A nonhormonal model for emergency contraception: prostaglandin synthesis inhibitor effects on luteal function and lifespan, a pilot study

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Abstract

Objectives: The purpose of this study is to determine if the use of a specific prostaglandin endoperoxide-2 inhibitor will prevent luteal development in women. Study Design: Ovulatory reproductive-aged women not using or needing hormonal contraception were prospectively followed for three menstrual cycles. Women were randomized into two groups using a crossover design [Group 1: control cycle, placebo cycle, active drug (celecoxib 400 mg orally) cycle; Group 2: control cycle, celecoxib cycle, placebo cycle]. Study drug was dosed daily until the onset of the next menses. Demographics, menstrual cycle length and twice-weekly progesterone (P) levels during the placebo and active drug cycles were recorded. End points included the change in luteal phase P levels and menstrual cycle length (days) during active drug exposure. Results: A total of 11 women completed the study (Group 1, n=7; Group 2, n=4). No demographic differences were found between groups [age, race, body mass index (BMI), control cycle length]. A comparison of the control and active drug cycles for all participants demonstrated a trend toward a longer menstrual cycle with active drug exposure [control, 27.2 days (SD, 2.4); study drug, 28.5 days (SD, 2.5), p=.09]. Five women had a delay in the rise of their luteal phase P levels, two women had lower peak P levels and two women had no elevation of luteal phase P levels during active drug cycle as compared to placebo cycle. Conclusion: Daily administration of a prostaglandin synthesis inhibitor may delay the timing of luteal events and, therefore, fertility in women. PTGS2 inhibitors may hold potential as an emergency contraceptive.

Original languageEnglish (US)
Pages (from-to)496-500
Number of pages5
JournalContraception
Volume81
Issue number6
DOIs
StatePublished - Jun 2010

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Postcoital Contraception
Prostaglandin Antagonists
Corpus Luteum
Celecoxib
Menstrual Cycle
Luteal Phase
Placebos
Pharmaceutical Preparations
Drug and Narcotic Control
Prostaglandin Endoperoxides
Postcoital Contraceptives
Demography
Control Groups
Menstruation
Cyclooxygenase 2
Contraception
Cross-Over Studies
Progesterone
Fertility
Body Mass Index

Keywords

  • COX2 inhibitor
  • Emergency contraception
  • Prostaglandin inhibitor
  • PTGS2 inhibitor

ASJC Scopus subject areas

  • Reproductive Medicine
  • Obstetrics and Gynecology

Cite this

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title = "A nonhormonal model for emergency contraception: prostaglandin synthesis inhibitor effects on luteal function and lifespan, a pilot study",
abstract = "Objectives: The purpose of this study is to determine if the use of a specific prostaglandin endoperoxide-2 inhibitor will prevent luteal development in women. Study Design: Ovulatory reproductive-aged women not using or needing hormonal contraception were prospectively followed for three menstrual cycles. Women were randomized into two groups using a crossover design [Group 1: control cycle, placebo cycle, active drug (celecoxib 400 mg orally) cycle; Group 2: control cycle, celecoxib cycle, placebo cycle]. Study drug was dosed daily until the onset of the next menses. Demographics, menstrual cycle length and twice-weekly progesterone (P) levels during the placebo and active drug cycles were recorded. End points included the change in luteal phase P levels and menstrual cycle length (days) during active drug exposure. Results: A total of 11 women completed the study (Group 1, n=7; Group 2, n=4). No demographic differences were found between groups [age, race, body mass index (BMI), control cycle length]. A comparison of the control and active drug cycles for all participants demonstrated a trend toward a longer menstrual cycle with active drug exposure [control, 27.2 days (SD, 2.4); study drug, 28.5 days (SD, 2.5), p=.09]. Five women had a delay in the rise of their luteal phase P levels, two women had lower peak P levels and two women had no elevation of luteal phase P levels during active drug cycle as compared to placebo cycle. Conclusion: Daily administration of a prostaglandin synthesis inhibitor may delay the timing of luteal events and, therefore, fertility in women. PTGS2 inhibitors may hold potential as an emergency contraceptive.",
keywords = "COX2 inhibitor, Emergency contraception, Prostaglandin inhibitor, PTGS2 inhibitor",
author = "Alison Edelman and Jeffrey Jensen and Jon Hennebold",
year = "2010",
month = "6",
doi = "10.1016/j.contraception.2010.01.004",
language = "English (US)",
volume = "81",
pages = "496--500",
journal = "Contraception",
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number = "6",

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T2 - prostaglandin synthesis inhibitor effects on luteal function and lifespan, a pilot study

AU - Edelman, Alison

AU - Jensen, Jeffrey

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PY - 2010/6

Y1 - 2010/6

N2 - Objectives: The purpose of this study is to determine if the use of a specific prostaglandin endoperoxide-2 inhibitor will prevent luteal development in women. Study Design: Ovulatory reproductive-aged women not using or needing hormonal contraception were prospectively followed for three menstrual cycles. Women were randomized into two groups using a crossover design [Group 1: control cycle, placebo cycle, active drug (celecoxib 400 mg orally) cycle; Group 2: control cycle, celecoxib cycle, placebo cycle]. Study drug was dosed daily until the onset of the next menses. Demographics, menstrual cycle length and twice-weekly progesterone (P) levels during the placebo and active drug cycles were recorded. End points included the change in luteal phase P levels and menstrual cycle length (days) during active drug exposure. Results: A total of 11 women completed the study (Group 1, n=7; Group 2, n=4). No demographic differences were found between groups [age, race, body mass index (BMI), control cycle length]. A comparison of the control and active drug cycles for all participants demonstrated a trend toward a longer menstrual cycle with active drug exposure [control, 27.2 days (SD, 2.4); study drug, 28.5 days (SD, 2.5), p=.09]. Five women had a delay in the rise of their luteal phase P levels, two women had lower peak P levels and two women had no elevation of luteal phase P levels during active drug cycle as compared to placebo cycle. Conclusion: Daily administration of a prostaglandin synthesis inhibitor may delay the timing of luteal events and, therefore, fertility in women. PTGS2 inhibitors may hold potential as an emergency contraceptive.

AB - Objectives: The purpose of this study is to determine if the use of a specific prostaglandin endoperoxide-2 inhibitor will prevent luteal development in women. Study Design: Ovulatory reproductive-aged women not using or needing hormonal contraception were prospectively followed for three menstrual cycles. Women were randomized into two groups using a crossover design [Group 1: control cycle, placebo cycle, active drug (celecoxib 400 mg orally) cycle; Group 2: control cycle, celecoxib cycle, placebo cycle]. Study drug was dosed daily until the onset of the next menses. Demographics, menstrual cycle length and twice-weekly progesterone (P) levels during the placebo and active drug cycles were recorded. End points included the change in luteal phase P levels and menstrual cycle length (days) during active drug exposure. Results: A total of 11 women completed the study (Group 1, n=7; Group 2, n=4). No demographic differences were found between groups [age, race, body mass index (BMI), control cycle length]. A comparison of the control and active drug cycles for all participants demonstrated a trend toward a longer menstrual cycle with active drug exposure [control, 27.2 days (SD, 2.4); study drug, 28.5 days (SD, 2.5), p=.09]. Five women had a delay in the rise of their luteal phase P levels, two women had lower peak P levels and two women had no elevation of luteal phase P levels during active drug cycle as compared to placebo cycle. Conclusion: Daily administration of a prostaglandin synthesis inhibitor may delay the timing of luteal events and, therefore, fertility in women. PTGS2 inhibitors may hold potential as an emergency contraceptive.

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