BACKGROUND: We aimed to assess whether lipiodol alters endometrial gene expression through a uterine bathing effect that might enhance receptivity to embryo implantation. METHODS: An open-label randomised controlled trial design in a single-centre tertiary infertility service. Twelve women with endometriosis (n [Formula: see text] 11) or previous successful lipiodol procedure (n [Formula: see text] 1) were randomised to receive immediate or delayed lipiodol hysterosalpingography, followed by endometrial biopsy. Endometrial samples were assessed for gene expression, using Affymetrix microarrays and validation studies using reverse transcriptase quantitative polymerase chain reaction analysis. Subsequent endometrial gene expression responses to treatment and clinical fertility outcomes were assessed. RESULTS: Eleven of 12 women had successful endometrial sampling procedures. Nine women had successful pregnancies within the 9-month follow-up phase. Following lipiodol bathing we identified 20 down-regulated and 13 up-regulated genes with p [Formula: see text] 0.05 and with magnitude of change [Formula: see text]1.5-fold in at least three of the four women, with osteopontin being the only gene down-regulated in all four women. CONCLUSIONS: This study supports the concept of a uterine bathing effect of lipiodol altering endometrial biology and gene expression. Whether regulation of inflammation and immune response pathways by lipiodol might contribute to an increase in endometrial receptivity to embryo implantation merits further investigation.
BACKGROUND: Lipiodol has a dramatic short term fertility enhancing effect for women with endometriosis. Microarray studies have shown transcriptomic regulation of molecular markers of endometrial inflammation, most notably a consistent down-regulation of endometrial osteopontin. We further explored the endometrial bathing effect of lipiodol on leukocyte expression in endometrium. METHODS: A cohort of four women, nested within a randomised trial of twelve women assessing the lipiodol uterine bathing effect, was studied as an ‘own control’ group, with their mid-luteal endometrium assessed before and after endometrial lipiodol exposure. Pipelle endometrial sampling allowed endometrial assessment by immunochemistry. Endometrial tissue samples were assessed by immunochemistry for total CD45+ leukocytes, CD68+ macrophages, CD3+ T-cells and CD56+ uterine natural killer cells. RESULTS: There was a statistically significant increase in the mean density of uterine natural killer cells in the endometrium of women post-lipiodol. No other significant differences were found in the mean densities of all leukocytes, macrophages or T cells in the endometrium of women post-lipiodol. CONCLUSIONS: These preliminary data further support the concept of a uterine bathing effect of lipiodol. Whether the increase in the mean density of uterine natural killer cells in the endometrium might contribute to an improvement in endometrial receptivity to embryo implantation merits further investigation.
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