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Distribution of polycystic ovary syndrome (PCOS) phenotypes in Iranian women: a cross-sectional study

BMC Research Notes volume 18, Article number: 215 (2025) Cite this article

Abstract

Objective

Polycystic ovary syndrome (PCOS) is a heterogeneous disorder characterized by diverse clinical and metabolic manifestations. This study aimed to investigate the prevalence of PCOS phenotypes and their association with hematological, biochemical, and hormonal parameters in PCOS, with a particular focus on infertile women and those with recurrent pregnancy loss (RPL).

Results

Phenotype A was the most prevalent phenotype overall and within both infertile and RPL subgroups. However, no significant differences in hematological, biochemical, or hormonal parameters were observed among the PCOS phenotypes, except for lower RBC and hematocrit levels in phenotype F. PCOS women with RPL demonstrate significantly lower levels of RBC, hemoglobin, and hematocrit in phenotype F.

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Introduction

Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder affecting approximately 5–7% of women of reproductive age [1]. It is characterized by a constellation of symptoms including irregular menstrual cycles, hyperandrogenism, and polycystic ovarian morphology, and is associated with a range of metabolic disturbances such as insulin resistance, obesity, and inflammation [2, 3]. The revised consensus Rotterdam criteria, which incorporate clinical, biochemical, and ultrasound findings or elevated anti-mullerian hormone (AMH) levels [4], provide a standardized diagnostic framework for PCOS [5]. While the precise etiology remains elusive, genetic, epigenetic, and environmental factors are implicated in the pathogenesis of PCOS [6, 7].

Recognizing the heterogeneity of PCOS, researchers have increasingly focused on identifying distinct phenotypic subpopulations within the syndrome. These PCOS phenotypes, characterized by specific combinations of clinical and biochemical features, offer a more nuanced understanding of the disorder [8]. Early attempts at phenotype classification primarily relied on clinical criteria, but advancements in diagnostic technology and molecular biology have enabled a more comprehensive approach that includes metabolic and ovarian characteristics [9]. This phenotypic heterogeneity underscores the complex pathophysiology of PCOS [8]. Given this complexity, researchers emphasize the need for tailored treatment strategies. Phenotype-specific approaches can optimize treatment outcomes and facilitate risk stratification for associated comorbidities, such as metabolic syndrome, cardiovascular disease, infertility [10].

Women with phenotype A often face the greatest challenges in achieving and maintaining pregnancy due to irregular ovulation and hormonal imbalances. In contrast, women with phenotype B, who may have regular ovulation but still exhibit metabolic disturbances, can also experience infertility and recurrent pregnancy loss (RPL), albeit potentially to a lesser extent. The underlying pathophysiological mechanisms, such as hormonal imbalances, insulin resistance, chronic inflammation, ovarian follicle development and endometrial dysfunction, contribute to the increased risk of infertility and miscarriage across all PCOS phenotypes [10,11,12,13]. In addition, obesity, age, family history, and metabolic syndrome can increase the likelihood of developing PCOS, infertility and miscarriage. Understanding these differences is essential for altering management strategies to improve reproductive outcomes for women with PCOS, as each phenotype may require specific interventions to address their unique challenges related to fertility and pregnancy loss [10, 13, 14].

It is notable that the clinical presentation of PCOS exhibits significant heterogeneity across geographical and ethnic populations [15]. The current study aims to investigate the clinical manifestations of PCOS phenotypes and the prevalence of PCOS phenotypes in Iranian women. Furthermore, we investigated the relationship between PCOS phenotypes and a range of hematological, biochemical, and hormonal markers, with particular attention to infertile and RPL subgroups.

Materials and methods

Study population

In this study, the inclusion criteria were women aged 22 to 40 years who were diagnosed with PCOS according to the Rotterdam criteria, which requires the presence of at least two of the following three features: oligo- or anovulation, clinical or biochemical signs of hyperandrogenism, and polycystic ovaries on ultrasound [5]. Additionally, infertile women, defined as those unable to achieve pregnancy despite engaging in regular unprotected sexual intercourse for 12 months or longer, and women with a history of recurrent pregnancy loss, defined as two or more consecutive pregnancy losses before the 20th week, were included.

Exclusion criteria included individuals with Cushing’s syndrome, thyroid dysfunction, androgen-secreting tumors, or those who had undergone hormonal treatment or used drugs such as steroids that could induce insulin resistance for at least 6 months prior to the evaluation. Participants with parathyroid disorders, chronic kidney disease, or other chronic illnesses were also excluded.

