Lactation suppression with bromocriptine. [Puerperal inhibition of lactation with metergoline or bromocriptine]. Lactation inhibition by the dopamine agonist CV 205-502. Inhibition of puerperal lactation. A double blind study of bromocriptine and placebo. Serum prolactin and the suppression of lactation. Suppression of lactation. A comparison of bromocriptine and prostaglandin E2. Lactation inhibition by a single injection of a new depot-bromocriptine. The combined oral contraceptive pill versus bromocriptine to suppress lactation in puerperium: a randomized double blind study. Inhibition of lactation by cyclofenil and bromocriptine.
The efficacy and acceptability of bromocriptine in suppressing postpartum lactation was determined in a double blind study in which bromocriptine 2.5 mg twice daily for 14 days was compared with a placebo. Forty women who decide during the antenatal period not to breast feed entered the study. The bromocriptine treated group had significantly less mammary secretion and breast engorgement than the control group and also required less analgesia. The most noticeable side effects during the trial were dizziness, headache and abdominal pain. The only statistical difference between the two groups was a higher incidence of dizziness in the bromocriptine treated group. In a controlled, randomised, prospective, clinical study, the effect of prolactin suppression and clinical course of the lactation suppressors Bromocriptine and Metergoline were investigated. During 7 months 150 patients were studied. 81 of those patients, who did not nurse, were treated by Bromocriptine (primary lactation suppression: n = 62, secondary suppression: n = 19) and 69 of the patients were treated by Metergoline (primary suppression: n = 54, secondary suppression: n = 15). The drugs were administrated orally to all subjects, dosed 2 x 2.5 mg/d of Bromocriptine for 14 days and 3 x 4 mg/d of Metergoline for 10 days, starting in average after 13 hours. Puerperal suppression of prolactine were compared with randomised breast feeding subjects (n = 30). In Bromocriptine treated women the average plasma prolactin level decreased from 78.4 +/- 22 ng/ml to 17.0 +/- 3.3 ng/ml during five days of treatment. In Metergoline treated women the plasma prolactin level decreased from 129.7 +/- 15.1 ng/ml to 56.9 +/- 10.0 ng/ml during the first days of treatment. Prolactin level of breast feeding subjects decreased from 233.6 +/- 21.4 ng/ml to 185.8 +/- 23.7 ng/ml during the same period (p < 0.05). There is no statistical significancy of clinical difference of both drugs, but a statistical trend was seen. With Bromocriptine treated women were suppressed efficiently in 71 of 81 cases, 10 refused. Refusals were divided in two quality levels, level I with subjects with moderate complaints and little puerperal lactation, level II with subjects with considerable complaints including strong puerperal lactation. With Metergoline suppressed women, treatment was efficiently in 51 of 69 cases, but refusals of level I were observed in 11 cases and refusals of level II were observed in 7 cases. The results show that Bromocriptine and Metergoline are effective on suppression of lactation. Under the current drug dose of Metergoline an advantage of Bromocriptine were observed. Only further studies could investigate, whether an adaptation of drug dose would improve the clinical efficiency of Metergoline. In an open pilot study with a parallel group design 30 bottle feeding women were randomly assigned in a two to one ratio to receive either the new dopamine agonist CV 205-502 or bromocriptine for lactation inhibition. Ten women who intended to breast feed served as normal controls. All treated women reached prepregnant prolactin levels within 72 h with once-daily 0.075 mg of CV 205-502 or twice-daily 2.5 mg of bromocriptine, at starting doses of 0.05 mg and 2.5 mg respectively. Fifteen of the 20 women treated with CV 205-502 reported breast symptoms, 50% occurring on days 3 and 4 of treatment. Three of the 10 women treated with bromocriptine had breast symptoms between days 2 and 28. Overall efficacy and tolerance in the two groups was very good. Side effects did not differ between the groups, with the exception of pulse rate in the standing position, which was significantly higher in the bromocriptine treated group than in either the CV 205-502 group (P = 0.02) or the breast feeding group (P less than 0.01). The coagulation tests (fibrinogen, AT III, PTT and APTT) showed no significant differences between the three groups. Bromocriptine and placebo were randomly allocated for three weeks to 52 postpartum patients requiring lactation suppression. Bromocriptine significantly