TY - JOUR
T1 - Serum inhibin A, VEGF and TNFα levels after triggering oocyte maturation with GnRH agonist compared with HCG in women with polycystic ovaries undergoing IVF treatment
T2 - A prospective randomized trial
AU - Babayof, Rachel
AU - Margalioth, Ehud J.
AU - Huleihel, Mahmoud
AU - Amash, Alaa
AU - Zylber-Haran, Edit
AU - Gal, Michael
AU - Brooks, Baruch
AU - Mimoni, Tzvia
AU - Eldar-Geva, Talia
PY - 2006/1/1
Y1 - 2006/1/1
N2 - Background: We aimed to examine the serum levels of inhibin A, vascular endothelial growth factor (VEGF), tumour necrosis factor α (TNFα), estradiol (E2) and progesterone levels after triggering of final oocyte maturation with GnRH agonist compared with HCG in patients with polycystic ovaries (PCO) and to investigate the relationship between these markers and ovarian hyperstimulation syndrome (OHSS). Methods: Twenty-eight patients with PCO, undergoing controlled ovarian hyperstimulation with FSH and GnRH antagonist for IVF-embryo transfer treatment, were randomized for triggering of final oocyte maturation with GnRH agonist (GnRH agonist group, n = 15) or HCG (HCG group, n = 13). Blood samples were obtained on the day of randomization and thereafter every 2-7 days. Serum levels of inhibin A, VEGF, TNFα, E2 and progesterone, the incidence of OHSS, ovarian size and pelvic fluid accumulation were evaluated. Results: Serum inhibin A, E2 and progesterone levels were significantly lower in the GnRH agonist group compared with the HCG group, particularly on the day of embryo transfer (P < 0.0001). Serum VEGF and TNFα levels were similar between the two groups. Four patients in the HCG group developed severe OHSS, whereas no patient had any symptoms or signs of OHSS in the GnRH-agonist group (P < 0.05). Conclusions: In patients with PCO treated with FSH/GnRH antagonist, final oocyte maturation with GnRH agonist instead of HCG reduces significantly inhibin A, E2 and progesterone levels during the luteal phase. This phenomenon reflects the inhibition of the corpus luteum function and may explain, at least in part, the mechanism of OHSS prevention in high-risk patients. Our results do not support a crucial role for VEGF or TNFα in OHSS.
AB - Background: We aimed to examine the serum levels of inhibin A, vascular endothelial growth factor (VEGF), tumour necrosis factor α (TNFα), estradiol (E2) and progesterone levels after triggering of final oocyte maturation with GnRH agonist compared with HCG in patients with polycystic ovaries (PCO) and to investigate the relationship between these markers and ovarian hyperstimulation syndrome (OHSS). Methods: Twenty-eight patients with PCO, undergoing controlled ovarian hyperstimulation with FSH and GnRH antagonist for IVF-embryo transfer treatment, were randomized for triggering of final oocyte maturation with GnRH agonist (GnRH agonist group, n = 15) or HCG (HCG group, n = 13). Blood samples were obtained on the day of randomization and thereafter every 2-7 days. Serum levels of inhibin A, VEGF, TNFα, E2 and progesterone, the incidence of OHSS, ovarian size and pelvic fluid accumulation were evaluated. Results: Serum inhibin A, E2 and progesterone levels were significantly lower in the GnRH agonist group compared with the HCG group, particularly on the day of embryo transfer (P < 0.0001). Serum VEGF and TNFα levels were similar between the two groups. Four patients in the HCG group developed severe OHSS, whereas no patient had any symptoms or signs of OHSS in the GnRH-agonist group (P < 0.05). Conclusions: In patients with PCO treated with FSH/GnRH antagonist, final oocyte maturation with GnRH agonist instead of HCG reduces significantly inhibin A, E2 and progesterone levels during the luteal phase. This phenomenon reflects the inhibition of the corpus luteum function and may explain, at least in part, the mechanism of OHSS prevention in high-risk patients. Our results do not support a crucial role for VEGF or TNFα in OHSS.
KW - GnRH agonist
KW - Inhibin A
KW - OHSS
KW - PCOS
KW - TNFα
UR - http://www.scopus.com/inward/record.url?scp=33645847254&partnerID=8YFLogxK
U2 - 10.1093/humrep/dei475
DO - 10.1093/humrep/dei475
M3 - Article
AN - SCOPUS:33645847254
SN - 0268-1161
VL - 21
SP - 1260
EP - 1265
JO - Human Reproduction
JF - Human Reproduction
IS - 5
ER -