Over recent months, the links between prenatal growth restraint and postnatal endocrinology and metabolism have been strengthened and their spectrum has been broadened. Recent progress has come from complementary angles, including the following: (1) Small for gestational age (SGA) and the human genetics of insulin-like growth factor (IGF)-I and its receptor: (a) IGF-I receptor mutations [1]; (b) single copy of IGF-I receptor gene [2]; (c) IGF-I gene polymorphisms [3]. (2) Adrenarche and polycystic ovary syndrome: (a) prenatal and postnatal weight gain: opposite effects on adrenarche in girls and boys [4]; (b) metformin therapy in low-birth-weight girls to prevent progression from precocious pubarche to polycystic ovary syndrome [5]. (3) Gynecological and pregnancy complications in women born SGA: (a) hypergonadotropinaemia and small uterus-ovaries [6]; (b) identification of low maternal birth weight as a risk factor for: (i) gestational diabetes, (ii) pregnancy-induced hypertension (with SGA offspring) [7, 8]. (4) Growth hormone (GH) therapy for short children born SGA: (a) efficacy of long-term, continuous GH therapy [9]; (b) normal puberty in short GH-treated SGA children [10]. Our knowledge of SGA and post-SGA endocrinology and metabolism continues to expand swiftly. Children born SGA may continue to experience SGA consequences or correlates, and SGA adults may confer intergenerational SGA risk. Given the dynamics of this research frontier, it is anticipated that multiple facets of GH therapy in short SGA children will regularly be challenged in the future. May those questions be welcomed and may their responses ultimately lead to optimal GH regimens that benefit not only SGA children themselves but also, in due course, their progeny.

1.
Abuzzahab MJ, Schneider A, Goddard A, et al, for the Intrauterine Growth Retardation (IUGR) Study Group: IGF-I receptor mutations resulting in intrauterine and postnatal growth retardation. N Engl J Med 2003;349(23):2211–2222.
2.
Okubo Y, Siddle K, Firth H, et al: Cell proliferation activities on skin fibroblasts from a short child with absence of one copy of the type 1 insulin-like growth factor receptor (IGF1R) gene and a tall child with three copies of the IGF1R gene. J Clin Endocrinol Metab 2003;88(12):5981–5988.
3.
Johnston LB, Dahlgren J, Léger J, et al: Association between insulin-like growth factor I (IGF-I) polymorphisms, circulating IGF-I, and pre- and postnatal growth in two European small for gestational age populations. J Clin Endocrinol Metab 2003;88(10):4805–4810.
4.
Ong KK, Potau N, Petry CJ, et al: Opposing influences of prenatal and postnatal weight gain on adrenarche in normal boys and girls. J Clin Endocrinol Metab 2004, June.
5.
Ibáñez L, Ferrer A, Ong K, et al: Insulin sensitization early after menarche prevents progression from precocious pubarche to polycystic ovary syndrome. J Pediatr 2004;144(1):23–29.
6.
Ibáñez L, Potau N, Enriquez G, et al: Hypergonadotrophinaemia with reduced uterine and ovarian size in women born small-for-gestational-age. Hum Reprod 2003;18(8):1565–1569.
7.
Innes KE, Byers TE, Marshall JA, et al: Association of a woman’s own birth weight with subsequent risk for gestational diabetes. J Am Med Assoc 2002;287(19):2534–2541. Erratum in: J Am Med Assoc 2002;287(24):3212.
8.
Innes KE, Byers TE, Marshall JA, et al: Association of a woman’s own birth weight with her subsequent risk for pregnancy-induced hypertension. Am J Epidemiol 2003;158(9):861–870.
9.
Van Pareren Y, Mulder P, Houdijk M, et al: Adult height after long-term, continuous growth hormone (GH) treatment in short children born small for gestational age: Results of a randomized, double-blind, dose-response GH trial. J Clin Endocrinol Metab 2003;88(8):3584–3590.
10.
Boonstra V, van Pareren Y, Mulder P, Hokken-Koelega A: Puberty in growth hormone-treated children born small for gestational age (SGA). J Clin Endocrinol Metab 2003;88(12):5753–5758.
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