scholarly journals Inverse correlation between baseline inhibin B and FSH after stimulation with GnRH: a study of serum levels of inhibin A and B, pro alpha-C and activin A in women with ovulatory disturbances before and after stimulation with GnRH

2000 ◽  
pp. 77-84 ◽  
Author(s):  
FW Casper ◽  
RJ Seufert ◽  
K Pollow

OBJECTIVE: Interest has focused recently on the influences of the polypeptide factors inhibin and activin on the selective regulation of the pituitary secretion of gonadotropins. DESIGN: Measurement of the concentrations of inhibin-related proteins in relation to the changes in pituitary gonadotropin (FSH, LH) parameters, after GnRH stimulation with a bolus injection of 100 microg gonadorelin, in 19 women with ovulatory disturbances. METHODS: Serum levels of inhibin A and B, activin A, and pro alpha-C were measured using sensitive ELISA kits. RESULTS: Within 60 min after GnRH stimulation, FSH values doubled from 5 to 10 mU/ml (P < 0.001). LH increased 12-fold from 2 to 24 mU/ml (P < 0.001). Activin A showed a significant decrease from 0.47 to 0.36 ng/ml (P < 0.001), whereas pro alpha-C increased from 127 to 156 pg/ml (P = 0.039). The median inhibin A concentration did not show a significant change between baseline and the 60 min value, whereas inhibin B was characterized by a minor, but not significant, increase in the median from 168 to 179 pg/ml (P = 0.408). A significant inverse correlation (P = 0.014) with a mean coefficient of correlation of 0.5516 was found, demonstrating a strong relationship between high inhibin B baseline levels and a small increase of FSH after 60 min. CONCLUSION: Our results show an interesting correlation between the baseline inhibin B and the change in FSH before and after GnRH stimulation. A high baseline inhibin B implies only a minor increase of FSH after 60 min.

2001 ◽  
Vol 45 (3) ◽  
pp. 180-187 ◽  
Author(s):  
DANIEL YAIR ◽  
TALMA ESHED-ENGLENDER ◽  
MICHAEL J. KUPFERMINC ◽  
ELI GEVA ◽  
JENNY FRENKEL ◽  
...  
Keyword(s):  

2002 ◽  
pp. 785-793 ◽  
Author(s):  
NA Bersinger ◽  
N Groome ◽  
S Muttukrishna

OBJECTIVE: Pre-eclampsia is a placental disease of unknown cause. Maternal circulating concentrations of a number of protein markers are altered (mainly increased) in pre-eclampsia in comparison with controls of matched gestational age. Inhibin A and activin A were found to be elevated even before the onset of the disease. The aim of this study was to compare the levels of inhibin A, activin A: follistatin ratio, leptin, pregnancy-associated plasma protein-A (PAPP-A), human placental lactogen (HPL), placenta growth factor (PLGF) and pregnancy-specific beta1-glycoprotein (SP1) in placental extracts of normal pregnant women and pre-eclampsia patients at term. METHODS: Placental tissue from normal pregnancies (n=14) and patients with pre-eclampsia (n=13) were collected at term (> or =37 weeks of gestation) and stored at -80 degrees C. The frozen tissue pieces were homogenised and the above-mentioned proteins were measured by specific enzyme-linked immunosorbent assays. RESULTS: Placental contents of inhibin A and PAPP-A were significantly higher (P<0.05) in pre-eclampsia placental extracts compared with the controls. Activin A:follistatin ratio was higher (23) in pre-eclampsia extracts than in the controls (15). Leptin, PLGF, SP1 and HPL levels were not altered in the term pre-eclampsia placenta. Inhibin A and PAPP-A contents were increased in the placental extracts of pre-eclampsia patients. CONCLUSION: Our data suggest that the placenta, possibly by a compensatory mechanism, is at least in part responsible for the altered serum levels observed in pre-eclampsia.


1998 ◽  
Vol 13 (12) ◽  
pp. 3530-3536 ◽  
Author(s):  
P. A. Fowler ◽  
L. W. Evans ◽  
N. P. Groome ◽  
A. Templeton ◽  
P. G. Knight

2019 ◽  
Vol 104 (12) ◽  
pp. 6371-6384 ◽  
Author(s):  
Stine Gry Kristensen ◽  
Ajay Kumar ◽  
Bhanu Kalra ◽  
Susanne Elisabeth Pors ◽  
Jane Alrø Bøtkjær ◽  
...  

Abstract Context Members of the TGF-β family have been implicated in aberrant follicle development in women with polycystic ovaries (PCO). Objective Are there quantitative differences in the concentrations of TGF-β family members in fluid from human small antral follicles (hSAFs) in women with or without PCO? Design and Setting Follicle fluids (FFs) were collected from 4- to 11-mm hSAFs obtained from women undergoing ovarian tissue cryopreservation for fertility preservation. Patients FFs from 16 women with PCO (FF = 93) and 33 women without PCO (FF = 92). Main Outcome Measures Intrafollicular concentrations of growth differentiation factor-9 (GDF9); anti-Müllerian hormone (AMH); inhibin-A and inhibin-B; total inhibin; activin-A, activin-B, and activin-AB; follistatin; follistatin-like-3; estradiol; and testosterone. Results Activin-B concentrations were reported in hSAFs, and concentrations were 10 times higher than activin-A and activin-AB concentrations. Activin-B showed significant associations with other growth factors. Concentrations of inhibin-A and inhibin-B were significantly lower in FFs from women with PCO, especially in hSAFs <8 mm in diameter. AMH concentrations did not differ between the groups in hSAFs <8 mm; however, AMH remained high in hSAFs >8 mm in women with PCO but decreased in women without PCO. Estradiol was significantly lower in FFs from women with PCO and showed significant associations with AMH. Concentrations of GDF9 showed significantly higher concentrations in PCO FFs of follicles >6 mm. Conclusions Altered concentrations of TGF-β family members in hSAFs from women with PCO highlight altered growth factor signaling as a potential mechanism for follicle growth arrest.


2000 ◽  
Vol 85 (1) ◽  
pp. 270-274 ◽  
Author(s):  
F. Debieve ◽  
S. Beerlandt ◽  
C. Hubinont ◽  
K. Thomas

Using specific enzyme-linked immunosorbent assays we measured inhibin A, inhibin B, and activin A in relation to LH, FSH, and PRL in normal human fetal midpregnancy serum obtained by in utero cord venipuncture (n = 25) and compared 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 three midpregnancy males (3 of 14). Inhibin B, however, was detected in midpregnancy 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 between 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. PRL 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 midpregnancy vs. +0.445 at term. Serum from fetuses with intrauterine growth retardation or trisomy 21 did not show any different hormonal profiles. These data suggest that inhibin B is probably an additional factor in FSH inhibition at midpregnancy, whereas activin A is not associated with any change in the different studied populations. We speculate that inhibin A could be a method to detect maternal blood contamination in cord venipuncture.


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