Induction of delayed follicular rupture in the human by the selective COX-2 inhibitor rofecoxib: a randomized double-blind study

M. Pall
In: Human Reproduction · 2001 · vol. 16(7) , pp. 1323–1328 · doi:10.1093/humrep/16.7.1323 · PMID:11425807 · W2109760209
article OA: bronze CC0 ⤵ 13 in-corpus citations
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This randomized double-blind study found that periovulatory administration of the selective COX-2 inhibitor rofecoxib delayed follicular rupture in women without affecting peripheral hormonal cyclicity.

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Abstract

BACKGROUND: The aims of the present study were to examine whether periovulatory administration of a cyclo-oxygenase (COX)-2 inhibitor affects human ovulation and endocrine parameters. METHODS: Thirteen healthy women, 30-40 years of age, without hormonal treatment and with regular menstrual cycles (27-34 days), were given the selective COX-2 inhibitor rofecoxib (n = 6) or placebo (n = 7) in a random double-blind fashion. In an initial control cycle, serial hormonal analyses, detection of a measurable mid-cycle urine LH peak and transvaginal ultrasound scans were performed to confirm normal ovulatory and endocrinological cyclic patterns, in all participating women. During the subsequent treatment cycle, serial ultrasound scans were performed. When the dominant follicle reached 14-16 mm in diameter, 25 mg rofecoxib or placebo was taken orally, once daily for 9 consecutive days, during which follicle size was monitored daily by ultrasound scans and serial hormone analyses were performed. RESULTS: Four of the six women who received rofecoxib demonstrated delayed follicle rupture, >48 h after the LH peak, when compared with the placebo group, who all had follicular rupture >36 h after the detected LH peak. No differences in peripheral serum concentrations of progesterone, oestradiol, LH and FSH were observed between placebo and rofecoxib groups, when analysed at specified time intervals. CONCLUSIONS: This study suggests that selective COX-2 inhibition has a negative, local effect on human ovulation, resulting in delayed follicular rupture, without affecting peripheral hormonal cyclicity.

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