# Comparison of serum inhibin A and estradiol levels for monitoring ovarian stimulation in IVF: a preliminary study

Maxime Chaillot, Anaïs Inquel, Arnaud Reignier, Sophie Loubersac, Thomas Fréour

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## To cite this version:

Maxime Chaillot, Anaïs Inquel, Arnaud Reignier, Sophie Loubersac, Thomas Fréour. Comparison of serum inhibin A and estradiol levels for monitoring ovarian stimulation in IVF: a preliminary study. Journal of Gynecology Obstetrics and Human Reproduction, 2025, 54 (8), pp.102988. 10.1016/j.jogoh.2025.102988. inserm-05269541

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Original Article

# Comparison of serum inhibin A and estradiol levels for monitoring ovarian stimulation in IVF: a preliminary study

Maxime Chaillot<sup>a, *</sup> <sup>ID</sup>, Anaïs Inquel<sup>a</sup>, Arnaud Reignier<sup>a, ID</sup>, Sophie Loubersac<sup>a, b</sup>, Thomas Fréour<sup>a, b ID</sup>

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ARTICLE INFO

Keywords:

Inhibin A

Estradiol

Ovarian stimulation

IVF

Follicular monitoring

ABSTRACT

**Introduction:** Controlled Ovarian Hyperstimulation (COH) is crucial in Assisted Reproductive Techniques (ART), as it determines the number of mature oocytes retrieved, a key factor in pregnancy success. Serum estradiol (E2) is commonly used alongside transvaginal ultrasound (TVUS) to monitor ovarian response, but its accuracy is limited due to secretion from multiple follicular categories. In contrast, serum Inhibin A, primarily secreted by mature antral follicles, may offer a more accurate reflection of follicular maturity.

**Materials and methods:** This retrospective study involved women undergoing COH for in vitro fertilization (IVF) using an antagonist protocol. Serum levels of E2 and Inhibin A were measured on the day of hCG trigger. The study assessed their association with ovarian response, specifically the number of mature follicles and mature oocytes retrieved.

**Results:** The study included 84 IVF cycles. The total number of oocytes retrieved and the number of mature oocytes were significantly correlated with serum levels of Inhibin A (R² = 0.253 and R² = 0.267, respectively; *p* < 0.001) and estradiol (R² = 0.344 and R² = 0.259, respectively; *p* < 0.001). The correlation with Inhibin A strengthened with increasing follicular size, while the correlation with estradiol remained stable.

**Conclusion:** These findings suggest that serum Inhibin A, combined with transvaginal ultrasound, could help improve the timing of the hCG trigger. It may offer a more accurate assessment of follicular maturity compared to estradiol alone. Further studies are needed to confirm its role in routine IVF monitoring.

Introduction

In vitro fertilization (IVF) and intra-cytoplasmic sperm injection (ICSI) are advanced assisted reproductive technologies (ART) that rely on controlled ovarian hyperstimulation (COH), followed by oocyte retrieval, fertilization, and embryo transfer after in vitro culture. The number of mature oocytes retrieved during COH is a critical determinant of ART success [1,2]. Exogenous gonadotropins are employed to stimulate multi-follicular growth, aiming to increase the number of oocytes available for fertilization. Effective monitoring of follicular development during COH is essential for optimizing ovulation triggering and minimizing the risk of ovarian hyperstimulation syndrome (OHSS).

The most common methods for monitoring follicular development are transvaginal ultrasound (TVUS) and the measurement of serum estradiol (E2) levels. TVUS assesses the number and size of growing

follicles, while serum E2 levels reflect the hormonal output of all follicles, including smaller pre-antral ones [3]. However, due to the multi-follicular nature of stimulation and the variability in follicle size, serum E2 levels often become supraphysiological and highly variable, limiting their utility as a sole marker for determining follicular maturity [4].

