Polyendocrine Metabolic Ovarian Syndrome (PMOS), previously known as Polycystic Ovary Syndrome (PCOS), is a common endocrine–metabolic disorder affecting adolescent girls and young women. The recent international consensus recommended the term PMOS as this better describes the multisystem endocrine-metabolic nature of the disorder, as opposed to PCOS which mainly points to ovarian morphology¹.Clinically, it is associated with menstrual irregularity, hyperandrogenic features, insulin resistance, metabolic disturbance and sometimes ovarian dysfunction, and diagnosis in adolescents can be difficult due to the overlap between the features of irregular cycles, acne and hormonal variation and normal pubertal maturation². Menstrual irregularity with clinical or biochemical hyperandrogenism is the most important feature of the clinical picture for diagnosis within this age group³.

Today, PMOS is known as a systemic disorder with complex interactions among the hypothalamic-pituitary-ovarian axis, insulin signaling, androgen production, adipose tissue function, inflammation and cardiovascular regulation⁴. Adolescents with PMOS may present with oligomenorrhea, acne, hirsutism, obesity, acanthosis nigricans, dyslipidemia, insulin resistance, and psychological stress, and these abnormalities may persist into adulthood with increased risk of metabolic syndrome, type 2 diabetes mellitus, hypertension, infertility, and cardiovascular disease⁵.

The burden of PMOS is all the more significant in Pakistan where the adolescent girls may not receive early diagnosis due to lack of awareness, social avoidance of talking about menstruation, inadequate access to specialist endocrinologist, and under recognition of metabolic risk in adolescent females⁶. In many local clinical scenarios, the management of menstrual irregularity may be symptomatic, and associated insulin resistance, central adiposity, dyslipidaemia, autonomic and neuroendocrine abnormalities remain under-assessed⁷. Other factors like dietary transition, reduced physical activity, and urban life style patterns, early weight gain and familial predisposition to diabetes further add to the clinical significance of PMOS in the Pakistani adolescent population⁸.

Adolescent endocrine care in the United States is now focused on early cardiometabolic screening, lifestyle and prevention-based care, multidisciplinary care, and long-term risk reduction in patients with PCOS/PMOS⁹. Current international guidelines advocate that all aspects of reproductive, metabolic, psychological and cardiometabolic characteristics be assessed in adolescents and young women with this condition¹⁰. Since the present study includes clinical data from Pakistan with academic contribution from the United States, it evaluates PMOS within both a South Asian risk profile and an internationally recognized clinical framework, allowing broader interpretation of adolescent cardiometabolic and neuroendocrine risk¹¹.

There is a growing concern about cardiovascular autonomic dysfunction in PMOS as the normal regulation of the cardiovascular system is dependent on balance between sympathetic and parasympathetic activity¹². While the sympathetic activity would accelerate heart rate, increase vascular tone and blood pressure, the parasympathetic activity would provide the vagal modulation and cardioprotective regulation. Heart rate variability is a non-invasive technique which can measure this balance, and decreases in HRV, decreases in parasympathetic and increases in sympathetic predominance may be markers of early cardiovascular dysregulation prior to the clinical detection of hypertension or structural cardiovascular disease¹³.

There are multiple mechanisms that can lead to autonomic dysfunction in adolescents with PMOS. Insulin resistance and compensatory hyperinsulinemia can increase sympathetic nervous system activity and worsen androgen excess¹⁴. Hyperandrogenemia may affect vascular tone, endothelial function, adipose tissue biology, and neuroendocrine signaling¹⁵. Central adiposity and chronic low-grade inflammation may further impair autonomic regulation and increase cardiometabolic risk, particularly in South Asian adolescents who may develop metabolic complications at lower body mass index thresholds compared with many Western populations¹⁶.