lowered plasma prolactin levels and suppressed breast milk, breast pain and engorgement quicker than placebo. No side-effects were noted and rebound lactation did not occur. Menstruation appeared to re-start sooner when Bromocriptine was given. Bromocriptine (2 bromo-alpha-ergocryptine), stilboestrol, clomiphene citrate, testosterone propionate and a placebo were given to 75 postpartum women for the suppression of puerperal lactation. An additional 15 women who breast-fed their babies served as a control group. Blood samples were taken for the determination of serum prolactin levels by a specific homologous double antibody radioimmunoassay. Concurrently, the clinical effectiveness of the various treatments was assessed. High levels of prolactin were found at the time of delivery. Bromocriptine effectively reduced serum prolactin and prevented lactation; stilboestrol increased serum prolactin and partially suppressed lactation; clomiphene citrate and testosterone propionate both lowered serum prolactin levels and partially suppressed lactation. The placebo showed almost no effect on serum prolactin. It appeared that bromocriptine was the drug of choice in the suppression of puerperal lactation. Women in the puerperium who requested lactation suppression were randomly allocated to receive bromocriptine from puerperal day 1 to 14 or prostaglandin E2 from day 3 or 4 for 24 hours. Subjectively, lactation suppression was satisfactory in all cases. Objective measurements showed a trend toward more-effective early suppression with bromocriptine. After discharge from the hospital, 3 of the 21 women who received prostaglandin E2 complained of mild breast tenderness, whereas 10 of the 22 who received bromocriptine reported severe "rebound" breast tenderness. Recently, long-acting injectable forms of bromocriptine have become available for the prevention of lactation. The first developed depot-form was very effective, but had the disadvantage of a slowly metabolized carrier. we investigated the pharmacokinetics, efficacy, tolerance and safety of 40 and 50 mg of a new rapidly eliminated depot-form in 61 postpartum women. Bromocriptine rapidly increased after injection and prolactin was effectively suppressed during the study-period of 60 days. Overall efficacy was very good or good in 98% and no rebound lactation occurred. Sixteen women experienced side effects. Tolerance at the injection site was good and safety tests did not show abnormalities. There were no differences between the two dosages. We conclude that this new depot-bromocriptine is a safe, well tolerated and effective drug in the suppression of prolactin and the prevention of post-partum lactation. A randomised double blind comparative study of 230 HIV infected mothers who had a normal delivery at 37-42 weeks' gestation were divided into two groups; 116 combined pill users and 114 bromocriptine users to suppress lactation. There were 33 cases (28.5%) of combined pills users and 29 cases (25.4%) of bromocriptine users who had breast engorgement without statistical difference. All of them had mild breast engorgement without any treatment except one case (0.9%) in the bromocriptine group had severe breast engorgement with puerperal fever and needed an analgesic drug. There were no side effects of the drugs. This study showed that combined pills were beneficial to suppress lactation in HIV infected mothers to prevent postnatal mother-to-child transmission because of low risk and low cost. In a double blind controlled study of the inhibition of lactation 13 women received 300 mg of cyclofenil and 11 women 2.5 mg of bromocriptine twice daily for 14 days. Lactation was effectively inhibited by both drugs, but with bromocriptine there was a significantly higher frequency of relapse. The plasma concentration of prolactin, which decreased rapidly with bromocriptine, returned to the pretreatment level the day after drug treatment stopped, but with cyclofenil it remained low. Plasma oestradiol followed a similar pattern. Plasma FSH increased more rapidly with bromocriptine than with cyclofenil. There was no significant difference between the treatment groups at any stage for haematology, coagulation or liver function tests. The more sustained effect of cyclofenil on prolactin secretion with a reduced frequency of relapse, and the lower oestradiol level, which might indicate a reduced risk of thromboembolism, suggest that this drug has some advantage over bromocriptine in the inhibition of postpartum lactation.
There are insufficient data to draw any firm conclusions. Treatment with bromocriptine appears promising, although women would be unable to breastfeed due to suppression of lactation.