Inhibin A, a dimeric glycoprotein member of the activin family, has emerged as a potential alternative marker for monitoring follicular development. During the follicular phase, inhibin A is part of a negative feedback loop regulating the hypothalamic-pituitary-gonadal axis. It is primarily secreted by the granulosa cells in follicles larger than 12 mm in diameter [5] under the influence of Follicular Stimulating Hormone (FSH). Inhibin A acts at the pituitary level to selectively suppress FSH secretion, without significantly affecting LH. This feedback mechanism helps prevent the recruitment of additional follicles once a dominant

<footnote><sup>a</sup> Service de médecine et biologie de la reproduction, gynécologie médicale, CHU Nantes, Nantes, France</footnote>

<footnote><sup>b</sup> Nantes Université, CHU Nantes, INSERM, Center for Research in Transplantation and Translational Immunology, UMR 1064, F-44000 Nantes, France</footnote>

<footnote>* Corresponding author at: Service de médecine et biologie de la reproduction, gynécologie médicale, CHU Nantes, 38 boulevard Jean Monnet, 44093 Nantes, France.</footnote>

<footnote>E-mail address: maxime.chaillot@chu-nantes.fr (M. Chaillot).</footnote>
follicle is established, thereby promoting monofollicular development in natural cycles.

It has been shown that inhibin A has a more restricted secretion profile compared to E2 by reflecting follicular differentiation rather than a simple proliferation. This suggests that it may more specifically reflect the population of mature follicles and could serve as a relevant hormonal marker for monitoring ovarian response during COH [6–8], especially for refining the timing of hCG administration and potentially improving oocyte maturity and cycle outcomes.

Since the development of specific assay methods for each inhibin (i. e., inhibin A and inhibin B), several studies have reported serum inhibin A levels during ovarian stimulation [6] and their correlation with ART outcomes [9,10]. Unlike estradiol, whose levels rise throughout follicular development, inhibin A levels increase significantly only when follicles reach a size of 12–15 mm. The role of inhibin A assays in guiding clinical decisions during IVF remains controversial and has been explored only to a limited extent. However, incorporating inhibin A measurement into IVF monitoring protocols may support more individualized and physiologically targeted stimulation strategies.

This preliminary retrospective study aims to compare the predictive value of serum inhibin A and E2 levels for ovarian response during COH using a GnRH antagonist protocol in IVF. Specifically, we assess the correlations between inhibin A and E2 levels measured on the day of hCG administration and two key outcomes: the total number of oocytes retrieved and the number of mature (MII) oocytes. By evaluating these associations, we aim to determine whether inhibin A could serve as a complementary or superior marker to E2 for monitoring follicular development and optimizing ovulation trigger timing.

## Materials and methods

### Study design

This retrospective, single-center study was conducted at a university-affiliated ART center in France between December 2019 and March 2020. All consecutive IVF ± ICSI cycles were eligible for inclusion if a serum sample was available on the day of hCG administration and analyzed in the center's local hormonology laboratory. Cycles were excluded if hormonal assays were performed the day before ovulation triggering or in an external laboratory.

This retrospective study used anonymized clinical and laboratory data collected during routine care at a French university hospital. In line with French regulations, patients are informed that their data may be used for research unless they object. No additional sampling or intervention was conducted. As such, formal ethics committee approval was not required.

### Ovarian stimulation protocols

All patients underwent COH for IVF using a GnRH antagonist protocol. The initial dose of gonadotropins (either recombinant or urinary) was determined based on patient age, ovarian reserve, body mass index (BMI), and history of previous IVF cycles. Follicular development was monitored according to standard practice, including TVUS and serum hormone assays (LH, estradiol, and progesterone) every 2–3 days.

The GnRH antagonist was introduced on day 6 of stimulation. Ovulation was triggered using recombinant hCG (Ovitrelle®) when at least three follicles reached a diameter of 17 mm, or with a GnRH agonist (0.2 mg Decapeptyl®) in cases of high OHSS risk. Oocyte retrieval was scheduled 35–36 h after the trigger. Fertilization was performed by conventional IVF or ICSI, depending on semen quality. All embryos were cultured to the blastocyst stage. A freeze-all strategy was employed in cases of OHSS risk, elevated premature progesterone levels, or when >18 oocytes were retrieved.

