European Journal of Cardiovascular Medicine

Concerns have become more common among females in the reproductive age range. While drastic measures are being taken to limit the population in emerging countries like India, issues like infertility are also rising, especially among girls from higher socioeconomic backgrounds. According to the WHO study, the prevalence of primary infertility in India is between 4 and 17%, with urban inhabitants accounting for the majority of cases. It can be linked to a number of variables that contribute to a rise in infertility, such as obesity, poor eating habits, an unhealthy lifestyle, an older age of conception, an advanced age of marriage, and stress.¹

One of the main causes of infertility is obesity, and the gold standard for determining obesity is an excessive body mass index (BMI) and body fat. The subject's height and weight are evaluated in order to calculate their BMI. Women who weigh more than 25 kg/m2 are classified as overweight, while those who weigh more than 30 kg/m2 are classified as obese. It is crucial to classify and evaluate obesity since it has negative effects on the entire body and puts people at risk for a number of illnesses, the most prevalent of which are diabetes mellitus and hypertension. Obesity is known to impact oocyte development and folliculogenesis in the ovary when it comes to the female reproductive system.²

In females of reproductive age, PCOD (polycystic ovarian disease) is a heterogeneous endocrine condition that manifests in a variety of ways, including hyperandrogenism, irregular menstruation, and obesity. Approximately 5–10% of females in the reproductive age range suffer from one of the most prevalent endocrine disorders. Anovulation follows an increase in testosterone levels and LH (luteinizing hormone) levels, which is the distinctive pattern.³

An evaluation of AMH (anti-mullerian hormone) levels is a helpful test for determining ovarian reserve and ovarian function. Because it shows the ovarian reserve—an additional indirect indicator of a woman's ability to procreate—estimating AMH levels is a common test for infertile individuals. After puberty, the ovary's granulosa cells release a glycoprotein called AMH. Ovarian follicle growth and oocyte maturation are aided by AMH.⁴

AMH primarily inhibits the early folliculogenesis stage's FSH (follicle stimulating hormone)-dependent selection mechanism. Additionally, it reduces the quantity of LH receptors in granulosa cells, a process that is similarly triggered by FSH. Because AMH levels are rather stable throughout the menstrual cycle, its evaluation is not time-dependent, which makes it easier to utilize.⁵
The normal range for AMH is 2–6.8 ng/ml, and as people age, their levels decline. AMH levels are absent during menopause. AMH levels are typically used to grade a female's fertility; females with AMH levels less than 1 ng/ml are thought to have inadequate ovarian reserve.

Obese women have elevated AMH levels, and PCOD is typically associated with high BMI. Females with PCOD are predicted to have high amounts of AMH, as the number of antral tiny follicles can boost AMH release.5 With a particular focus on participants with PCOD, the current investigation sought to determine if serum AMH levels and BMI were related in females presenting with infertility

The current cross-sectional clinical study was carried out at the Institute's Department of Obstetrics and Gynecology. Prior to their involvement in the study, all participants provided written and verbal informed consent. Every female who complained of infertility to the Institute during the designated study period was evaluated.

Females who presented with infertility and were willing to participate in the study between the ages of 20 and 40 met the inclusion criteria. Participants with premature ovarian failure (FSH level > 15 IU/ml), a history of ovarian surgery, diabetes, congenital adrenal hyperplasia, Cushing's syndrome, hyperprolactinemia, thyroid dysfunction, and those who did not consent to participate in the trial were excluded. Additionally, participants with proven male infertility were not included in the study.

Every participant got a thorough evaluation at baseline, which included a gynecological, physical, and general examination, a gynecological history, and a basic assessment of infertility that included a transvaginal ultrasound (TVS) on the second day of the menstrual cycle.

Regardless of the day of the cycle, serum AMH (anti-mullerian hormone) was measured at the initial visit. After drawing blood from the cubital vein and waiting for lot retraction, the sample was centrifuged at 2000 rpm for five minutes. The obtained serum was then kept between 2 and 80 degrees Celsius. Chemiluminescent immunoassay (CLIA) was used to measure AMH levels in mg/ml. AMH samples were collected using a comparable test.

After then, the subjects were split into two groups: Group I, which included people with PCOD, and Group II, which included those without PCOD. According to the Rotterdam criteria, patients who met two of the three criteria—hyperandrogenism, oligo/anovulation, and/or polycystic ovaries on ultrasound—were diagnosed with PCOD.

