, acne, alopecia, or laboratory tests indicating elevated androgens like testosterone. Polycystic ovarian morphology requires assessment via standardized ultrasound.
With advancements in diagnostic technology, researchers are also exploring more objective and convenient assessment methods. The review mentions that highly sensitive detection techniques like liquid chromatography-tandem mass spectrometry can be used for more accurate measurement of total testosterone; high-frequency transvaginal ultrasound can be used to assess antral follicle count; and anti-Müllerian hormone levels are also being studied as one of the surrogate markers for polycystic ovarian morphology. Some studies show that in women aged 23 to 35, an AMH level above 3.2 ng/mL can serve as a potential surrogate marker for assessing polycystic ovarian morphology, with a sensitivity of 88.6% and specificity of 80.3%. However, researchers emphasize that AMH cannot be used alone to diagnose PCOS/PMOS.
The complexity of PMOS is also reflected in its high heterogeneity. Different patients may present with different predominant symptoms: some primarily experience menstrual irregularities and infertility, others mainly have acne, hirsutism, and alopecia, while still others more prominently exhibit insulin resistance, obesity, dyslipidemia, or diabetes risk. The review points out that different phenotypes may correspond to different metabolic risks. Patients with concurrent hyperandrogenism, ovulatory dysfunction, and polycystic ovarian morphology often face a higher risk of insulin resistance, metabolic syndrome, and dyslipidemia; whereas patients presenting only with ovulatory dysfunction and polycystic ovarian morphology have relatively milder metabolic risks.
From a pathogenesis perspective, PMOS is not a disease caused by a single factor. The review summarizes that genetic, epigenetic, environmental, metabolic, and neuroendocrine factors may all contribute to the disease's onset. Research shows that PMOS has a strong genetic predisposition; a significant proportion of daughters born to mothers with PMOS will eventually be diagnosed with the condition themselves. Genome-wide association studies have identified multiple gene loci associated with PMOS, many of which are related to insulin signaling, sex hormone function, and metabolic regulation.
The mutual reinforcement between insulin resistance and hyperandrogenism is a key link in the pathogenesis of PMOS. A hyperinsulinemic state can lower sex hormone-binding globulin levels, increasing free androgens. Simultaneously, insulin can directly act on ovarian theca cells, promoting androgen production. Elevated androgens can further disrupt follicular development, leading to ovulatory dysfunction and menstrual abnormalities. Obesity, insulin resistance, and metabolic stress can exacerbate this cycle, but not all PMOS patients have obesity or insulin resistance, which also explains why the disease presentation varies so significantly.
Besides metabolic factors, neuroendocrine abnormalities are receiving increasing attention. The review notes that abnormal gonadotropin-releasing hormone pulsatility is common in PMOS patients, subsequently affecting the ratio of luteinizing hormone to follicle-stimulating hormone and driving excessive ovarian androgen production. Some studies also suggest that GABA, kisspeptin, neurokinin B, dynorphin, and AMH-related signaling pathways may be involved in the disease's pathogenesis. These mechanisms also provide direction for developing more precise therapeutic targets in the future.
The long-term health impacts of PMOS are equally significant and cannot be ignored. Besides infertility and menstrual abnormalities, patients may face an increased risk of insulin resistance, type 2 diabetes, dyslipidemia, hypertension, and cardiovascular disease. At the same time, depression, anxiety, eating disorders, and body image concerns are also more common in PMOS patients and can significantly affect quality of life. For this reason, viewing PMOS merely as a "gynecological disease" or a "fertility issue" easily underestimates its value for lifelong health management.
In terms of treatment, current clinical practice still primarily focuses on symptom management. Combined hormonal contraceptives are commonly used to improve menstrual irregularities, acne, and hirsutism; lifestyle interventions and metformin can be used to improve weight and insulin resistance; for patients with fertility needs and ovulatory dysfunction, letrozole is increasingly recommended by guidelines as a first-line ovulation induction agent. The review mentions that compared to traditional clomiphene citrate, letrozole can lead to higher live birth rates in ovulation induction therapy.
At the same time, new therapeutic directions are being explored. Drugs such as neurokinin 3 receptor antagonists, GLP-1 receptor agonists, and multi-agonists are showing potential for improving hyperandrogenic states, metabolic abnormalities, and reproductive features. Some drug repurposing studies also suggest that artemisinin-related compounds may improve hyperandrogenism, menstrual cycle abnormalities, and reduced fertility in animal models by affecting ovarian androgen synthesis. However, many new therapies are still in early or preclinical stages, and safety needs to be evaluated more cautiously, especially for populations involving pregnancy planning and gestation.
The review suggests that the key to future PMOS management will shift from a "one-size-fits-all" treatment approach to precise phenotyping and individualized intervention. With the advancement of technologies like machine learning, genetics, multi-omics, and organ-on-a-chip, clinicians may in the future be able to identify high-risk individuals earlier, more accurately distinguish between reproductive, metabolic, or mixed phenotypes, and develop personalized treatment plans based on different risk trajectories.