## Hormonal analysis

Blood samples were collected on the morning of the hCG trigger day. Estradiol, LH, and progesterone levels were measured within two hours of collection using routine clinical protocols. For inhibin A analysis, samples were frozen at –20 °C and stored until batch analysis. Estradiol concentrations were measured using an automated competitive immunoassay on the Roche Cobas® platform. Serum inhibin A levels were measured using the iFlash-Inhibin A assay (Orgentec®), a fully automated sandwich-type chemiluminescent immunoassay performed on the iFlash 1800 analyzer.

## Statistical analysis

Statistical analyses were performed using Prism5®, BiostatsGV, and Microsoft Excel®. Pearson's correlation coefficient was used to assess the relationship between continuous variables. A p-value < 0.05 was considered statistically significant. All analyses were conducted in the overall study population.

## Results

A total of 84 IVF cycles from 84 couples were included in the analysis. The patients' baseline characteristics—including age, body mass index (BMI), ovarian reserve, and smoking status—are summarized in Table 1. The stimulation cycle characteristics are detailed in Table 2.

The total number of oocytes retrieved and the number of mature oocytes were significantly correlated with serum inhibin A levels ($R^2$ = 0.253 and $R^2$ = 0.267, respectively; *p* < 0.001) and estradiol levels ($R^2$ = 0.344 and $R^2$ = 0.259, respectively; *p* < 0.001) in the overall study population (Table 3).

Serum levels of inhibin A and estradiol were also significantly correlated with the number of follicles in each size category (10–13 mm, 14–15 mm, and >16 mm). The strength of the correlation between inhibin A and follicle count increased with follicular size, whereas the correlation with estradiol remained relatively stable across all follicle size categories (Table 3).

We analyzed the results by defining subgroups based on age and ovarian response. Patients were divided into two age groups: under 35 years (*n* = 42) and over 35 years (*n* = 42). Additionally, patients were categorized according to ovarian response and the number of oocytes retrieved: poor responders (≤ 5 oocytes), normo-responders (6–18 oocytes), and hyper-responders (> 18 oocytes).

In the under-35 age group, both the total number of oocytes collected and the number of mature oocytes were significantly correlated with serum inhibin A ($R^2$ = 0.376 and $R^2$ = 0.308, respectively; *p* < 0.001) and estradiol levels ($R^2$ = 0.321 and $R^2$ = 0.315, respectively; *p* < 0.001). In contrast, the over-35 age group showed weaker correlations between serum inhibin A and the number of oocytes collected ($R^2$ = 0.178; *p* < 0.01). Regarding follicle size, the correlation between follicle size and inhibin A increased significantly for follicles measuring 14–15 mm, but this was observed only in the under-35 age group ($R^2$ = 0.245; *p* < 0.001).

For ovarian response subgroups, significant correlations with serum

<table><caption>**Table 1**

Patients' characteristics.</caption><thead><tr><td>Parameter</td><td>Mean</td><td>SD</td></tr></thead><tbody><tr><td>Age</td><td>34 (23–43)</td><td>4.7</td></tr><tr><td>BMI (kg/m<sup>2</sup>)</td><td>25.1 (17.7–49.9)</td><td>6.1</td></tr><tr><td>AMH (ng/mL)</td><td>2.61</td><td>1.9</td></tr><tr><td>AFC (n)</td><td>20.3</td><td>12.5</td></tr><tr><td>Smoking patients (n, %)</td><td>14 (16.7 %)</td><td></td></tr></tbody></table>

