Endocrine Abstracts

Background: Considerable overlap of IGF-I levels exists between normal subjects and those with severe GHD determined by conventional testing of GH status. Recognised factors influencing IGF-I status in GHD patients include age, gender, timing of onset of GHD and exogenous oestrogen therapy, but these do not fully explain the GH/IGF-I discordance in severe GHD. The primary structures of prolactin and GH are similar. Effects of hypoprolactinaemia are not well described in humans but laboratory studies have suggested a role for prolactin in hepatic IGF-I release, possibly through the STAT5B pathway. A potential impact of prolactin status on IGF-I status in severely GHD adults is investigated here.

Patients and methods: The study was approved by the hospital and local research ethics committees. Using multiple regression analysis techniques the contributions of the following variables to age-adjusted IGF-I SDS were evaluated in 162 (86 female, 76 male) GHD adults; Gender, timing of onset of GHD (childhood; CO or adult; AO), presence or absence of prolactin deficiency, BMI, number of additional pituitary deficits and underlying pathology.

Results: Timing of onset of GHD (P<0.0001) and presence of prolactin deficiency (P<0.0001) were independently associated with reduced IGF-I status. The contributions of CO-GHD and prolactin deficiency to IGF-I SDS were −2.64 and −2.36 respectively. Gender (P=0.07), BMI (P=0.99), number of additional pituitary deficits (P=0.65) and underlying pathology (P=0.06) did not significantly influence IGF-I status.

Conclusions: Prolactin deficiency is independently associated with reduced IGF-I status in hypopituitary adults with GHD. The prolactin deficiency may simply reflect the severity of the GHD, implying a GHD paradigm undetected by conventional GH provocative tests, or alternatively that pituitary prolactin contributes to IGF-I release in GHD, possibly through the STAT5B pathway.