For patients, the change in the PMOS name and diagnostic/treatment concepts is not merely a simple term substitution. It signals that the healthcare system needs to view this disease more comprehensively. Irregular menstruation, acne, hirsutism, infertility, weight changes, abnormal blood glucose, and emotional issues may not be isolated symptoms but rather manifestations of the same systemic endocrine-metabolic disease at different stages and in different systems.
Overall, PMOS redefines the clinical boundaries of traditional PCOS. It reminds the public and physicians that common hormonal disorders in women should not only revolve around ovarian imaging or fertility needs but should incorporate long-term metabolic risk, mental health, cardiovascular risk, and individualized management. With the continuous advancement of diagnostic technologies and targeted therapies, PMOS management is expected to gradually shift from passively treating symptoms to early screening, early intervention, and lifelong health management.
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Published 2026-06-29
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News | Behind the Renaming of PCOS to PMOS: A Common Hormonal Disorder Is Being Redefined as a Systemic Disease
Behind the Renaming of PCOS to PMOS: A Common Hormonal Disorder Being Redefined as a Systemic Disease
For a long time, Polycystic Ovary Syndrome has been commonly understood by the public as a gynecological issue primarily affecting menstruation and fertility. However, the latest medical reviews indicate that this understanding is changing. Growing evidence shows that what was traditionally called PCOS is not just an ovarian disease, but a systemic condition involving reproduction, endocrinology, metabolism, cardiovascular risk, and mental health. To more accurately reflect the nature of the disease, the international academic community has proposed in recent years to rename it PMOS, or Polyendocrine Metabolic Ovarian Syndrome.
Recently, a comprehensive review published in the *Journal of Clinical Investigation* systematically summarized the diagnostic criteria, pathogenesis, long-term health impacts, and future treatment trends of PCOS/PMOS. The article points out that PCOS/PMOS is one of the most common endocrine disorders among women of reproductive age. Depending on the diagnostic criteria used, the global prevalence rate in women is estimated to be approximately 5% to 20%. However, due to its complex symptoms, highly variable presentations, and long-standing lack of unified diagnostic criteria, many patients may remain unidentified for extended periods or receive treatment only for a single symptom.
In the past, PCOS was widely regarded as a "fertility problem," mainly associated with irregular menstrual cycles, ovulatory dysfunction, and polycystic ovarian morphology. Many patients were diagnosed only during evaluations for difficulty conceiving or infertility. However, modern clinical research shows that the core of this disease is not limited to the ovaries but is related to multiple mechanisms, including elevated androgens, insulin resistance, neuroendocrine abnormalities, genetic susceptibility, environmental factors, and inflammatory states. In other words, the ovarian manifestation is just one part of the disease's presentation, behind which lies an imbalance in the systemic endocrine and metabolic network.
This is also a key reason why the name PMOS has garnered attention. PMOS stands for Polyendocrine Metabolic Ovarian Syndrome. Compared to "Polycystic Ovary Syndrome," this name de-emphasizes the central role of "ovarian cystic changes" in diagnosis, highlighting that the disease involves multiple endocrine organs and metabolic systems. Researchers point out that pathological ovarian cysts are not a necessary condition for diagnosing the disease; focusing the disease name on "polycystic ovaries" can easily lead to cognitive biases among the public and clinicians.
According to the 2023 International Evidence-Based Guideline, the diagnosis of adult PCOS/PMOS still recommends using the Rotterdam criteria. After excluding other hormonal diseases, patients must meet two of three main features: ovulatory dysfunction, clinical or biochemical hyperandrogenism, and ultrasound indicating polycystic ovarian morphology. Ovulatory dysfunction often manifests as menstrual cycles that are too short, too long, or irregular. Hyperandrogenism can include hirsutism, acne, alopecia, or laboratory tests indicating elevated androgens like testosterone. Polycystic ovarian morphology requires assessment via standardized ultrasound.
With advancements in diagnostic technology, researchers are also exploring more objective and convenient assessment methods. The review mentions that highly sensitive detection techniques like liquid chromatography-tandem mass spectrometry can be used for more accurate measurement of total testosterone; high-frequency transvaginal ultrasound can be used to assess antral follicle count; and anti-Müllerian hormone levels are also being studied as one of the surrogate markers for polycystic ovarian morphology. Some studies show that in women aged 23 to 35, an AMH level above 3.2 ng/mL can serve as a potential surrogate marker for assessing polycystic ovarian morphology, with a sensitivity of 88.6% and specificity of 80.3%. However, researchers emphasize that AMH cannot be used alone to diagnose PCOS/PMOS.