Neuroendocrine dysfunction is another key component to the pathophysiology of PMOS. Increased luteinizing hormone activity, elevated luteinizing hormone to follicle-stimulating hormone ratio, ovarian androgen excess, insulin resistance, and possible hypothalamic-pituitary-adrenal axis involvement may contribute to the clinical phenotype¹⁷. These perturbations can combine with metabolic and autonomic risk factors to generate a unique spectrum of reproductive, metabolic, cardiovascular and stress-axis dysfunction. This interaction is of significance given that adolescence is a vital age for prevention, counselling and long-term risk modification¹⁸.

Despite increasing global interest in PMOS, limited data are available regarding cardiovascular autonomic and neuroendocrine dysfunction in adolescents with PMOS, particularly in South Asian populations. Most existing studies have focused on menstrual irregularity, androgenic symptoms, obesity, metabolic disturbance, or fertility-related outcomes, while relatively few have evaluated heart rate variability, orthostatic cardiovascular response, resting autonomic tone, or the relationship between neuroendocrine markers and cardiovascular regulation¹⁹. Therefore, the present comparative study was conducted to assess cardiovascular autonomic and neuroendocrine dysfunction in adolescents with PMOS. The study compared affected adolescents with healthy age-matched controls to determine differences in autonomic regulation, sympathetic predominance, parasympathetic modulation, insulin resistance, and reproductive hormone profile. The findings may support early cardiometabolic screening, preventive intervention, and pre-anesthetic cardiovascular risk assessment in adolescents with PMOS²⁰.

Study Design and Duration

This comparative cross-sectional study aimed to assess cardiovascular autonomic and neuroendocrine dysfunction in adolescents diagnosed with Polyendocrine Metabolic Ovarian Syndrome (PMOS), previously referred to as Polycystic Ovary Syndrome (PCOS). The results of impacted teenagers were contrasted with healthy age-matched controls. The study was conducted over 21 months, from January 2024 to September 2025.

Study Setting

The research was carried out at Khawaja Muhammad Safdar Medical College in Sialkot, Pakistan, in conjunction with the Department of Internal Medicine at the University at Buffalo, New York, United States. Supplementary clinical data were obtained from Shahida Islam Teaching Hospital in Lodhran, Punjab, Pakistan.

Study Cohort and Sample Size

The research encompassed adolescent females aged 13 to 19 years. One hundred fifty volunteers were recruited and allocated into two equal groups. Group I comprised 75 adolescents diagnosed with PMOS, whereas Group II consisted of 75 healthy age-matched controls devoid of monthly irregularity, clinical hyperandrogenism, or other endocrine-metabolic disorders.

Sampling Technique

A non-probability consecutive sampling technique was used. Eligible adolescents presenting to the outpatient departments and affiliated clinical units during the study period were enrolled after assessment according to the study criteria.

Inclusion Criteria

Adolescent girls aged 13 to 19 years were included in the PMOS group if they had persistent menstrual irregularity along with clinical or biochemical evidence of hyperandrogenism after exclusion of other endocrine disorders. Healthy adolescents of similar age were included in the control group if they had regular menstrual cycles, no clinical signs of androgen excess, and no previous diagnosis of endocrine, metabolic, cardiovascular, or chronic systemic disease.

Exclusion Criteria

Participants were excluded if they had thyroid dysfunction, hyperprolactinemia, congenital adrenal hyperplasia, Cushing syndrome, diabetes mellitus, chronic kidney disease, chronic liver disease, congenital heart disease, arrhythmia, diagnosed hypertension, acute febrile illness, active infection, or psychiatric illness requiring medication. Participants using steroids, hormonal therapy, oral contraceptive pills, anti-androgen therapy, insulin-sensitizing drugs, or any medication affecting autonomic or endocrine function during the previous three months were also excluded.

Data Collection Procedure

Data were collected using a structured study proforma. Demographic data, age, address, socioeconomic factors, age at menarche, regularity of menstruation, duration of symptoms, presence of acne, hirsutism, weight gain, family history of diabetes and family history of PMOS were documented. All subjects were clinically examined by trained clinical personnel.

