2-Methoxyoestradiol levels and placental catechol-O-methyltransferase expression in patients with late-onset preeclampsia

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Abstract

Purpose: Deficiencies in placental catechol-O-methyltransferase (COMT) and circulating 2-methoxyoestradiol (2-ME) have been shown to be related to early onset preeclampsia. The aim of this study was to investigate levels of 2-ME in the serum and urine of patients with late-onset preeclampsia and to compare those levels to those of normal pregnant women. In addition, we examined placental COMT expression in both groups. Methods: Fifteen patients with preeclampsia and 15 normal pregnant women were enrolled. 2-ME levels were evaluated by ELISA and placental COMT expression was examined by Western blot analysis. Results: 2-ME levels in serum [median 181.1 pg/mL, interquartile range (IQR) 119.6-244.3 vs. 61.2 pg/mL, IQR 12.0-133.7, respectively, p = 0.004] and urine (median 143.3 pg/mL, IQR 35.0-328.2 vs. 0.5 pg/mL, IQR 0.4-4.6, respectively, p < 0.001) were significantly increased in patients with late-onset preeclampsia compared to those in normal pregnant women at term. There was no significant difference in placental COMT expression between the two groups. Conclusion: Increased levels of 2-ME in patients with late-onset preeclampsia might be a product of a compensatory mechanism in patients with late-onset preeclampsia.

Original languageEnglish
Pages (from-to)881-886
Number of pages6
JournalArchives of Gynecology and Obstetrics
Volume287
Issue number5
DOIs
Publication statusPublished - 2013 May 1

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Catechol O-Methyltransferase
Pre-Eclampsia
Pregnant Women
Urine
Serum
2-methoxyestradiol
Western Blotting
Enzyme-Linked Immunosorbent Assay

Keywords

  • 2-Methoxyoestradiol
  • Catechol-O-methyltransferase
  • Placenta
  • Preeclampsia

ASJC Scopus subject areas

  • Obstetrics and Gynaecology

Cite this

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title = "2-Methoxyoestradiol levels and placental catechol-O-methyltransferase expression in patients with late-onset preeclampsia",
abstract = "Purpose: Deficiencies in placental catechol-O-methyltransferase (COMT) and circulating 2-methoxyoestradiol (2-ME) have been shown to be related to early onset preeclampsia. The aim of this study was to investigate levels of 2-ME in the serum and urine of patients with late-onset preeclampsia and to compare those levels to those of normal pregnant women. In addition, we examined placental COMT expression in both groups. Methods: Fifteen patients with preeclampsia and 15 normal pregnant women were enrolled. 2-ME levels were evaluated by ELISA and placental COMT expression was examined by Western blot analysis. Results: 2-ME levels in serum [median 181.1 pg/mL, interquartile range (IQR) 119.6-244.3 vs. 61.2 pg/mL, IQR 12.0-133.7, respectively, p = 0.004] and urine (median 143.3 pg/mL, IQR 35.0-328.2 vs. 0.5 pg/mL, IQR 0.4-4.6, respectively, p < 0.001) were significantly increased in patients with late-onset preeclampsia compared to those in normal pregnant women at term. There was no significant difference in placental COMT expression between the two groups. Conclusion: Increased levels of 2-ME in patients with late-onset preeclampsia might be a product of a compensatory mechanism in patients with late-onset preeclampsia.",
keywords = "2-Methoxyoestradiol, Catechol-O-methyltransferase, Placenta, Preeclampsia",
author = "Seol, {Hyun Joo} and Geum-Joon Cho and Oh, {Min Jeong} and Kim, {Hai Joong}",
year = "2013",
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language = "English",
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pages = "881--886",
journal = "Archives of Gynecology and Obstetrics",
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T1 - 2-Methoxyoestradiol levels and placental catechol-O-methyltransferase expression in patients with late-onset preeclampsia

AU - Seol, Hyun Joo

AU - Cho, Geum-Joon

AU - Oh, Min Jeong

AU - Kim, Hai Joong

PY - 2013/5/1

Y1 - 2013/5/1

N2 - Purpose: Deficiencies in placental catechol-O-methyltransferase (COMT) and circulating 2-methoxyoestradiol (2-ME) have been shown to be related to early onset preeclampsia. The aim of this study was to investigate levels of 2-ME in the serum and urine of patients with late-onset preeclampsia and to compare those levels to those of normal pregnant women. In addition, we examined placental COMT expression in both groups. Methods: Fifteen patients with preeclampsia and 15 normal pregnant women were enrolled. 2-ME levels were evaluated by ELISA and placental COMT expression was examined by Western blot analysis. Results: 2-ME levels in serum [median 181.1 pg/mL, interquartile range (IQR) 119.6-244.3 vs. 61.2 pg/mL, IQR 12.0-133.7, respectively, p = 0.004] and urine (median 143.3 pg/mL, IQR 35.0-328.2 vs. 0.5 pg/mL, IQR 0.4-4.6, respectively, p < 0.001) were significantly increased in patients with late-onset preeclampsia compared to those in normal pregnant women at term. There was no significant difference in placental COMT expression between the two groups. Conclusion: Increased levels of 2-ME in patients with late-onset preeclampsia might be a product of a compensatory mechanism in patients with late-onset preeclampsia.

AB - Purpose: Deficiencies in placental catechol-O-methyltransferase (COMT) and circulating 2-methoxyoestradiol (2-ME) have been shown to be related to early onset preeclampsia. The aim of this study was to investigate levels of 2-ME in the serum and urine of patients with late-onset preeclampsia and to compare those levels to those of normal pregnant women. In addition, we examined placental COMT expression in both groups. Methods: Fifteen patients with preeclampsia and 15 normal pregnant women were enrolled. 2-ME levels were evaluated by ELISA and placental COMT expression was examined by Western blot analysis. Results: 2-ME levels in serum [median 181.1 pg/mL, interquartile range (IQR) 119.6-244.3 vs. 61.2 pg/mL, IQR 12.0-133.7, respectively, p = 0.004] and urine (median 143.3 pg/mL, IQR 35.0-328.2 vs. 0.5 pg/mL, IQR 0.4-4.6, respectively, p < 0.001) were significantly increased in patients with late-onset preeclampsia compared to those in normal pregnant women at term. There was no significant difference in placental COMT expression between the two groups. Conclusion: Increased levels of 2-ME in patients with late-onset preeclampsia might be a product of a compensatory mechanism in patients with late-onset preeclampsia.

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