Serum inhibin levels in XXXX : basal levels and response to luteinizing hormone-releasing hormone agonist and exogenous gonadotropin administration.

@entity1 @entity3610 @entity249 @entity53
Serum inhibin levels were measured by RIA twice weekly for 4 weeks in 5 @entity1 with the @entity3610 ( @entity3610 ). These were compared to those in 10 @entity1 with normal menstrual cycles. Serum inhibin levels were similar in the 5 @entity3610 @entity1 (mean, 199; range, 126-266 U/L) and were not significantly different from those in the normal @entity1 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 @entity1 compared to those in the @entity3610 group. Serum inhibin levels were also measured in @entity3610 (n = 8) and @entity249 (n = 14) @entity1 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 @entity53 and inhibin before suppression ( @entity3610 @entity1 : r = 0.71; P less than 0.001; n = 108; @entity249 @entity1 : r = 0.42; P less than 0.05; n = 163). All hormone levels, including inhibin, decreased during continued LHRH administration. Five @entity3610 @entity1 underwent ovulation induction using combined LHRH agonist and @entity1 menopausal gonadotropin administration. Serum @entity53 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 @entity1 with @entity3610 in terms of either basal or gonadotropin-stimulated (exogenous or endogenous) secretion.