BMI: Body Mass Index, AMH: Anti-Müllerian-Hormone, AFC: Antral Follicle Count, SD: standard deviation.
<table><caption>**Table 2**
Cycle's characteristics.</caption><thead><tr><th>Parameter</th><th>Mean</th><th>SD</th></tr></thead><tbody><tr><td>Stimulation days</td><td>10.3</td><td>1.58</td></tr><tr><td>Mean E2 level (pg/mL)</td><td>3034.8</td><td>1172.5</td></tr><tr><td>Mean Inhibin A level (pg/mL)</td><td>233.3</td><td>208.6</td></tr><tr><td>Total dose gonadotropins (IU)</td><td>2307</td><td>890</td></tr><tr><td>Number of follicles of 10–13 mm</td><td>5.4</td><td>3.9</td></tr><tr><td>Number of follicles of 14–15 mm</td><td>3.6</td><td>2.4</td></tr><tr><td>Number of follicles > 16 mm</td><td>6.9</td><td>3.1</td></tr><tr><td>Number of retrieved oocytes</td><td>13.6</td><td>7.9</td></tr><tr><td>Total number of mature oocytes</td><td>10</td><td>5.5</td></tr><tr><td>IVF fertilisation rate (%)</td><td>79.8</td><td>20</td></tr><tr><td>ICSI fertilisation rate (%)</td><td>67.3</td><td>22</td></tr><tr><td>Number of embryos obtained (blastocyst stage)</td><td>7.1</td><td>5</td></tr><tr><td>Number of cycles with recombinant FSH</td><td>40</td><td>47.6</td></tr><tr><td>Number of cycles with urinary FSH</td><td>44</td><td>52.4</td></tr></tbody></table>

IVF: In Vitro Fertilization, ICSI: Intra-Cytoplasmic Sperm Injection, SD: standard deviation.

<table><caption>**Table 3**
Correlations between follicular development and hormonal levels on hCG trigger day.</caption><thead><tr><th>Follicle number on the day of final oocyte maturation</th><th>E2 (pg/mL)</th><th>Inhibin A (pg/mL)</th></tr></thead><tbody><tr><td>Total number of follicles</td><td>R<sup>2</sup> = 0.344<br>* p &lt; 0.001;.<br>R<sup>2</sup> = 0.259<br>* p &lt; 0.01.</td><td>R<sup>2</sup> = 0.253*<br>R<sup>2</sup> = 0.267*<br>R<sup>2</sup> = 0.200<br>* R<sup>2</sup> = 0.132*<br>R<sup>2</sup> = 0.0184*<br>R<sup>2</sup> = 0.0168<br>* R<sup>2</sup> = 0.258*</td></tr><tr><td>Total number of mature oocytes</td><td>R<sup>2</sup> = 0.344<br>* p &lt; 0.001;.<br>R<sup>2</sup> = 0.259<br>* p &lt; 0.01.</td><td>R<sup>2</sup> = 0.253*<br>R<sup>2</sup> = 0.267*<br>R<sup>2</sup> = 0.200<br>* R<sup>2</sup> = 0.132*<br>R<sup>2</sup> = 0.0184*<br>R<sup>2</sup> = 0.0168<br>* R<sup>2</sup> = 0.258*</td></tr><tr><td>Number of follicles 10–13 mm</td><td>R<sup>2</sup> = 0.344<br>* p &lt; 0.001;.<br>R<sup>2</sup> = 0.259<br>* p &lt; 0.01.</td><td>R<sup>2</sup> = 0.253*<br>R<sup>2</sup> = 0.267*<br>R<sup>2</sup> = 0.200<br>* R<sup>2</sup> = 0.132*<br>R<sup>2</sup> = 0.0184*<br>R<sup>2</sup> = 0.0168<br>* R<sup>2</sup> = 0.258*</td></tr><tr><td>Number of follicles 14–15 mm</td><td>R<sup>2</sup> = 0.344<br>* p &lt; 0.001;.<br>R<sup>2</sup> = 0.259<br>* p &lt; 0.01.</td><td>R<sup>2</sup> = 0.253*<br>R<sup>2</sup> = 0.267*<br>R<sup>2</sup> = 0.200<br>* R<sup>2</sup> = 0.132*<br>R<sup>2</sup> = 0.0184*<br>R<sup>2</sup> = 0.0168<br>* R<sup>2</sup> = 0.258*</td></tr><tr><td>Number of follicles ≥ 16 mm</td><td>R<sup>2</sup> = 0.344<br>* p &lt; 0.001;.<br>R<sup>2</sup> = 0.259<br>* p &lt; 0.01.</td><td>R<sup>2</sup> = 0.253*<br>R<sup>2</sup> = 0.267*<br>R<sup>2</sup> = 0.200<br>* R<sup>2</sup> = 0.132*<br>R<sup>2</sup> = 0.0184*<br>R<sup>2</sup> = 0.0168<br>* R<sup>2</sup> = 0.258*</td></tr></tbody></table>

Significance level:.

