Premium
Soluble CD40 Ligand Levels during Controlled Ovarian Hyperstimulation – A Possible Culprit of Systemic Inflammation
Author(s) -
Orvieto Raoul,
Schachter Benny,
YulzariRoll Vered,
Marca Antonio La,
Bar Jacob,
Fisch Benjamin
Publication year - 2006
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/j.1600-0897.2006.00424.x
Subject(s) - ovarian hyperstimulation syndrome , human chorionic gonadotropin , androstenedione , medicine , gonadotropin , endocrinology , testosterone (patch) , controlled ovarian hyperstimulation , ovulation induction , ovary , ovulation , in vitro fertilisation , hormone , biology , pregnancy , androgen , genetics
Aim To investigate the behavior and association of serum sex‐steroids and serum CD40 ligand in patients undergoing controlled ovarian hyperstimulation (COH) for in vitro fertilization (IVF). Design Prospective, observational study. Setting The IVF unit of an academic medical center. Patients and methods Blood was drawn three times during the COH cycle from 17 patients undergoing the long gonadotropin‐releasing hormone‐analog protocol: (i) day on which adequate suppression was obtained (Day‐S); (ii) day of or prior to administration of human chorionic gonadotropin (Day‐hCG); and (iii) day of ovum pick‐up (Day‐OPU). Levels of sex steroids and serum CD40 ligand were compared among the three time points. Results During gonadotropin treatment, serum ovarian sex steroids (estradiol, progesterone, free testosterone and androstenedione) significantly increased while CD40 ligand levels nonsignificantly decreased. After hCG administration, there was a significant increase in the levels of serum CD40 ligand, ovarian androgens, and progesterone, with a significant decrease in estradiol levels. No correlations were observed between CD40 ligand and ovarian sex‐steroid levels or other treatment variables. Conclusion The administration of hCG leads to activation of systemic inflammation, as reflected by CD40 ligand levels. This, in turn, may lead to the development of ovarian hyperstimulation syndrome via several mechanisms, including an increase in several angiogenic factors.