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POSTPARTUM HYPOGONADOTROPHINISM: EVIDENCE FOR INCREASED OPIOID INHIBITION
Author(s) -
ISHIZUKA B.,
QUIGLEY M. E.,
YEN S. S. C.
Publication year - 1984
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.1984.tb00106.x
Subject(s) - endocrinology , medicine , (+) naloxone , naloxone hydrochloride , opioid peptide , hypogonadotrophic hypogonadism , prolactin , opioid , postpartum period , hormone , chemistry , pregnancy , biology , receptor , genetics
SUMMARY To investigate a proposed role for endogenous opioids in the inhibition of LH: RH‐gonadotrophin release in the postpartum hypogonadotrophic state, LH and FSH responses to naloxone infusion (1·6 mg/h for 2 h) and to a pulse of LHRH (10 μg) were measured in five non breast‐feeding women. Sequential studies were made at four intervals during the first 25 d postpartum. LH and FSH responses to naloxone were absent on Day 10 postpartum, but significant increments were observed in all studies performed between Days 13–25 postpartum. The relative increments of FSH and LH during naloxone varied as the puerperium progressed; a 3‐fold greater release of FSH than LH was found on Day 13 to 15 while the reverse was observed on Day 25. The intermediate days (17–20) yield an equal response. There was a positive linear correlation between the LH and FSH responses to naloxone infusion and to LHRH. These data suggest that the hypogonadotrophinism of the puerperium is due at least in part to increased opioid inhibition of LHRH secretion.