Absent biologically relevant associations between serum inhibin B concentrations and characteristics of polycystic ovary syndrome in normogonadotrophic anovulatory infertility

Abstract

In conclusion, inhibin B serum concentrations are normal in WHO 2 and PCOS women, suggesting a normal number of healthy early antral follicles despite increased overall follicle numbers in PCOS.

Luteal-phase inhibin A and follicular-phase inhibin B levels are not characteristic of patients with an elevated LH-to-FSH ratio

“…It was previously shown that, similar to ovaries of healthy women, inhibin B is the predominant form of inhibin in the follicular fluid of polycystic ovaries and each individual follicle in PCOS produces a similar amount of inhibin B to that secreted by small antral follicles in normally cycling women [10]. Taken together with the fact that we found similar serum concentrations of inhibin B in the early follicular phase in ELF patients and controls, which is in line with the results of previous reports [1,13], this suggests certain mechanisms within the follicles that concentrate and sequester hormones in the follicular fluid. The idea of individual hormone-dependent transport mechanisms is further corroborated by the finding that the ratio between follicular fluid and serum levels is different for E 2 , inhibin A, and inhibin B [7].…”

“…Some authors reported raised concentrations of total immunoreactive inhibins [19], α-inhibin [9,13] or inhibin B [20,21,22], supporting the above hypotheses, while others observed normal levels of total immunoreactive inhibin [12] or inhibin B [1,10,13,23] in the early follicular phase.…”

“…Instead, the role of LH in deficient production of inhibin subunits through premature luteinization and inhibition of proliferation seems plausible. despite an increased total number of follicles in PCOS [1,13,15,16,28]. Inhibin B levels have been shown to be inversely related to BMI [13,15,16] and a positive correlation has been demonstrated with serum LH levels [15,16].…”

“…Chronic anovulation is a major cause of infertility, with approximately 80% of anovulatory patients presenting with normal FSH concentrations [1]. The most common cause of normogonadotropic normoestrogenic ovulatory disorders (constituting the so-called WHO 2 group) is polycystic ovary syndrome (PCOS), characterized by chronic anovulation, hyperandrogenism [2], and often by hyperinsulinemia [3].…”

“…Recent studies have reported an inverse correlation between inhibin B levels and body mass index (BMI) in PCOS, suggesting a role of some factor responsible for decreased inhibin B levels observed in obese PCOS patients [1,13,14]. More recently, it was shown that the negative effect of obesity on inhibin B levels is not specific to PCOS [15], and it was demonstrated by an interventional study that insulin is involved in the negative regulation of inhibin B secretion [16], which is in line with reports on the resumption of follicular growth and ovulation that occur with the use of insulin-lowering agents [17,18].…”