The study involved 242 women with PCOS (aged 22 to 40 years), including 143 infertile patients and 99 individuals with a history of recurrent pregnancy loss. Participants were selected from the Obstetrics and Gynecology Department of the Ibn Sina Infertility Center in Tehran, Iran. We utilized the Rotterdam criteria for patient selection, while also acknowledging the various phenotypes of PCOS as defined by the AES criteria, which allows for the identification of patients with a single feature as having a mild phenotype of PCOS [16]. Therefore, patients were categorized into seven distinct phenotypes based on the presence or absence of hyperandrogenemia/hirsutism, oligo/anovulation, and polycystic ovaries [17]. As shown in Table 1, participants with PCOS were categorized into seven phenotypic subtypes: phenotype A (hyperandrogenism/hirsutism, oligo/anovulation and polycystic ovaries); phenotype B (hyperandrogenism/hirsutism and oligo/anovulation); phenotype C (hyperandrogenism/hirsutism and polycystic ovaries); phenotype D (oligo/anovulation and polycystic ovaries); phenotype E (hyperandrogenism/hirsutism); phenotype F (polycystic ovaries), and phenotype G (oligo/anovulation).

Table 1 Clinical manifestations of PCOS phenotypes [17]
Full size table

All study procedures involving human participants were conducted in accordance with ethical guidelines established by institutional and national review boards and the 1975 Helsinki Declaration (as revised in 2008). This study was approved by the Ethics Committee of the Ibn Sina Infertility Center (IR.ACER.Avicenna.Res.1395.6).

Laboratory analysis

Blood samples were collected from fasting participants (12 h) under strict aseptic conditions at the follicular phase (days 7–14) of menstrual cycle. Samples were processed and stored at -80 °C for subsequent analysis. Hematological, biochemical and hormonal parameters, including FBS, insulin, lipid profile, urea, creatinine, HomoCys, RBC, WBC, PLT, Hb, Hct, MCV, MCH, MCHC, FSH and LH, were quantified as detailed in our previous publications [18,19,20].

Statistical analysis

Statistical analyses were performed with IBM SPSS Statistics for Windows, Version 25.0 (IBM Corp., Armonk, NY, USA). The Shapiro-Wilk test was used to evaluate data normality. For normally distributed data, the ANOVA test was applied. Post hoc comparisons utilized the Bonferroni method. A two-tailed p-value of less than 0.05 was considered statistically significant.

Results

A total of 242 women with PCOS were classified into seven phenotypic subgroups (A-G) for this study. The frequencies of phenotypes D and G were zero; therefore, these phenotypes were excluded from the analysis. As outlined in Table 2, phenotype A was the most prevalent among PCOS women overall and maintained this predominance within both infertile and RPL subpopulations. The distribution of phenotypes A, B, C, E, and F within the total PCOS population was 68.6%, 4.5%, 21.9%, 4.1%, and 0.8%, respectively. The phenotypic distribution was similar across infertile and RPL subgroups. However, a higher proportion of women with phenotype A (81%) was identified in the infertile compared to the RPL (50.5%) subgroup. Conversely, the RPL subgroup exhibited a higher prevalence of phenotypes C, B, and F relative to the infertile group.

Table 2 Distribution of various PCOS phenotypes
Full size table

Table 3 presents the clinical characteristics of each PCOS phenotype. No significant differences were observed among the phenotypes regarding hematologic, biochemical, or hormonal parameters. However, phenotype F exhibited significantly lower levels of red blood cell (RBC) and hematocrit compared to the other phenotypes (3.8 ± 0.3, p = 0.006).

Table 3 Hematological, biochemical, and hormonal characteristics among the PCOS phenotypes in Iranian women with PCOS
Full size table

Within the infertile PCOS subgroup, phenotypes showed a significant difference in mean corpuscular volume (MCV) (Table 4) (Phenotypes A, B, and C; 84.1 ± 7.07, 63.6 ± 39.7,and 84.5 ± 3.9, respectively, p = 0.001).

Table 4 Hematological, biochemical, and hormonal characteristics among the PCOS phenotypes in PCOS women with infertility
Full size table

Among PCOS women with a history of RPL, Table 5 demonstrates significantly lower levels of RBC, hemoglobin, and hematocrit in phenotype F compared to the remaining phenotypes.