Anthropometric Assessment

The height was measured in centimetres using a stadiometer and the weight was measured in kilos using a calibrated weight scale. BMI was calculated as weight (in kg) divided by height (in m) squared. Waist circumference was measured at the level midway between the bottom of the rib cage and the hip. The hip circumference was measured at the widest part of the hip. Waist-to-hip ratio (WHR) was calculated as an indicator of central obesity.

Cardiovascular Assessment

BP was taken after a minimum of 5 minutes rest in a sitting position. A cuff of the correct size was used for all measurements. Both systolic and diastolic blood pressures were recorded and the average of the two taken for analysis. After adequate rest, the resting heart rate (RHR) was recorded in beats per minute (bpm).

Cardiovascular Autonomic Function Assessment.

Cardiovascular autonomic function was measured in a controlled environment under uniform conditions. Participants were asked to avoid caffeine, large meals and excessive physical activity before the test. The autonomic examination comprised resting heart rate, heart rate reaction to orthostatic changes, blood pressure response to orthostatic changes, deep breathing evaluation, and heart rate variability analysis. Heart rate variability served as a non-invasive indicator of autonomic control. The time-domain parameters comprised the standard deviation of normal-to-normal intervals and the root mean square of sequential differences. Frequency-domain characteristics encompassed low-frequency power, high-frequency power, and the ratio of low-frequency to high-frequency power. Decreased parasympathetic activity was evidenced by diminished high-frequency power and a lower root mean square of consecutive differences. An elevated low-frequency to high-frequency ratio indicated sympathetic predominance. Given that autonomic imbalance may affect perioperative haemodynamic responses, these parameters were also evaluated for their potential significance in pre-anesthetic cardiovascular risk assessment in adolescents with PMOS.

Orthostatic Response Assessment

For orthostatic assessment, heart rate and blood pressure were recorded in the supine position after rest and again after standing. The change in heart rate and blood pressure after standing was documented. A greater rise in heart rate or an abnormal blood pressure response was considered suggestive of altered autonomic cardiovascular control.

Neuroendocrine Assessment

Venous blood samples were obtained from all participants in the morning under aseptic conditions. Blood samples were examined for fasting blood glucose, fasting serum insulin, luteinizing hormone, follicle-stimulating hormone, total testosterone, thyroid-stimulating hormone, prolactin, and morning cortisol levels. The ratio of luteinizing hormone to follicle-stimulating hormone was computed. Insulin resistance was evaluated with the homeostatic model assessment of insulin resistance.

Biochemical Assessment

Fasting blood glucose and fasting insulin levels were evaluated to determine glucose metabolism and insulin resistance. The lipid profile, comprising total cholesterol, triglycerides, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol, was evaluated. The metrics were utilised to assess the metabolic profile of adolescents with PMOS and healthy controls.

Operational Definitions

PMOS was defined as persistent menstrual irregularity in adolescence with clinical or biochemical hyperandrogenism after exclusion of other endocrine disorders. Menstrual irregularity was defined as persistence of abnormal cycle length beyond expected pubertal maturation. Clinical hyperandrogenism was assessed by the presence of hirsutism, acne, or other androgenic features. Biochemical hyperandrogenism was assessed by raised serum total testosterone according to the laboratory reference range. Insulin resistance was assessed using HOMA-IR.

Data Management

All collected data were checked for completeness and accuracy before entry. Each participant was assigned a study code to maintain confidentiality. Data from the Pakistani centers and the collaborating United States department were compiled in a secure dataset for final statistical analysis. No personal identifying information was used during analysis.

