Background: Polycystic ovary syndrome (PCOS) is a common endocrine disorder among women of reproductive age, characterised by menstrual irregularity, hyperandrogenism and polycystic ovarian morphology. Obesity and central adiposity are known to exacerbate hormonal and metabolic dysfunction in PCOS. Methods: A total of 140 women aged 18–45 years diagnosed with PCOS (according to Rotterdam criteria) were consecutively recruited. Demographic and clinical features (menstrual dysfunction, hirsutism, acne, alopecia) and anthropometrics (BMI, waist-hip ratio) were recorded. Fasting blood samples were obtained in early follicular phase and assayed for LH, FSH, LH/FSH ratio, total testosterone and SHBG. Participants were stratified into non-obese (BMI < 30 kg/m²; n = 90) and obese (BMI ≥ 30 kg/m²; n = 50) subgroups. Independent sample t-tests (or ANOVA) compared hormonal and anthropometric variables between subgroups; Pearson correlation coefficients assessed relationships between anthropometric and hormonal variables. P-value < 0.05 was considered statistically significant. Results: The cohort’s mean age was 27.0 ± 5.1 years, mean BMI 28.5 ± 5.4 kg/m², and mean waist-hip ratio 0.89 ± 0.07. In the obese subgroup, total testosterone was significantly higher (46.4 ± 12.2 vs 41.2 ± 11.9 ng/dL; p = 0.015) and SHBG significantly lower (33.8 ± 13.2 vs 40.9 ± 13.9 nmol/L; p = 0.005) compared to the non-obese subgroup. The LH/FSH ratio was significantly lower in the obese group (1.72 ± 0.65 vs 1.92 ± 0.73; p = 0.033). Correlation analyses showed BMI positively correlated with total testosterone (r = 0.31; p < 0.001) and negatively with SHBG (r = −0.28; p = 0.002) and LH/FSH ratio (r = −0.18; p = 0.034). Waist-hip ratio correlated positively with LH/FSH ratio (r = 0.22; p = 0.010) and total testosterone (r = 0.26; p = 0.003). Conclusions: In this tertiary-care PCOS cohort, increased adiposity — notably higher BMI and central fat distribution — was associated with greater androgen excess (higher total testosterone, lower SHBG) and a comparatively attenuated LH/FSH ratio in obese women.
Polycystic ovary syndrome (PCOS) is emerging as a major endocrine-metabolic disorder in women of reproductive age, presenting a complex interplay of reproductive, hormonal and metabolic disturbances.
Globally, PCOS affects an estimated 5 %–10 % of women of reproductive age, though prevalence may vary depending on diagnostic criteria and population studied [1]. Historically first described by Stein and Leventhal in 1935 in the context of amenorrhea, hirsutism and
polycystic ovaries, PCOS now is recognized as a heterogeneous syndrome with far-reaching implications beyond the ovary. The diagnosis of PCOS is fundamentally anchored in criteria such as the 2003/2004 Rotterdam consensus, which requires the presence of at least two of the three hallmarks: oligo-/anovulation, clinical/biochemical hyperandrogenism, and polycystic ovarian morphology on ultrasound, after excluding other etiologies [2]. Despite this shared framework, the clinical spectrum of PCOS remains vast ranging from menstrual irregularities, infertility and hyperandrogenic symptoms (hirsutism, acne, hair loss) to metabolic derangements such as insulin resistance, dyslipidemia, obesity and an elevated risk for type 2 diabetes and cardiovascular disease [1]. From a hormonal-pathophysiology viewpoint, PCOS is characterized by a disrupted gonadotropin axis, where luteinizing hormone (LH) is often elevated relative to follicle-stimulating hormone (FSH), contributing to excess androgen production, follicular arrest and anovulation [3]. Concurrently, hyperinsulinemia and insulin resistance amplify ovarian androgen synthesis, reduce sex-hormone binding globulin (SHBG) and promote further metabolic dysfunction. These hormonal disturbances underscore the dual reproductive-metabolic nature of PCOS [4].
Clinically, women with PCOS often present in youth or early adulthood with irregular menstrual cycles (oligomenorrhea or amenorrhea), weight gain or obesity, hirsutism, and features of metabolic syndrome. For example, a descriptive cross-sectional study in Nepal found that 86 % of PCOS patients presented with menstrual irregularity, and 83 % had LH/FSH ratio ≥ 2 [1]. Similarly, a Bangladeshi adolescent cohort reported 88 % with oligomenorrhea, nearly 70 % overweight/obese, 33.7
% with biochemical hyperandrogenism and 90.9 % with dyslipidemia [4]. Such data highlights not only the reproductive burden of PCOS but also the mounting metabolic risk that may accompany it early in the course of disease. In many tertiary-care settings and resource-limited contexts, the recognition of the full spectrum of PCOS is critical. Not only do these patients require evaluation for immediate reproductive concerns (infertility, menstrual dysfunction), but they also merit longitudinal surveillance for metabolic complications—insulin resistance, type 2 diabetes, cardiovascular disease and endometrial morbidity. For instance, in a Bangladeshi hospital-based study, PCOS patients exhibited varied
phenotypes with clear differences in hormonal and anthropometric profiles across phenotypic groups, underscoring the heterogeneity of this condition in real-world settings [2]. Accordingly, the present cross-sectional study in a tertiary-care hospital aimed to delineate the “clinical spectrum” (i.e., the presenting symptoms, anthropometric features, menstrual and hyperandrogenic signs) and to map the “hormonal profiles” (gonadotropins, androgens, LH/FSH ratio, SHBG, etc.) of women diagnosed with PCOS. Given the emerging burden of PCOS and its potential long-term sequelae, especially in younger women in diverse populations, it is imperative to characterize local epidemiological patterns. Such characterization aids in understanding the interplay of ethnicity, body-mass index (BMI), lifestyle factors and hormonal milieu and in identifying at-risk sub-groups for targeted prevention. Evidence suggests that higher BMI and hyperandrogenic phenotypes are linked to more deranged hormonal and metabolic profiles in PCOS [5].
To assess the clinical manifestations and hormonal profiles of women with polycystic ovarian syndrome in a tertiary care hospital.