The complexity of PMOS is also reflected in its high heterogeneity. Different patients may present with different predominant symptoms: some primarily experience menstrual irregularities and infertility, others mainly have acne, hirsutism, and alopecia, while still others more prominently exhibit insulin resistance, obesity, dyslipidemia, or diabetes risk. The review points out that different phenotypes may correspond to different metabolic risks. Patients with concurrent hyperandrogenism, ovulatory dysfunction, and polycystic ovarian morphology often face a higher risk of insulin resistance, metabolic syndrome, and dyslipidemia; whereas patients presenting only with ovulatory dysfunction and polycystic ovarian morphology have relatively milder metabolic risks.
From a pathogenesis perspective, PMOS is not a disease caused by a single factor. The review summarizes that genetic, epigenetic, environmental, metabolic, and neuroendocrine factors may all contribute to the disease's onset. Research shows that PMOS has a strong genetic predisposition; a significant proportion of daughters born to mothers with PMOS will eventually be diagnosed with the condition themselves. Genome-wide association studies have identified multiple gene loci associated with PMOS, many of which are related to insulin signaling, sex hormone function, and metabolic regulation.
The mutual reinforcement between insulin resistance and hyperandrogenism is a key link in the pathogenesis of PMOS. A hyperinsulinemic state can lower sex hormone-binding globulin levels, increasing free androgens. Simultaneously, insulin can directly act on ovarian theca cells, promoting androgen production. Elevated androgens can further disrupt follicular development, leading to ovulatory dysfunction and menstrual abnormalities. Obesity, insulin resistance, and metabolic stress can exacerbate this cycle, but not all PMOS patients have obesity or insulin resistance, which also explains why the disease presentation varies so significantly.
Besides metabolic factors, neuroendocrine abnormalities are receiving increasing attention. The review notes that abnormal gonadotropin-releasing hormone pulsatility is common in PMOS patients, subsequently affecting the ratio of luteinizing hormone to follicle-stimulating hormone and driving excessive ovarian androgen production. Some studies also suggest that GABA, kisspeptin, neurokinin B, dynorphin, and AMH-related signaling pathways may be involved in the disease's pathogenesis. These mechanisms also provide direction for developing more precise therapeutic targets in the future.
The long-term health impacts of PMOS are equally significant and cannot be ignored. Besides infertility and menstrual abnormalities, patients may face an increased risk of insulin resistance, type 2 diabetes, dyslipidemia, hypertension, and cardiovascular disease. At the same time, depression, anxiety, eating disorders, and body image concerns are also more common in PMOS patients and can significantly affect quality of life. For this reason, viewing PMOS merely as a "gynecological disease" or a "fertility issue" easily underestimates its value for lifelong health management.
In terms of treatment, current clinical practice still primarily focuses on symptom management. Combined hormonal contraceptives are commonly used to improve menstrual irregularities, acne, and hirsutism; lifestyle interventions and metformin can be used to improve weight and insulin resistance; for patients with fertility needs and ovulatory dysfunction, letrozole is increasingly recommended by guidelines as a first-line ovulation induction agent. The review mentions that compared to traditional clomiphene citrate, letrozole can lead to higher live birth rates in ovulation induction therapy.
At the same time, new therapeutic directions are being explored. Drugs such as neurokinin 3 receptor antagonists, GLP-1 receptor agonists, and multi-agonists are showing potential for improving hyperandrogenic states, metabolic abnormalities, and reproductive features. Some drug repurposing studies also suggest that artemisinin-related compounds may improve hyperandrogenism, menstrual cycle abnormalities, and reduced fertility in animal models by affecting ovarian androgen synthesis. However, many new therapies are still in early or preclinical stages, and safety needs to be evaluated more cautiously, especially for populations involving pregnancy planning and gestation.
The review suggests that the key to future PMOS management will shift from a "one-size-fits-all" treatment approach to precise phenotyping and individualized intervention. With the advancement of technologies like machine learning, genetics, multi-omics, and organ-on-a-chip, clinicians may in the future be able to identify high-risk individuals earlier, more accurately distinguish between reproductive, metabolic, or mixed phenotypes, and develop personalized treatment plans based on different risk trajectories.
For patients, the change in the PMOS name and diagnostic/treatment concepts is not merely a simple term substitution. It signals that the healthcare system needs to view this disease more comprehensively. Irregular menstruation, acne, hirsutism, infertility, weight changes, abnormal blood glucose, and emotional issues may not be isolated symptoms but rather manifestations of the same systemic endocrine-metabolic disease at different stages and in different systems.
Overall, PMOS redefines the clinical boundaries of traditional PCOS. It reminds the public and physicians that common hormonal disorders in women should not only revolve around ovarian imaging or fertility needs but should incorporate long-term metabolic risk, mental health, cardiovascular risk, and individualized management. With the continuous advancement of diagnostic technologies and targeted therapies, PMOS management is expected to gradually shift from passively treating symptoms to early screening, early intervention, and lifelong health management.
Story Source:
Online Collection