* p < 0.001;

s p < 0.01.

inhibin A levels were primarily found in normo-responders. No significant correlations were observed in poor responders or hyper-responders.

## Discussion

TVUS and serum E2 measurements are currently the primary criteria used to adjust ovarian stimulation in ART. However, the predictive value of these markers in determining the number of oocytes retrieved during IVF remains limited. Numerous studies have assessed the role of E2 measurement during ovarian stimulation, with results showing that E2 levels do not lead to a higher number of mature oocytes compared to ultrasound monitoring alone [11–14]. Nonetheless, E2 remains a useful marker for predicting the risk of OHSS, particularly when excessively high E2 levels coincide with a large follicular cohort, which may necessitate a freeze-all strategy. The search for alternative biomarkers to improve the assessment of follicular growth and oocyte maturity is a critical clinical objective. To our knowledge, only a few studies, notably by Lawrenz et al. (2020) and Millot et al. (2002), have explored the potential of inhibin A measurement for optimizing ovulation timing and its correlation with follicular development compared to serum E2 [10, 15]. Previous research has largely focused on the role of inhibin A assays in ovarian stimulation monitoring for IVF, without directly comparing it to E2. Furthermore, the few older studies that did compare inhibin and E2 assays often employed assay methods that did not differentiate between the two types of inhibin.

## Correlation between inhibin A levels and follicular development assessed by ultrasound

Inhibin A is produced by dominant follicles at the end of their maturation and is considered to reflect follicular maturity and oocyte quality. Previous research has shown a hormonal shift in follicles measuring 9–10 mm in diameter, where inhibin A concentration increases with follicular size [16]. Although our study measured inhibin A in serum rather than follicular fluid, our findings are consistent with previous work, demonstrating a strong correlation between inhibin A levels and follicles ≥16 mm. These results align with studies by Eldar-Geva et al. and Lawrenz et al., which found significant inhibin A secretion primarily from larger follicles [10,17]. While both E2 and inhibin A correlate with follicular size, inhibin A appears to be a more specific marker for larger follicles (>15 mm) [6]. Despite the moderate and generally similar Pearson correlation coefficients for inhibin A and E2 in our study, E2 is not a reliable marker for predicting the number of follicles observed on TVUS. In contrast, we observed a significant increase in correlation for follicles larger than 16 mm. Our findings suggest that inhibin A is predominantly secreted by the largest follicles, reinforcing the potential of inhibin A as a new marker for monitoring ovarian response [9,18]. Integrating inhibin A with E2 and ultrasound may improve the precision of ovulation trigger timing, particularly in cases where estradiol levels plateau or rise unusually, or when follicular size on ultrasound is discordant with the expected endocrine profiles. In situations at risk of OHSS, the inhibin A assay could help trigger ovulation earlier, while ensuring an adequate number of mature oocytes are retrieved.

## Association of inhibin A and estradiol with oocyte retrieved

Gonadotropin-stimulated serum inhibin A concentrations significantly correlate with oocyte retrieval outcomes. Hall et al. reported a correlation of *r* = 0.54 for inhibin A and *r* = 0.58 for E2, which aligns with our findings of *r* = 0.503 for inhibin A in the general population [9]. Additionally, several studies have identified a significant correlation between serum inhibin A concentrations and the number of oocytes retrieved on the day before hCG injection (R = 0.50), consistent with our results [17]. Beyond the number of follicles and oocytes retrieved, it is also important to consider the maturity of the oocytes. Lawrenz et al. proposed a threshold inhibin A level of 668.1 pg/mL, above which the likelihood of retrieving ≥10 mature oocytes significantly increases [10]. These findings further support the potential of inhibin A as a marker for ovulation timing and oocyte retrieval planning.