Table 5 Hematological, biochemical, and hormonal characteristics among the PCOS phenotypes in PCOS women with a history of recurrent pregnancy loss
Full size table

Discussion

PCOS is a multifactorial endocrine disorder among women of reproductive age [7]. To account for the heterogeneity of PCOS, patients have been classified into distinct phenotypes based on clinical and biochemical characteristics [21]. These phenotypic variations consider factors including hyperandrogenism, ovulatory dysfunction, and polycystic ovary morphology [22]. To date, some studies have reported the prevalence of PCOS phenotypes across different populations and ethnicities [8, 23,24,25]. This study aimed to determine the prevalence of these phenotypes in an Iranian cohort of women with PCOS. Additionally, the study assessed the prevalence of PCOS phenotypes among Iranian women with PCOS who have infertility and RPL.

Some studies focused on biochemical parameters in different PCOS phenotypes [26,27,28,29]. However, the infertility and abortion approach in various PCOS phenotypes was ignored, so far. This study represents a novel investigation into the association between hematological, biochemical, and hormonal parameters and distinct PCOS phenotypes among infertile and RPL patients.

Consistent with findings from Sachdeva et al. and Głuszak et al., phenotype A was the most prevalent among women with PCOS in the present study [8, 23]. Phenotype A is the most commonly reported PCOS manifestation in the majority of published clinical studies [30]. However, in contrast to these findings, a study conducted in Sudan by Elasam et al. reported phenotype D as the most prevalent among Sudanese women with PCOS [24]. The study findings revealed that the prevalence of phenotype A (characterized by hyperandrogenism/hirsutism, oligo/anovulation and polycystic ovaries) was 68.7%. Phenotypes B (hyperandrogenism/hirsutism and oligo/anovulation), C (hyperandrogenism/hirsutism and polycystic ovaries), E (hyperandrogenism/hirsutism), and F (polycystic ovaries) had prevalence rates of 4.5%, 21.9%, 4.1%, and 0.8%, respectively. In this context, Farhadi-Azar identified classical phenotypes A and B as the most prevalent among Iranian women with PCOS [25]. Our findings suggest that most Iranian women diagnosed with PCOS according to the Rotterdam criteria present with all three primary features: hyperandrogenism, polycystic ovaries, and ovulatory dysfunction. Approximately 22% of patients exhibited hyperandrogenism and polycystic ovaries. To date, no studies have reported the prevalence of PCOS phenotypes in PCOS women with infertility and RPL. Our findings indicate that phenotype A remains the most prevalent phenotype among infertile and RPL subgroups. Phenotype A of PCOS, which recognized as full Rotterdam criteria, probably is associated with an increased risk of infertility and miscarriage. The anovulation characteristic can lead to irregular menstrual cycles and difficulty in conceiving. Additionally, women with this phenotype may experience hormonal imbalances that can affect pregnancy outcomes, increasing the likelihood of abortion. It seems that proper management and treatment are essential for women with this phenotype who are trying to conceive or are pregnant.

Chang et al. reported that biochemical profiles exhibit significant differences across these phenotypes [31]. This study investigated the relationship between PCOS phenotypes and hematological, biochemical, and hormonal parameters. Compared to phenotype C and D, patients with phenotype A and B (classical phenotype) are more often obese, with hirsutism, more likely to have insulin resistance, dyslipidemia, and metabolic syndrome in later life.

PCOS is a complex syndrome associated with metabolic disturbances such as insulin resistance, dyslipidemia, and obesity. Although previous studies have suggested that classical phenotypes (A and B) are more strongly linked to these abnormalities [32, 33], our study did not find significant differences in metabolic parameters such as BMI, fasting insulin, and lipid profile among the phenotypes. These findings align with some studies on Iranian women with PCOS [28]. The limited sample size or ethnic, epigenetic and environmental and developmental differences may have influenced these results [34]. However, the metabolic aspect of PCOS remains crucial. Future studies with larger sample sizes and more detailed metabolic assessments, including HOMA-IR and inflammatory markers, could further clarify the relationship between PCOS phenotypes, infertility, and recurrent pregnancy loss.

In the current study, phenotype A have shown the most level of insulin resistance and LH/FSH ratio in PCOS with infertility, which did not receive to significant level. Our findings did not reveal significant differences in BMI, fasting blood sugar (FBS), insulin, lipid profile, urea, creatinine, LH, FSH, homocysteine, WBC, Hb, MCV, MCHC, MCH and platelet counts among the different PCOS subgroups. These results align with the observations of Elasam et al. regarding BMI and LH/FSH levels [24]. Similarly, our lipid profile findings concur with those of Gluszak et al. [23]. However, these results contrast with those of several other studies, including Sachdeva et al., Jamil et al., and Abashova et al., which reported significant variations in lipid and glucose profiles across PCOS phenotypes [8, 35, 36]. Nevertheless, Hosseinpanah et al. in line with our findings showed there was no difference regarding metabolic characteristics between different PCOS phenotypes in Iranian women [28]. These discrepancies may be attributed to differences in study populations, diagnostic criteria, sample sizes, or other methodological factors. Further research is warranted to elucidate the complex interplay between PCOS phenotypes and metabolic disturbances.

