Serum Inhibin Levels in Polycystic Ovary Syndrome: Basal Levels and Response to Luteinizing Hormone-Releasing Hormone Agonist and Exogenous Gonadotropin Administration*

Abstract

Serum inhibin levels were measured by RIA twice weekly for 4 weeks in 5 women with the polycystic ovary syndrome (PCOS). These were compared to those in 10 women with normal menstrual cycles. Serum inhibin levels were similar in the 5 PCOS women (mean, 199; range, 126-266 U/L) and were not significantly different from those in the normal women during the early follicular phase (227; 100-485 U/L) or midfollicular phase (243; 143-412 U/L) of their cycles. Inhibin levels were higher (P less than 0.001) in the late follicular phase (408; 227-732 U/L), at midcycle (623; 367-1058 U/L), and during the midluteal phase (1245; 898-1727 U/L) in the normal women compared to those in the PCOS group. Serum inhibin levels were also measured in PCOS (n = 8) and infertile (n = 14) women after the rise and subsequent diminished gonadotropin secretion that occurred during LHRH agonist administration. In both groups, serum LH and FSH increased after initiation of LHRH agonist administration; this increase was accompanied by parallel rises in serum estradiol and inhibin before suppression (PCOS women: r = 0.71; P less than 0.001; n = 108; infertile women: r = 0.42; P less than 0.05; n = 163). All hormone levels, including inhibin, decreased during continued LHRH administration. Five PCOS women underwent ovulation induction using combined LHRH agonist and human menopausal gonadotropin administration. Serum estradiol and inhibin rose in parallel in response to exogenous gonadotropins (r = 0.92; P less than 0.001; n = 77). In conclusion, we found no evidence of a primary defect in ovarian inhibin physiology in women with PCOS in terms of either basal or gonadotropin-stimulated (exogenous or endogenous) secretion.

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

“…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.…”

“…Decreased inhibin concentrations during the midluteal phase may be at least in part responsible for impaired corpus luteum function often present in PCOS. However, to the best of our knowledge, only total immunoreactive inhibin levels have been compared in the second half of the menstrual cycle between PCOS patients and normal controls [12].…”

Serum α-Inhibin Levels in Polycystic Ovary Syndrome: Relationship to the Serum Androstenedione Level1

“…Some studies have evaluated the hypothesis that the endocrine or paracrine influence of inhibin might be enhanced in PCOS. However, these studies were performed by measuring either ␣-inhibin or dimeric inhibin, and generally did not find a difference in serum inhibin levels between control women and PCOS patients (25)(26)(27), with one exception (28). In these studies no relationship between either serum androgen or FSH and inhibin levels in PCOS women was noted.…”

Changes in Serum Immunoreactive Inhibin during Ovulation Induction in Women with Amenorrhea.

“…E2 during ovulation induction in normal women [7][8][9] or women with polycystic ovarian syndrome [10], and indeed a significant correlation between the two hormones was shown in women undergoing ovulation induction by pFSH [15]. However these findings were obtained under conditions where the effect of endogenous LH was present.…”

“…Both hormones are produced and released by the granulosa cells during the menstrual cycle [3][4][5][6]. In fact a parallel increase in the two hormones in response to exogenous gonadotropin has been demonstrated in normal women [7][8][9] and in amenorrheic women with polycystic ovarian disease (PCOD) [10]. These reports indicate that measurement of inhibin can be a useful marker for evaluating granulosa cell function [6] or predicting the clinical outcome of the treatment [7][8][9], but there is still a lack of knowledge of inhibin secretion during ovulation induction.…”