Statistical Analysis

Data were analysed utilising SPSS version 27.0. Quantitative variables were presented as mean ± standard deviation or median with interquartile range, contingent upon data distribution. Qualitative factors were displayed as frequency and percentage. Independent-samples t-test was used for continuous variables with a normal distribution, and the Mann–Whitney U test was used for continuous variables with a non-normal distribution. For categorical variables, the chi-square test or Fisher's exact test was used. Correlation analysis was performed to assess the relationship between autonomic and neuroendocrine-metabolic indices. Statistically significant results were set at a p-value of <0.05.

Ethical Considerations

The project was approved by the relevant institutional ethical review committee before it was started. Parental/guardian informed consent was obtained and adolescent assent was obtained. All participants were informed of the study goal, confidentiality of information, and that they could withdraw from the study at any time without affecting their clinical treatment.

Baseline Clinical and Anthropometric Characteristics

There were 150 adolescent females in the study. A total of 75 adolescents were diagnosed with Polyendocrine Metabolic Ovarian Syndrome (PMOS), while 75 age-matched healthy adolescents were used as controls. There was no significant difference in the average age and age at menarche between the two groups. The adolescents with PMOS had significantly higher BMI, WC, and WHR than the healthy controls. The prevalence of clinical symptoms of androgen excess and metabolic disturbances was increased in the PMOS group. It was clear that menstrual irregularity, acne, hirsutism, acanthosis nigricans and family history of diabetes were significantly more common in teens with PMOS. Results show that the affected group had more adverse clinical and metabolic risk profile at baseline as shown in Table 1.

Table 1. Baseline clinical and anthropometric characteristics of study participants

Cardiovascular and Autonomic Function Parameters

Resting cardiovascular assessment showed that adolescents with PMOS had significantly higher resting heart rate, systolic blood pressure, diastolic blood pressure, and mean arterial pressure compared with controls. Although most participants did not meet criteria for established hypertension, the higher cardiovascular values in the PMOS group suggested early hemodynamic alteration.

Cardiovascular autonomic assessment demonstrated clear autonomic imbalance among adolescents with PMOS. The PMOS group had significantly lower SDNN, RMSSD, and high-frequency power, indicating reduced parasympathetic modulation. In contrast, low-frequency power and LF/HF ratio were significantly higher in the PMOS group, suggesting sympathetic predominance. Orthostatic testing also showed a greater rise in heart rate after standing among affected adolescents, as shown in Table 2.

Table 2. Cardiovascular and autonomic function parameters in both groups

The reduction in RMSSD and high-frequency power reflects lower vagal activity in adolescents with PMOS. The increased LF/HF ratio and greater orthostatic heart rate rise further support sympathetic dominance and impaired autonomic cardiovascular adaptation in the affected group.

Neuroendocrine and Metabolic Profile

Neuroendocrine assessment showed significantly higher luteinizing hormone, LH/FSH ratio, total testosterone, prolactin, and morning cortisol levels in adolescents with PMOS compared with controls. Follicle-stimulating hormone and thyroid-stimulating hormone levels were not significantly different between the two groups. These findings suggest hypothalamic-pituitary-ovarian axis disturbance with hyperandrogenemia in adolescents with PMOS.

Metabolic assessment showed significantly higher fasting blood glucose, fasting insulin, HOMA-IR, total cholesterol, triglycerides, and LDL-C in the PMOS group. HDL-C was significantly lower among adolescents with PMOS. These results indicate that the affected group had greater insulin resistance and a more adverse lipid profile compared with healthy controls, as shown in Table 3.

Table 3. Neuroendocrine and metabolic parameters in both groups

The PMOS group demonstrated a combined pattern of endocrine and metabolic dysfunction. Increased LH/FSH ratio and total testosterone confirmed androgen-related neuroendocrine abnormality, while elevated fasting insulin and HOMA-IR indicated significant insulin resistance. The presence of dyslipidemia further supports increased cardiometabolic risk in adolescents with PMOS.

