Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2006) 11 P226

ECE2006 Poster Presentations Cytokines and growth factors (33 abstracts)

Prolactin deficiency is independently associated with reduced IGF-I status in severely GHD adults

A Mukherjee , WDJ Ryder , A Jostel & SM Shalet


Christie Hospital, Manchester, United Kingdom.


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.

Volume 11

8th European Congress of Endocrinology incorporating the British Endocrine Societies

European Society of Endocrinology 
British Endocrine Societies 

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