Hum. Reprod. Advance Access originally published online on September 12, 2007
Human Reproduction 2007 22(11):3042; doi:10.1093/humrep/dem290
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Letters to the Editor |
Vascular endothelial growth factor production by circulating immune cells is elevated in ovarian hyperstimulation syndrome
Infertility and IVF Unit, Department of Obstetrics and Gynecology, Barzilai Medical Center, Ashkelon 78078, Israel
1 Correspondence address. Tel: +972-8-6745932/3; Fax: +972-8-6745134; E-mail: raoulo{at}barzi.health.gov.il
We read with interest the study by Kosaka et al. (2007)
, on vascular endothelial growth factor (VEGF) production by circulating immune cells in ovarian hyperstimulation syndrome (OHSS) patients. In this study, they demonstrated an elevated basal VEGF production by peripheral blood mononuclear cells of OHSS patients and concluded that their study provides ‘new evidence’ to suggest that circulating immune cells are involved in the pathogenesis of OHSS.
Surprisingly, our 10 years of research on controlled ovarian hyperstimulation, OHSS and systemic inflammation went unnoticed (Orvieto, 2004). In our studies, we have suggested that the hyperstimulated human ovaries produce and secrete factor/s, which cause OHSS, probably by activating a systemic inflammatory response. This notion was based on the similarity of vascular leak syndrome to the clinical picture of OHSS (Orvieto et al., 1995), the significantly higher cytokines' concentration in the follicular fluid at the time of oocyte retrieval in patients in whom OHSS subsequently developed (Orvieto and Ben Rafael, 1998), and the neutrophil and endothelial activations following hCG administration (Orvieto et al., 1999, 2000, 2001).
Moreover, due to the observed direct depressive effect of hCG on interleukin (IL)-2 production by human peripheral lymphocyte and mononuclear cells in vitro (Orvieto et al., 2003), we suggested that that hCG probably causes OHSS by stimulating the ovaries to produce and secrete a still unknown intermediate factor which causes the increase in capillary permeability, rather than by directly stimulating the peripheral lymphocytes and mononuclear cells to secrete IL-2.
Furthermore, in accordance with Kosaka et al. (2007), we also could not find any correlation between the inflammatory mediators and estradiol (E2) levels, which to our opinion, reinforces the ongoing debate on the role of E2 in the pathogenesis or prediction of OHSS (Orvieto, 2003).
References
Kosaka K, Fujiwara H, Yoshioka S, Fujii S. Vascular endothelial growth factor production by circulating immune cells is elevated in ovarian hyperstimulation syndrome. Hum Reprod (2007) 22:1647–1651.
Orvieto R. Prediction of OHSS—challenging the estradiol mitos. Hum Reprod (2003) 18:665–667.
Orvieto R. Controlled ovarian hyperstimulation—an inflammatory state. J Soc Gynecol Invest (2004) 11:424–426.[CrossRef][Web of Science][Medline]
Orvieto R, Ben-Rafael Z. Ovarian hyperstimulation syndrome: a new insight into an old enigma. J Soc Gynecol Invest (1998) 5:110–113.[Web of Science][Medline]
Orvieto R, Voliovitch I, Fishman P, Ben-Rafael Z. Interleukin-2 and ovarian hyperstimulation syndrome—a pilot study. Hum Reprod (1995) 10:24–27.
Orvieto R, Ben-Rafael Z, Abir R, Bar Hava I, Fisch B, Molad Y. Controlled ovarian hyperstimulation—a state of neutrophil activation. Am J Reprod Immunol (1999) 42:288–291.[Medline]
Orvieto R, Schwartz A, Bar Hava I, Abir R, Ashkenazi J, La-Marca A, Ben-Rafael Z. Controlled ovarian hyperstimulation—a state of endothelial activation. Am J Reprod Immunol (2000) 44:257–260.[Medline]
Orvieto R, Ben Rafael Z, Schwartz A, Abir R, Fisch B, La-Marca A, Bar-Hava I. Soluble L-selectin levels during controlled ovarian hyperstimulation. Gynecol Endocrinol (2001) 15:29–33.[Web of Science][Medline]
Orvieto R, Leites T, Abir R, Bar J, Yoeli R, Feldberg D, Fisch B. Interleukin-2 production in whole blood cell cultures of women undergoing controlled ovarian hyperstimulation for assisted reproductive technology cycles. Am J Reprod Immunol (2003) 50:220–223.[Medline]
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