## Subgroup analysis

Our analysis revealed stronger correlation coefficients for serum inhibin A levels in patients under 35 years old, suggesting that inhibin A secretion may decline with age, which could impact its predictive capacity in older women. Furthermore, no significant correlations were observed in poor responders or hyper-responders, indicating that inhibin A secretion may be more variable in patients who do not respond predictably to ovarian stimulation. Therefore, inhibin A may serve as a more reliable predictor of oocyte number and follicle count, as visualized by ultrasound, in patients who respond appropriately to stimulation. These findings underscore the novelty of this study and emphasize the need for further research to better define the indications for using inhibin A in predicting controlled ovarian response.

## OHSS prediction

The aim of our study was to compare the correlation between inhibin A, E2, and ovarian stimulation response. Although OHSS data were not available for our cohort, some studies suggest that serum inhibin A concentrations could serve as an additional predictor of OHSS risk [19,
[20]. This potential role should be further explored in prospective studies, particularly in high-risk patient populations.

## Comparative interest of inhibin B

Inhibin B, primarily secreted by small antral follicles, has been studied as a marker of ovarian reserve and follicular recruitment [21]. It has been shown that inhibin B rises earlier, peaking on day 7, before inhibin A and E2 [15]. This early elevation could make it valuable for early adjustments to stimulation protocols or cycle cancellation in cases of poor response. However, unlike inhibin A, it does not appear to correlate with final follicular maturity or pregnancy rates [22].

## Strengths and limitations

A strength of our study is its inclusion of unselected patients, which reflects the typical population seen in IVF centers. Our findings confirm that inhibin A is correlated with mature follicles and retrieved oocytes, reinforcing its potential as an additional or alternative biomarker to E2.

Personalized ovarian stimulation is an emerging concept aimed at optimizing ART outcomes by tailoring treatment protocols to individual patient characteristics. While antral follicle count (AFC) and anti-Müllerian hormone (AMH) are widely used to predict ovarian response before stimulation, few biomarkers have been validated for real-time monitoring during stimulation. This study highlights the potential role of inhibin A as a dynamic biomarker that could complement existing parameters. By incorporating inhibin A levels into clinical algorithms, it may be possible to refine gonadotropin dose adjustments or modify the timing of ovulation triggering, ultimately improving clinical pregnancy rates and reducing cycle cancellations.

However, this study has several limitations. Its retrospective design limits causal interpretation. Only one stimulation protocol (GnRH antagonist) was evaluated, which may reduce the generalizability of the findings. The sample size was relatively small (84 cycles), and subgroup analyses by age or ovarian response further limited statistical power. Inhibin A was measured only once per cycle, on the day of hCG administration, based on conventional criteria. Additionally, prior stimulation cycles in some patients may have influenced ovulation triggering. Inhibin B, although proposed as a predictive marker, was not assessed.

While inhibin A appears to be a promising marker for optimizing ovulation trigger timing, its clinical integration requires prospective studies to define optimal thresholds and assess its impact on outcomes. Provided that rapid and cost-effective assays are available, randomized trials comparing monitoring strategies—ultrasound plus inhibin A versus ultrasound plus estradiol—could clarify its added value, particularly regarding mature oocyte yield.

Future research should also evaluate whether inhibin A offers meaningful advantages over current tools in predicting outcomes such as live birth rates. However, the potential cost and logistical implications of routine inhibin A measurement must be considered. It remains to be determined whether inhibin A could complement or replace existing monitoring strategies, or if it would add unnecessary complexity. This preliminary study provides initial data to support the development of larger prospective trials and potential funding applications.

## Conclusion

Serum inhibin A shows potential as an additional biomarker for monitoring ovarian stimulation in IVF. Its correlation with mature oocytes and larger follicles suggests it may complement estradiol in evaluating follicular development. However, given the limitations of this preliminary study, including its retrospective design and limited sample size, further prospective research is needed to determine its clinical relevance and utility in improving patient management.

## Funding

This research was conducted without specific funding, relying on institutional resources to ensure its completion.

## Declaration of competing interest

The authors Chaillot et al. declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

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