Determination of endometrial prolactin in vivo as a marker for endometrialdevelopment in spontaneous ovulatory cycles and in vitro fertilization cycles
Jjml. Dekker et al., Determination of endometrial prolactin in vivo as a marker for endometrialdevelopment in spontaneous ovulatory cycles and in vitro fertilization cycles, GYNECOL END, 15(3), 2001, pp. 210-218
Decidual prolactin was directly determined in endometrial tissue in order t
o assess its potential role in improving the accuracy of the diagnosis of l
uteal-phase defect (LPD). Endometrial biopsies of 124 women with regular cy
cles (group 1) and 13 women with controlled ovarian hyperstimulation and pr
ogesterone-supported cycles (group 2) were evaluated in the secretory phase
. In addition, decidual prolactin was measured in the luteal phase of the i
n vitro fertilization (IVF) cycles. The biopsies dated on or after day 25 s
howed a significant increase in the slope of the regression line of the cyc
le day versus decidual prolactin content (p < 0.05). Delayed endometrium wa
s not characterized by a lower amount of decidual prolactin compared with b
iopsies with the same histological dating. On day 27 of the cycle, less pro
lactin was measured in the out-of-phase biopsies (p < 0.05). A large inter-
individual variation in endometrial prolactin tissue content was noticed. I
n group 2 all biopsies but one were in phase. Compared to the in-phase biop
sies of group 1, a significantly higher amount of prolactin was found in gr
oup 2.
Production of endometrial prolactin in vivo is associated with decidualizat
ion of the stromal cells. However, because of the large inter-individual va
riation, determination of prolactin is not of adjuvant diagnostic value for
clinical assessment of LPD. Three factors might explain the higher amount
of decidual prolactin in group 2 compared to group 1: (2) a higher serum pr
ogesterone concentration owing to an increased production by multiple corpo
ra lutea, or because of the administered progesterone; (2) increased estrad
iol levels and thus progesterone receptors; and (3) direct stimulation of d
ecidualization by gonadotropins.