Increased ENA-78 in the follicular fluid of patients with endometriosis

Background. It is known that endometriosis is an inflammatory disease and those patients seem to have lower pregnancy rates. The aim of the study was to investigate the concentrations of chemokines and proinflammatory cytokines in the follicular fluid of patients with and without endometriosis. Meth...

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Veröffentlicht in:Acta obstetricia et gynecologica Scandinavica 2006-01, Vol.85 (3), p.336-342
Hauptverfasser: Wunder, Dorothea M., Mueller, Michael D., Birkhäuser, Martin H., Bersinger, Nick A.
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Sprache:eng
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Zusammenfassung:Background. It is known that endometriosis is an inflammatory disease and those patients seem to have lower pregnancy rates. The aim of the study was to investigate the concentrations of chemokines and proinflammatory cytokines in the follicular fluid of patients with and without endometriosis. Methods. Follicular aspiration, recovering follicular fluid during assisted reproductive treatment, follicular fluid storage and analysis of chemokines and proinflammatory cytokines were carried out. Tumor necrosis factor- , interleukin-1 , interleukin-6, interleukin-8, interleukin-15, leukemia inhibitory factor, epithelial neutrophil-activating peptide 78, regulated upon activation, normal T-cell expressed and secreted, and growth-regulated oncogene- were analyzed in the follicular fluid and compared between women with (n=47) and without endometriosis (n=279). Results. The above cytokines were detected in the follicular fluid samples. Epithelial neutrophil-activating peptide 78 levels were significantly higher in follicular fluid from endometriosis patients than from controls (p=0.008). Increases (to twice the control level) were also observed for tumor necrosis factor- and for interleukin-6. Conclusions. Increased follicular fluid levels of epithelial neutrophil-activating peptide 78, tumor necrosis factor- and interleukin-6 indicate that these cytokines may influence oocyte quality and fecundability of women with endometriosis by deteriorating the microenvironment in the human follicle.
ISSN:0001-6349
1600-0412
DOI:10.1080/00016340500501715