Previous research has linked increased oxidative stress in PCOS to shortened RBC lifespan due to membrane alterations [37]. While studies have reported varying RBC parameters among PCOS women [38, 39], others have found no significant differences in blood-related factors between women with and without PCOS [40]. We investigate that phenotype F in PCOS women with RPL, probably suffer from anemia like megaloblastic anemia, because of higher level of RBC and MCV, as well as lower level of Hct and Hb. Interestingly, this pattern was not found in PCOS women with infertility. A decrease in red blood cell count, hematocrit, and hemoglobin can be associated with folic acid deficiency. Folic acid, a member of the B vitamin group, plays a vital role in the production and proliferation of blood cells [41]. This vitamin is especially essential for DNA and RNA synthesis and is necessary for the production of healthy red blood cells. Folic acid has crucial role in the one-carbon metabolism cycle. This cycle contributes to the production of methionine and other essential compounds that are critical for fetal growth and development. Disruptions in this cycle can increase the risk of abortion [42, 43]. PCOS women with phenotype F known as” non-hyperandrogenic” PCOS which is characterized only by PCO on ultrasound. This phenotype has unknown and unclear pathophysiology. The observed hematological changes within phenotype F is intriguing and warrants further exploration with a larger sample size about the role of one-carbon metabolism cycle to validate these preliminary findings.

Conclusion

Our study investigate the possible impact of PCOS phenotypes in an Iranian population in relation to reproductive outcomes. The findings indicate that women with PCOS, especially those exhibiting phenotype A, face increased challenges regarding infertility and a higher risk of repeated pregnancy loss. These results indicate that comprehensive metabolic screening may not be necessary for different phenotypes of PCOS. To gain a deeper understanding of hematological parameters effect in women with various PCOS phenotypes who experience pregnancy loss, further research through larger population-based studies is essential.

Limitations

Despite the novel nature of this investigation, certain limitations warrant consideration. The relatively small sample size limits the generalizability of our findings. Additionally, the study’s focus on Iranian women restricts definitive conclusions about racial and environmental factors. Future research involving larger and more diverse populations is necessary to validate and expand upon these results. Another limitation of this study was the inability to assess additional factors such as QUICKI, G/I ratio, and biomarkers like free and bound testosterone, SHBG, estradiol, and DHEA-sulphate and AMH due to financial constraints. Future research incorporating these parameters may offer a more comprehensive understanding of the pathophysiology of PCOS.

Data availability

All data generated or analyzed during this study are included in this published article.

Abbreviations

BMI:

Body Mass Index

FBG:

Fasting Blood Glucose

FSH:

Follicle-Stimulating Hormone

HDL-C:

High-Density Lipoprotein Cholesterol

HOMA-IR:

Homeostasis Model Assessment of IR

LDL-C:

Low-Density Lipoprotein Cholesterol

LH:

Luteinizing Hormone

PCOS:

Polycystic Ovary Syndrome

TC:

Total Cholesterol

RPL:

Recurrent Pregnancy Loss

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Acknowledgements

The authors are grateful to the University of Tehran for the support of this project.

Funding

This study was supported by the University of Tehran.

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Authors and Affiliations

  1. Department of Comparative Biosciences, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran

    Asma Kheirollahi, Hediyeh Hamidi & Akram Vatannejad

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Contributions

AK: Conceptualization and Supervision; HH: Writing original draft, Investigation; AV: Conceptualization and Statistical Analysis. All authors reviewed and edited the manuscript and approved the final version of the manuscript.

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Correspondence to Akram Vatannejad.

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All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1975 Helsinki declaration as revised in 2008. The present research was approved by the Ethics Committee of Ibn Sina Infertility Center. Informed consent was obtained through a written consent form before starting the study.

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Kheirollahi, A., Hamidi, H. & Vatannejad, A. Distribution of polycystic ovary syndrome (PCOS) phenotypes in Iranian women: a cross-sectional study. BMC Res Notes 18, 215 (2025). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s13104-025-07202-6

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