Correlation of Autonomic Dysfunction With Neuroendocrine and Metabolic Markers

Correlation analysis was performed within the PMOS group to determine the relationship between autonomic dysfunction and endocrine-metabolic markers. HOMA-IR, fasting insulin, total testosterone, waist circumference, morning cortisol, and LH/FSH ratio showed positive correlations with LF/HF ratio. These variables also showed negative correlations with RMSSD.

The strongest positive correlation with LF/HF ratio was observed for HOMA-IR, followed by fasting insulin and waist circumference. These findings suggest that insulin resistance, central adiposity, androgen excess, and stress-axis activity were associated with sympathetic predominance and reduced parasympathetic modulation among adolescents with PMOS, as shown in Table 4.

Table 4. Correlation of autonomic parameters with neuroendocrine and metabolic variables in the PMOS group

The positive association of HOMA-IR, fasting insulin, and total testosterone with LF/HF ratio indicates that metabolic and androgenic dysfunction may contribute to sympathetic predominance. The negative relationship of these variables with RMSSD suggests that worsening endocrine-metabolic disturbance is associated with reduced parasympathetic activity. These findings support a linked pattern of autonomic, neuroendocrine, and metabolic dysfunction in adolescents with PMOS. Overall, adolescents with PMOS demonstrated significantly greater clinical, cardiovascular, autonomic, neuroendocrine, and metabolic abnormalities compared with healthy age-matched controls. The affected group had higher adiposity markers, increased resting heart rate, higher blood pressure, reduced parasympathetic heart rate variability, increased sympathetic predominance, insulin resistance, hyperandrogenemia, and dyslipidemia. These findings suggest that PMOS in adolescence is associated with early cardiovascular autonomic and neuroendocrine dysfunction, supporting the need for early cardiometabolic screening and preventive intervention.

The present comparative study demonstrated that adolescents with Polyendocrine Metabolic Ovarian Syndrome (PMOS) had significant clinical, cardiovascular autonomic, neuroendocrine, and metabolic abnormalities compared with healthy age-matched controls¹. Although both groups were comparable in age and age at menarche, the PMOS group showed higher body mass index, increased waist circumference, higher waist-to-hip ratio, and a greater frequency of acne, hirsutism, acanthosis nigricans, and family history of diabetes². These results indicate that PMOS in adolescence is not just a reproductive disorder, but also a systemic endocrine-metabolic disorder with early involvement in the cardiometabolic system³.

The key finding of this study was the change in the way the cardiovascular system was regulated in adolescents with PMOS⁴. PMOS group showed significantly elevated heart rate, SBP, DBP and MAP levels compared to controls⁵. While these tended to be within non-hypertensive limits, there was a trend towards higher cardiovascular values, which may be explained by greater sympathetic drive, decreased vagal modulation, insulin resistance, and the effect of central adiposity on vascular tone⁶.

Heart rate variability analysis further supported the presence of autonomic imbalance in adolescents with PMOS⁷. Significant decreases in SDNN, RMSSD and high frequency power were observed in the affected group, reflecting decreased parasympathetic activity⁸. Low-frequency power and LF/HF ratio, on the other hand, were significantly higher, indicating sympathetic predominance, which may be a precursor to overt hypertension, impaired glucose regulation and subsequent cardiovascular diseases⁹.

Adolescents with PMOS also had a higher increase in HR after standing, indicating poor autonomic adaptation to postural change. Usually, standing leads to a well-regulated autonomic response that helps to regulate blood pressure and blood flow to the brain. The exaggerated HRR in the PMOS group is suggestive of a diminished autonomic stability and sympathetic compensation, lending credence to the idea that autonomic dysfunction can already be seen in adolescence before clinically apparent cardiovascular disease occurs².

Neuroendocrine abnormalities were also prominent in the PMOS group¹³. Luteinizing hormone, LH/FSH ratio, total testosterone, prolactin and morning cortisol levels were significantly higher in adolescents with PMOS than in controls¹⁴. The elevated LH/FSH ratio and high levels of testosterone suggest hypothalamic-pituitary-ovarian axis dysfunction and hyperandrogenemia, which can lead to menstrual irregularity, acne, hirsutism, metabolic disturbance, and abnormal cardiovascular regulation¹⁵.

