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Insulin-Like Growth Factor Binding Protein-1 and Glycodelin Levels in Uterine Flushing Before and after Hysteroscopic Polypectomy by Manal M. Elbehery, Amal A. Nouh, Mohamed L. Mohamed, Amal A. Alanwar, Somia H. Abd-Allah, Sally M. Shalaby

Background: Endometrial polyps are one of the most common endometrial abnormalities and it may be associated with infertility and early pregnancy loss. The aim of this study was to investigate the levels of insulin-like growth factor 1 binding protein (IGFBP-1) and glycodelin levels in uterine flushings before and after hysteroscopic polypectomy.
Methods: Two-hundred fifty non pregnant women participated in this prospective interventional study. One-hundred women with a complaint of infertility had endometrial polyps diagnosed by two-dimensional ultrasound scan and confirmed by transvaginal sonohysterography were prepared for hysteroscopic polypectomy, and 150 women with a history of menorrhagia not responding to medical treatment were prepared for hysteroscopic endometrial biopsy. Paired samples of uterine flushings were taken from all patients prior to and post hysteroscopic intervention at the midluteal phase. Insulin-like growth factor binding protein-1 was analyzed using an immunoradio-metric assay. Enzyme-linked immunoassays were performed to analyze glycodelin. Glycodelin and IGFBP-1 levels were compared in both groups prior to and post hysteroscopic intervention.
Results: The glycodelin and IGFBP-1 levels are significantly lower in patients with uterine polyps than in patients having menorrhagia preoperatively (p <0.001 for each). In patients with uterine polyps, both glycodelin and IGFBP-1 were significantly increased postoperatively (p <0.001 for each), while no significant changes in their values were noted postoperatively in patients with menorrhagia undergoing endometrial biopsy.
Conclusions: Decreased levels of mid-secretory IGFBP-1 and glycodelin were associated with the presence of endometrial polyps and both were reversed following hysteroscopic polypectomy. This could explain the pathophysiological mechanisms by which endometrial receptivity is impaired in the presence of endometrial polyps.

DOI: Clin. Lab. 2011;57:953-957