F. Debieve et al., Gonadotropins, prolactin, inhibin A, inhibin B, and activin A in human fetal serum from midpregnancy and term pregnancy, J CLIN END, 85(1), 2000, pp. 270-274
Using specific enzyme-linked immunosorbent assays we measured inhibin A, in
hibin B, and activin A in relation to LH, FSH, and PRL in normal human feta
l midpregnancy serum obtained by in utero cord venipuncture (n = 25) and co
mpared these results to those in fetal serum from term pregnancies (n = 23)
. We also tested serum from fetuses with intrauterine growth retardation (n
= 6) or trisomy 21 (n = 6). We found no measurable inhibin A, except in th
ree midpregnancy males (3 of 14). Inhibin B, however, was detected in midpr
egnancy male fetuses (167 +/- 67 pg/mL) and was higher than that in females
(16 +/- 12 pg/mL). It was present in male term fetuses (125 +/- 32 pg/mL),
but not in females. The activin A levels did not significantly differ betw
een term and midpregnancy males and females.
LH and FSH were detected in midpregnancy male fetuses (4.4 +/- 3.3 and 0.77
+/- 0.49 mIU/mL, respectively), with higher levels in females (33.0 +/- 23
.2 and 54.4 +/- 27.7 mIU/mL, respectively), and were suppressed at term. PR
L did not exhibit sexual difference, but showed a higher level at term (322
.4 +/- 113.8 ng/mL) than at midpregnancy (33.0 +/- 26.1 ng/mL). Comparison
of inhibin B with FSH levels showed correlation coefficients of -0.565 at m
idpregnancy vs. + 0.445 at term. Serum from fetuses with intrauterine growt
h retardation or trisomy 21 did not show any different hormonal profiles.
These data suggest that inhibin B is probably an additional factor in FSH i
nhibition at midpregnancy, whereas activin A is not associated with any cha
nge in the different studied populations. We speculate that inhibin A could
be a method to detect maternal blood contamination in cord venipuncture.