Insulin resistance was another important finding in this study¹⁶. The levels of fasting insulin and HOMA-IR were significantly elevated in the PMOS group of adolescents when compared to the control group¹⁷. Insulin resistance may increase ovarian androgen production, worsen hyperandrogenemia, and promote sympathetic nervous system activation, which may explain why adolescents with greater insulin resistance demonstrated stronger autonomic imbalance¹⁸.

Adolescents with PMOS also had a negative lipid profile result.¹⁹ The PMOS group had significantly higher levels of total cholesterol, triglycerides, and LDL-C, and significantly lower levels of HDL-C²⁰. This dyslipidemic pattern, together with an increased waist circumference, insulin resistance, elevated blood pressure and autonomic imbalance, appears to indicate that adolescents with PMOS may already be on a trajectory towards metabolic syndrome and cardiovascular disease in the future.

Correlation analysis confirmed the association of endocrine-metabolic dysfunction with autonomic dysfunction². HOMA-IR, fasting insulin, total testosterone, waist circumference, morning cortisol, and LH/FSH ratio were positively associated with LF/HF ratio and negatively associated with RMSSD¹⁶. These associations suggest that insulin resistance, androgen excess, central adiposity, and stress-axis activity may contribute to sympathetic predominance and reduced parasympathetic modulation⁸.

The inclusion of participants and academic input from Pakistan and the United States gives this study broader clinical relevance¹. Adolescent girls with menstrual irregularity and androgenic symptoms may present late in Pakistan due social hesitation, less awareness and less availability of specialized endocrine assessment³. By comparison, the focus of adolescent endocrine care in the United States is on early cardiometabolic screening, multidisciplinary assessment, life-style based prevention, and long-term risk reduction⁹.

The findings of this study have practical clinical implications¹⁴. Adolescents with PMOS should not be evaluated only for menstrual irregularity and cosmetic symptoms; routine assessment should also include body mass index, waist circumference, blood pressure, fasting glucose, fasting insulin, lipid profile, and androgen levels¹⁷. Heart rate variability and orthostatic response testing may be useful non-invasive tools where available, especially for identifying early autonomic dysfunction in high-risk adolescents⁷.

The autonomic and metabolic abnormalities found in adolescents with PMOS could have implications from an anesthesiology perspective for pre-anesthetic evaluation5. Lower parasympathetic activity and higher sympathetic activity, elevated resting heart rate, increased blood pressure, insulin resistance, and obesity could affect the perioperative hemodynamic responses and cardiovascular stability during anesthesia. Hence, a thorough pre-operative cardiovascular and metabolic evaluation could be useful for identifying patients who are at higher risk during the perioperative period and to plan anesthetic care accordingly4-7.

Early intervention is essential because adolescence provides an important opportunity for prevention¹⁰. Lifestyle modification, regular physical activity, weight optimization, dietary improvement, sleep regulation, and psychological support may help reduce insulin resistance and improve autonomic balance⁹. Early identification of affected adolescents may help prevent progression to adult metabolic syndrome, type 2 diabetes mellitus, hypertension, infertility, and cardiovascular disease⁶.

The relationship between hyperandrogenism and metabolic abnormality is particularly important in interpreting the present findings¹⁵. Increased androgen levels may worsen insulin resistance, promote central adiposity, alter lipid metabolism, and contribute to endothelial dysfunction¹⁸. In adolescents, this interaction may create a cycle in which androgen excess and metabolic disturbance reinforce each other, leading to greater cardiometabolic risk over time²⁰.

