Alvarez-Tutor E, Forga-LLenas L, Rodriguez-Erdozain R, Goñi-Iriarte M J, Mendendez-Torre E, Alvarez-Tutor J
Arch Gynecol Obstet. 1999 Nov;263(1-2):45-50. doi: 10.1007/s004040050261.
The mechanism involved in estrogen induced hyperprolactinemia is not completely known, although one of the possible theories suggest inhibition of dopaminergic tone. Our objective was to study the mechanism implied in the increment of PRL levels as a consequence of oral contraceptive treatment and possible modifications in TSH levels.
We performed a trial on 21 healthy women, nulliparas. We administered 35 microg of Etinil-Estradiol (EE) and 2 mg of Ciproterone Acetate (CA) for a period of 12 months. Stimulation tests with Metoclopramide and TRH were carried out before treatment, after 3, 6 and 12 months of treatment and finally 6 months after cessation of treatment.
Basal levels of PRL (mean=12.62 ng/ml) increased significantly (p<0.05) during the year of treatment (mean12=17.04 ng/ml) and maintained higher levels 6 months after cessation (meanl8=17.53 ng/ml). Maximum values obtained in response to metoclopramide (mean1=154.78) were significantly higher after 12 months (mean12=173.29), persisting 6 months after cessation of treatment (mean18=245.28). We also observed significant differences in the maximum response of TSH to metoclopramide during the same period of study (mean6=2.45), (mean12=2.76) and (mean18=2.07) respectively (p<0.05). We did not find changes in PRL and TSH responses to TRH stimulation after a year of treatment with EE and CA.
Treatment with EE (35 microg) and CA (2 mg) induces an increase in PRL levels that persist 6 months after cessation of treatment. Our results rule out the possibility that this increase in PRL is due to a decrease in dopaminergic tone or an increase in TRH sensitivity.
