Is Dinoprostone Safe in Breastfeeding

I am a breastfeeding mother and i want to know if it is safe to use Dinoprostone? Is Dinoprostone safe for nursing mother and child? Does Dinoprostone extracts into breast milk? Does Dinoprostone has any long term or short term side effects on infants? Can Dinoprostone influence milk supply or can Dinoprostone decrease milk supply in lactating mothers?

Prostaglandin E2 is eventually used for induction of labor at term. Orally or vaginally administrated. At latest update no published data on excretion into breast milk were found.Pharmacokinetic data (very rapid removal and moderately high protein binding capacity) make it highly unlikely the passage into breast milk in significant amounts.It is a natural component of breast milk (Alzina 1986 Neu 1988) that increases in concentration in the first week postpartum (Hawkes 1999) and possibly plays an important role in the gastrointestinal function of the infant (Bedrick 1989, Shimizu 1992) and intestinal motility (Lucas 1980, Li 1994). Although dinoprostone can be used to inhibit lactation by reducing prolactin levels (Bremme 1980, England 1988, Toppozada 1992), it would be necessary to achieve a higher dose than that used at the time of partum for several days (Berić 1992). It would not be recommended to use it for relief of breast engorgement in women who are willing to breastfeed.The effect of reducing prolactin levels induced by dinoprostone only occurs during the first days postpartum (Caminiti 1980).

Dinoprostone (prostaglandin E2) has not been measured in human milk after exogenous administration, but it is a normal component of breastmilk in small amounts where it may help protect the infant's gastrointestinal tract. Use of vaginal dinoprostone to induce labor appears to have a negative effect on breastfeeding. Given orally in the first few days postpartum, dinoprostone can suppress lactation. Whether postpartum vaginal or endocervical administration suppresses lactation is not known, but it should probably not be used postpartum in mothers who wish to breastfeed. By one month postpartum, the drug appears not to suppress lactation.

A retrospective cohort study of birth records in Cardiff, Wales, UK found that the use of vaginal prostaglandins for the induction of labor resulted in an 11% decrease in the likelihood that mothers would be breastfeeding at 48 hours postpartum. The subgroup of first-time mothers had a 15% decrease.[10] A nonrandomized prospective study compared women who had spontaneous deliveries with those who had elective induction using dinoprostone vaginal gel. At hospital discharge, exclusive breastfeeding rates were similar between the two groups (88% and 89%). However, at 1 and 3 months postpartum, exclusive breastfeeding rates were significantly lower in mothers who had dinoprostone induction than in those who delivered spontaneously. Exclusive breastfeeding rates were 54% and 85% at 1 month and 46% and 59% at 3 months postpartum, respectively. Rates of supplemental and exclusive formula feeding were higher in the induced mothers at both time points also.[11] Dinoprostone has been used investigationally to inhibit postpartum lactation and engorgement by reducing serum prolactin concentrations.[12][13][14][15][16] The effect on prolactin levels, engorgement and lactation appears to be dose and duration related. Oral dosages of 3 mg daily for 4 days[17] or 0.5 mg three times daily were ineffective,[16] whereas oral dosages of 8 to 12 mg over 24 to 30 hours were effective.[12][14] These effects seem to be limited to the first few days postpartum; dinoprostone had no effect on serum prolactin or milk production when given to women 30 days postpartum.[12] Compared to oral bromocriptine 2.5 mg every 12 hours for 14 days, dinoprostone 12 mg orally in divided doses over 30 hours was as effective as bromocriptine, but resulted in less rebound breast tenderness.[14]