A systemic nature of PMOS may also be due to inflammation. Low grade inflammatory activity is associated with insulin resistance, adipose tissue dysfunction, endothelial changes and metabolic syndrome¹⁹. In the present study, the coexistence of central obesity, dyslipidemia, insulin resistance, and autonomic imbalance supports the possibility that inflammatory and metabolic pathways may jointly contribute to cardiovascular vulnerability in affected adolescents¹¹.

The current results are also in line with the hypothesis that PMOS can have heterogeneous phenotypes¹³. Some teens might have mainly hyperandrogenic and metabolic symptoms, while others might have more dominant neuroendocrine abnormalities¹⁶. This heterogeneity is clinically important because a single symptom-based approach may miss adolescents who already have cardiometabolic or autonomic risk despite variable reproductive manifestations¹.

The increased prevalence of diabetes in families in the PMOS group also provides evidence of inherited and familial metabolic susceptibility²⁰. There may be a genetic and familial influence that interacts with lifestyle factors, adiposity, insulin resistance and androgen excess, leading to earlier onset of metabolic dysfunction¹⁸. This is particularly relevant in adolescents because early identification of familial risk may allow preventive counseling before irreversible cardiometabolic complications develop⁶.

The diagnosis of PMOS in the adolescent may still be difficult due to the tendency of pubertal changes to mimic some of the features of the syndrome³. However, persistent menstrual irregularity combined with clinical or biochemical hyperandrogenism should prompt careful evaluation⁹. The results of this study reinforce the need to avoid both overdiagnosis and underdiagnosis, while ensuring that adolescents with true endocrine-metabolic dysfunction receive timely assessment and follow-up¹⁴.

The study also indicates the need to go beyond morphology of the ovary alone. The newer definition of PMOS focuses on the endocrine, metabolic, reproductive, psychological and cardiovascular aspects of the disease⁴. This more comprehensive approach is significant, as adolescents can initially come to a physician with menstrual or dermatologic issues, and the most important long-term consequences include insulin resistance, dyslipidemia, autonomic dysfunction and cardiovascular disease⁷.

There are certain limitations in this study. The design of the study is a cross-sectional study, which does not allow the causality of PMOS and autonomic dysfunction to be confirmed². Sample size is sufficient for comparison between groups but does not necessarily reflect the diversity of all adolescent populations in Pakistan and the United States³. Heart rate variability may be influenced by sleep, stress, physical activity, caffeine intake, and emotional state; therefore, future multicenter longitudinal studies are required to determine whether autonomic dysfunction predicts long-term cardiometabolic outcomes in adolescents with PMOS¹².

Overall, this study supports the concept that PMOS in adolescence is a multisystem disorder involving reproductive, metabolic, neuroendocrine, and cardiovascular autonomic pathways¹. Sympathetic predominance, decreased parasympathetic activity, insulin resistance, hyperandrogenemia, and dyslipidemia suggest that affected adolescents need to be evaluated comprehensively, in addition to symptom-based treatment, in the early stages⁹. The results encourage early detection, preventive advice and long-term monitoring and follow-up of cardiometabolic outcomes in adolescents with PMOS⁶.,

The cardiovascular autonomic and neuroendocrine function was significantly disordered in adolescents with Polyendocrine Metabolic Ovarian Syndrome. The affected group had greater adiposity markers, higher resting HR, higher blood pressure, lower P-HRV, higher sympathetic predominance, insulin resistance, higher blood insulin and hyperandrogenemia, altered gonadotropin profile, and dyslipidemia. The results show that although PMOS in adolescence is not restricted to menstrual and androgenic presentations, it is linked to early systemic cardiometabolic risk. Cardiovascular autonomic assessment, neuroendocrine evaluation, and metabolic screening might be of benefit in identifying high-risk adolescents earlier on. Early identification and preventive intervention is highly recommended. Weight control, regular exercise, diet advice and proper endocrine follow up could help to decrease the long-term risk of metabolic syndrome, type 2 diabetes mellitus, hypertension and cardiovascular disease in PMOS patients during adolescence.

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