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DOI 10.1111/j.1600-0897.2006.00424.x

Медицинская библиотека · American journal of reproductive immunology (New York, N.Y. : 1989) · 2006

Soluble CD40 ligand levels during controlled ovarian hyperstimulation--a possible culprit of systemic inflammation.

Orvieto Raoul, Schachter Benny, Yulzari-Roll Vered, La Marca Antonio, Bar Jacob, Fisch Benjamin

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Аннотация

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.

Для цитирования: Orvieto Raoul, Schachter Benny, Yulzari-Roll Vered, La Marca Antonio, Bar Jacob, Fisch Benjamin. Soluble CD40 ligand levels during controlled ovarian hyperstimulation--a possible culprit of systemic inflammation.. American journal of reproductive immunology (New York, N.Y. : 1989). 2006. DOI: 10.1111/j.1600-0897.2006.00424.x.

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