Polycystic Ovary Syndrome (PCOS) is one of the most common endocrine disorders affecting women of reproductive age group, with an estimated prevalence ranging between 5% and 21% globally1. In India the prevalence of PCOS has increased ranging from 3.7% to 22.5%.2  PCOS manifests as a spectrum of symptoms including amenorrhoea/oligomenorrhea, anovulation, hirsutism, infertility, weight gain or obesity, acne vulgaris and androgenic alopecia 3, The pathophysiology of PCOS is multifactorial and involves complex interactions between genetic, environmental and hormonal factors 4

The most common criteria employed for the diagnosis of Rotterdam Criteria5 which includes 1) Oligo-/anovulation + clinical or biochemical hyperandrogenemia + Polycystic ovaries on ultrasound, 2) Polycystic ovaries on ultrasound + Oligo-/anovulation, 3) clinical or biochemical hyperandrogenism + Oligo-/anovulation, and 4) Polycystic ovaries on ultrasound + clinical or biochemical hyperandrogenism.6

Biochemical alterations are central to the diagnosis and management of PCOS. Women with PCOS often exhibit elevated levels of Luteinizing hormone (LH) and Prolactin, reduced Follicle-Stimulating Hormone (FSH) ratios, hyperandrogenemia which is result of increased testosterone.7

Comparatively, women without PCOS generally demonstrate stable hormonal profiles, making the study of these biochemical differences pivotal in understanding the disease's underlying mechanisms and its systemic implications. Identifying these variations can aid in the development of targeted therapeutic strategies to mitigate the reproductive complications of PCOS.8

This study aims to analyze and compare the biochemical parameters in women with and without PCOS, focusing on hormonal profiles. The findings will contribute to a more comprehensive understanding of the biochemical changes associated with PCOS and their clinical relevance.

This study was conducted over a period of 8 months after approval of Ethical Committee. The cross sectional observational study was conducted in Department of Obstetrics and  Gynaecology (Zanana Hospital), J.L.N Medical College and Attached Group of Hospitals, Ajmer, India. The sample size was calculated using formula n = Z2 x P x Q /E2 resulting in sample size of 120. Participants were recruited based on predefined inclusion and exclusion criteria. Written informed consent was obtained from all the participants before inclusion in the study. Study population was divided into groups of 2; Group 1 consisted of 60 women diagnosed with Polycystic Ovary Syndrome (PCOS) as per the Rotterdam Criteria, Group 2 included 60 women without PCOS.

General demographic data was collected using a standardized questionnaire. All blood samples were drawn under aseptic precautions on day 3-7 of menstrual cycle to minimize the hormonal fluctuations. Follicle stimulating hormone (FSH) and Luteinizing hormone (LH) were measured using Maglumi chemiluminescent immunoassay analyzer. Prolactin and Testosterone were assessed using Beckman Coulter Access 2 immunoassay system.

Inclusion Criteria: The study included female participants, aged between 18-40 years. Participants diagnosed with PCOS as per the Rotterdam criteria. Participants not diagnosed with PCOS exhibiting normal menstrual cycles, no signs of hyperandrogenism and normal ovarian morphology on ultrasound.

Exclusion Criteria: Participants above the age of 40 years were excluded, as were those currently taking medication for any psychiatric or medical illness. In addition to this, participants diagnosed with gynecological conditions other than PCOS or those undergoing any form of fertility treatment were not included in the study

Statistical Analysis: Data were organized using Microsoft Excel and analyzed using SPSS version 24.0 (IBM Corp., USA). The Kolmogorov-Smirnov test was applied to assess data normality and guiding the choice of statistical tests. Descriptive statistics were calculated as percentages for categorical data and as mean ± standard deviation (SD) for continuous data. P value of <0.05 was considered statistically significant. For normally distributed continuous data, an independent t-test was applied, while Mann-Whitney U test was used for non-normally distributed data.

Table 1: Distribution of cases by age.

In the study comparing age distributions between PCOS and Non PCOS, the following observations were made: Among PCOS patients, 22 were aged 18-25 years, 27 aged between 26-30 years, 8 patients aged 31-35 years, and 3 patients were over 35 years old. In contrast, Non PCOS had 19 subjects aged 18-25 years, 20 subjects were 26-30 years, 14 subjects 31-35 years, and 7 subjects over 35 years old. This distribution shows a generally younger age profile among PCOS patients compared to Non PCOS, particularly in the 18-25 and 26-30 age groups

Table 2: Distribution of cases according to FSH, LH and Testosterone.

In comparing hormonal parameters between women with PCOS and those without, several key differences emerge. The mean levels of follicle-stimulating hormone (FSH) were observed to be lower in group with PCOS at 5.38 IU/mL compared to 5.5 IU/mL in non-PCOS women. Conversely, Luteinizing hormone (LH) levels were markedly higher in women with PCOS, averaging 11.83 IU/mL, compared to 7.34 IU/mL in non-PCOS women. Testosterone levels were significantly elevated in women with PCOS, averaging 1.24 ng/mL, compared to 0.51 ng/mL in non-PCOS women. The LH/FSH ratio, indicative of ovarian function, was significantly higher in group with PCOS at 1.88 compared to 1.26 in non-PCOS groups.

