The precise mechanism for the preventive effect of progesterone on preterm delivery is unknown.
The hormone seems to decrease the risk of preterm uterine contractions, whereas no effect is seen once
labour is initiated. This may be the result of an inhibitory effect of progesterone on the amount of gap
junctions in the myometrium by suppression of genes for gap junction proteins [27]. Progesterone also
suppresses gene transcription for calcium channels and oxytocin receptors [27]. In addition, progesterone
has been suggested to be anti-inflammatory and inhibits cervical ripening by suppressing
proinflammatory cytokines, which reduces concentration of prostaglandins in the cervix [28]. In-vitro
studies suggest that lymphocytes exposed to progesterone during pregnancy produce progesteroneinduced
blocking factor, which is capable of blocking lymphocyte function. Furthermore, Norwitz
et al. [29] found that medroxyprogesterone acetate, a synthetic variant of the human hormone,
inhibited the plasminogen activator system in decidual cells. Progesterone may also have pregnancyprolonging
actions by inhibiting decidual activation, which is believed to be necessary for spontaneous
onset of labour. Luo et al. [30] showed that progesterone may inhibit apoptosis in fetal membranes and
thereby prevent rupture of membranes and preterm labour.
As the pathophysiology of preterm delivery is likely to be different in singleton and twin pregnancies,
results from singleton pregnancies may not be directly transferred to twin or higher order of
multiple pregnancies. Until 2007, only one randomised-controlled trial had investigated the effect of
progesterone treatment in twin pregnancies [31]. The frequency of preterm delivery among twin
pregnancies was not reduced, but sample size was small (77 women) and the power of the study was
less than 0.4 (preterm delivery was found in 30.9% in the study group versus 23.7% in the control
group). More importantly, treatment was initiated late in pregnancy (28–33 weeks) [31]. Several
randomised-controlled trials that have included women with twin pregnancies were planned and
carried out since 2003, and more than 10 randomised placebo-controlled trials have been published
to date examining the effect of progesterone treatment in women with twin pregnancies (Table 1)
[18,32–41].
The precise mechanism for the preventive effect of progesterone on preterm delivery is unknown.
The hormone seems to decrease the risk of preterm uterine contractions, whereas no effect is seen once
labour is initiated. This may be the result of an inhibitory effect of progesterone on the amount of gap
junctions in the myometrium by suppression of genes for gap junction proteins [27]. Progesterone also
suppresses gene transcription for calcium channels and oxytocin receptors [27]. In addition, progesterone
has been suggested to be anti-inflammatory and inhibits cervical ripening by suppressing
proinflammatory cytokines, which reduces concentration of prostaglandins in the cervix [28]. In-vitro
studies suggest that lymphocytes exposed to progesterone during pregnancy produce progesteroneinduced
blocking factor, which is capable of blocking lymphocyte function. Furthermore, Norwitz
et al. [29] found that medroxyprogesterone acetate, a synthetic variant of the human hormone,
inhibited the plasminogen activator system in decidual cells. Progesterone may also have pregnancyprolonging
actions by inhibiting decidual activation, which is believed to be necessary for spontaneous
onset of labour. Luo et al. [30] showed that progesterone may inhibit apoptosis in fetal membranes and
thereby prevent rupture of membranes and preterm labour.
As the pathophysiology of preterm delivery is likely to be different in singleton and twin pregnancies,
results from singleton pregnancies may not be directly transferred to twin or higher order of
multiple pregnancies. Until 2007, only one randomised-controlled trial had investigated the effect of
progesterone treatment in twin pregnancies [31]. The frequency of preterm delivery among twin
pregnancies was not reduced, but sample size was small (77 women) and the power of the study was
less than 0.4 (preterm delivery was found in 30.9% in the study group versus 23.7% in the control
group). More importantly, treatment was initiated late in pregnancy (28–33 weeks) [31]. Several
randomised-controlled trials that have included women with twin pregnancies were planned and
carried out since 2003, and more than 10 randomised placebo-controlled trials have been published
to date examining the effect of progesterone treatment in women with twin pregnancies (Table 1)
[18,32–41].
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