Intrauterine growth retardation (IUGR) is encountered in 2.5% (-2 SD)
of newborns. Lack of postnatal catch-up growth is found in 8-20%. If G
H secretion is increased early postnatally in IUGR, then some persiste
ntly short IUGR children may present with GH insufficiency. However, t
he mechanism of postnatal catch-up growth is heterogenous. The respons
e to GH treatment with regard to plasma IGF-1, GH dose and growth velo
city was analyzed in persistently short idiopathic IUGR children and c
ompared to GH-deficient (GHD) and familial short stature (FSS) childre
n of similar age and degree of short stature. IUGR children require bo
th a greater basal and GH-induced plasma IGF-1 in order to achieve a g
rowth velocity of similar magnitude to that of FSS and GHD children. T
hese data suggest a different sensitivity to GH in IUGR compared to FS
S or GHD children, sustaining the hypothesis that these idiopathic IUG
R children may be partially IGF-1 resistant. The recent report of part
ial insulin resistance in IUGR subjects raises the possibility of an I
GF-1 receptor- or post-receptor-mediated defect.