Table 3: Distribution of cases according to Prolactin.

In comparing women with polycystic ovary syndrome (PCOS) to those without, several differences in biochemical parameters were noted. Women with PCOS exhibited a higher mean Prolactin level of 423.03 ng/mL, whereas non-PCOS women had a slightly lower mean of 403.25 ng/mL.

Polycystic ovary syndrome (PCOS) is linked to multiple reproductive, endocrine, and psychological challenges, posing a significant socioeconomic burden on healthcare systems. Stein and Leventhal made initial strides in understanding PCOS during the mid-nineteenth century, but it took nearly a century for its prevalence in India to gain prominence in medical literature. Nationally representative surveys conducted from 2010 to 2014 in India reported PCOS prevalence rates ranging from 6% to 46.8%.[9] Hence, PCOS is one of the most prevalent endocrinological disorder affecting females and a leading cause of menstrual disturbances during reproductive years.

AGE DISTRIBUTION

In our study, the age distribution among PCOS patients shows that 22 individuals were aged 18-25 years, 27 patients were 26-30 years, 8 were in between ages of 31-35 years, and 3 women were over 35 years old. In contrast, Non PCOS groups exhibited 19 subjects aged 18-25 years, 20 subjects between 26-30 years, 14 participants 31-35 years, and 7 individuals were over 35 years old. This indicates a generally younger age profile among PCOS patients, particularly noticeable in the 18-25 and 26-30 age groups.

Ahmadi et al.[9] reported a range of 17 to 47 years among women with PCOS. The mean age of women with PCOS was 28 ± 5.00 years, while those without PCOS were slightly older at 30 ± 5.00 years. Bazarganipour et al.[10] found that the mean age of their PCOS patients was 26.5 (SD 4.44) years. Dybciak et al.[11] detailed that among their PCOS group, 37.39% were aged 20-25 years, 44.35% were aged 26-30 years, and 18.26% were aged 31-40 years, showing a similar distribution in their control group with no significant difference

FSH, LH AND TESTOSTERONE

In our study, women with PCOS showed slightly lower mean levels of follicle-stimulating hormone (FSH) at 5.38 IU/mL compared to 5.5 IU/mL in non-PCOS women. Conversely, Luteinizing hormone (LH) levels were significantly higher in women with PCOS, averaging 11.83 IU/mL, compared to 7.34 IU/mL in non-PCOS women. Testosterone levels were notably elevated in PCOS women at 1.24 ng/mL, compared to 0.51 ng/mL in non-PCOS women. The LH/FSH ratio, indicative of ovarian function, was higher in women with PCOS at 1.88, where as in non PCOS groups it was 1.26.

Bazarganipour F et al[10]reported endocrine markers including mean levels of LH at 8.28 IU/L, FSH at 6.09 IU/L, testosterone at 1.24 nmol/L, and SHBG at 55.57 nmol/L, with a calculated free androgen index (FAI) of 10.21. Rajbanshi[12] I et al found that among PCOS patients, 19% had an LH/FSH ratio ≥ 2. The mean Prolactin level was 17.80 ± 15.89 ng/mL. Testosterone levels in PCOS participants were 35.8 ± 20.15 ng/mL, while progesterone levels were 1.73 ± 21.73 ng/mL.

Prolactin

We found that women suffering from polycystic ovary syndrome (PCOS) had higher mean Prolactin value (423.03 ng/mL)  compared to non-PCOS women, who had mean Prolactin levels of (403.25 ng/mL) Spandana et al.[13]reported that among 87 patients with prolactin levels below 25 ng/ml, the mean prolactin concentration was 14.76±14.07 ng/ml. Conversely, 13 patients had prolactin levels exceeding 25 ng/ml. Nizem FI et al.[14]observed in Benghazi, Libya, that 31% of patients had Hyperprolactinemia, and 26.4% had elevated testosterone levels. Kumar et al.[15]found that 10.7% of patients had elevated prolactin levels. Davoudi et al.[16]identified Hyperprolactinemia in 37% of patients, with a mean serum prolactin level of 48.42±5.44 ng/ml. In contrast, Rajbanshi et al.[12]reported Hyperprolactinemia in 21% of PCOS patients, with a mean prolactin level of 37.25±21.86 ng/ml, which was lower compared to the findings by Davoudi et al.[16]

The present study provides insights into the biochemical alterations especially of the hormonal parameters observed in women with Polycystic Ovary Syndrome (PCOS) compared to women without the condition.Key findings include significantly higher levels of Luteinizing hormone (LH), Testosterone, and LH/FSH ratio. These hormonal disruptions reflect core endocrine features that play a crucial role in it’s pathophysiology.

The findings reinforce the presence of hyperandrogenemia and hypothalamic-pituitary axis dysregulation as central component of the syndrome. Increase level of LH and testosterone have been closely linked to the clinical manifestations of PCOS, particularly menstrual irregularities, anovulation and hirsutism. These hormonal imbalances emphasize the importance of targeted endocrine evaluation in the diagnosis and management of PCOS

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