Postpartum hyperprolactinemia and hyporesponsiveness of growth hormone (GH) to GH-releasing peptide.

Abstract

Human PRL and GH as well as their respective receptors have closely related origins. In peripartal women, physiological hyperprolactinemia is associated with a pronounced hyposomatotropism that remains to be fully characterized. Through paracrine mechanisms, PRL-secreting "pregnancy cells" may modulate the secretory function of somatotropes, which are known to express PRL receptors. Within a randomized, placebo-controlled design, we examined GH responsiveness in 10 nonpregnant women and in 58 mothers either in early (median, 48 h; range, 42-54 h after delivery; all lactating) or late postpartum (median, 10 weeks; range, 3-25 weeks; lactating and nonlactating subgroups), using GH-releasing peptide-1 (GHRP-1; 100-micrograms i.v. bolus) as the GH secretagogue. Baseline serum PRL concentrations were low and similar (median, 5 micrograms/L) in nonpregnant controls and nonlactating, late postpartum women and were elevated in lactating women, particularly in the early postpartum period (median, 102 micrograms/L), compared to those in the late postpartum period (median, 27 micrograms/L). GHRP-1 elicited GH responses in all study groups; lactation was associated with lower and slower GH responses. Serum GH concentrations (20 min after GHRP-1 treatment) in controls (median, 78 micrograms/L) were 7- and 5-fold higher than those in lactating women studied, respectively, early or late postpartum. Baseline prolactinemia presented an inverse correlation with GH responsiveness; the higher baseline PRL concentration, the lower and the slower the GH response to GHRP-1. GH hyporesponsiveness in postpartum women is herewith further characterized to include the GHRP pathway. The inverse relationship between baseline prolactinemia and GH responsiveness is consistent with the concept that pregnancy cells may exert, either directly or indirectly, an inhibitory effect on the secretory capacity of somatotropes.