 Polycystic ovaries were defined as having at least 12 little antral follicles per ovary. BMI was calculated for each female by dividing weight in kilos by height in square meters.
Establishing a link between BMI and AMH levels in PCOD participants and evaluating the association in the Institute's non-PCOD infertile cohort were the main outcomes evaluated.

The Student t-test, ANOVA (analysis of variance), Spearman correlation test, and descriptive measures were evaluated using SPSS (Statistical Package for the Social Sciences) software version 24.0 (IBM Corp., Armonk, NY, USA). The mean, standard deviation, frequency, and percentages were used to express the results. A p-value of less than 0.05 was taken into

The goal of the current cross-sectional clinical investigation was to assess the association between blood AMH (anti-mullerian hormone) levels and BMI (bone mass index) in infertile females with and without PCOD (polycystic ovarian disease). 400 women who came to the Institute with infertility during the specified study period were evaluated. Three hundred participants had infertility due to causes other than polycystic ovarian disease, such as tubal factors, poor ovarian response, and unexplained infertility. One hundred subjects had been diagnosed with polycystic ovarian disease.

43% of the 400 study participants were between the ages of 25 and 30, followed by 32% who were between the ages of 31 and 35, 20% who were older than 35, and 5% who were younger than 25.

Table 1: Age, BMI, and AMH levels in the Gr I of study subjects

According to the study's findings, participants with polycystic ovarian disease (Group I) [Table 1] had significantly greater amounts of AMH (p<0.05) than those without PCOD (Group II) in terms of mean age, BMI, and AMH levels. Additionally, the study's findings revealed a statistically significant inverse association between AMH and BMI levels in Group I (p=0.04). But in group II, there was no correlation between AMH levels and BMI (p>0.05) (Table 2).

Table 2: Age, BMI, and AMH levels in the Gr II of study subjects

It was observed that there were considerably more lean PCOD subjects in the study (those with a BMI of less than 25) than non-lean PCOD patients (those with a BMI of more than 25 kg/m2).

The mean AMH levels were 11.16±2.62 ng/ml in lean PCOD patients and 10.09±4.24 ng/ml in non-lean PCOD subjects. However, with p>0.05, the difference was not statistically significant. [Table 3]

Table 3: Age, BMI, and AMH levels in overall study subjects

400 women who came to the Institute with infertility during the specified research period were evaluated in this study. Three hundred participants had infertility due to causes other than polycystic ovarian disease, such as tubal factors, poor ovarian response, and unexplained infertility. One hundred subjects had been diagnosed with polycystic ovarian disease. These parameters were similar to the causes of PCOD in the research subjects described by Amer SA et al. (2013) and Siefer DB et al. (2011).

According to the study's findings, 43% of the 400 participants were between the ages of 25 and 30, followed by 32% who were between the ages of 31 and 35, 20% who were older than 35, and 5% who were younger than 25. These findings were similar to those of research by Piouka A. et al. (2009) and Halawaty S. et al. (2010), whose authors also reported demographic information similar to the current study.

AMH levels were shown to be considerably greater in participants with polycystic ovarian disease when compared to the two study groups' mean age, BMI, and AMH levels (Group I) compared to subjects without PCOD (group II) with p<0.05. Additionally, the study's findings revealed a statistically significant inverse association between AMH and BMI levels in Group I (p=0.04).

However, group II's AMH levels and BMI did not correlate (p>0.05). These findings were in line with those of Freeman EW et al. (2007) and Jungheim ES et al. (2013), whose results for age, BMI, and AMH levels were similar to those of the current study.

The study's findings also revealed that the proportion of lean PCOD participants (those with a BMI of less than 25) was substantially greater than that of non-lean PCOD subjects (those with a BMI of more than 25 kg/m2).

The mean AMH levels were 11.16±2.62 ng/ml in lean PCOD patients and 10.09±4.24 ng/ml in non-lean PCOD subjects. However, with p>0.05, the difference was not statistically significant.

These results were consistent with those of Su Hi12 et al. and Teixeria J et al.13 in 2001, wherein the authors reported similar proportions of lean PCOD subjects (BMI <25) and non-lean PCOD subjects (BMI >25 kg/m2).

The current study concludes, within its constraints, that AMH and BMI levels in infertile females without PCOD do not significantly correlate. However, there is a strong negative relationship between blood AMH levels and BMI in females with PCOD.

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