RESUMEN
Short children born small for gestational age (SGA) are defined as having a birth weight below -2 SD for gestational age and a reduced height at four years of age (height < -2.5 SD). Growth hormone (GH) treatment significantly improves final height (mean height gain 12 centimetres) in such children. Consequently, GH therapy has been an approved indication in Europe since 2003 for SGA children who remain short at four years of age. The Danish consensus guidelines for diagnosis, treatment and control of short SGA children are described in this review.
Asunto(s)
Trastornos del Crecimiento/tratamiento farmacológico , Hormona del Crecimiento/administración & dosificación , Estatura/efectos de los fármacos , Preescolar , Femenino , Retardo del Crecimiento Fetal/etiología , Trastornos del Crecimiento/etiología , Hormona del Crecimiento/efectos adversos , Humanos , Recién Nacido , Recién Nacido Pequeño para la Edad Gestacional , Masculino , Guías de Práctica Clínica como Asunto , Ensayos Clínicos Controlados Aleatorios como AsuntoRESUMEN
Low birth weight has been associated with an increased incidence of ischaemic heart disease (IHD) and type 2 diabetes. Endocrine regulation of fetal growth by growth hormone (GH) and insulin-like growth factor (IGF)-I is complex. Placental GH is detectable in maternal serum from the 8th to the 12th gestational week, and rises gradually during pregnancy where it replaces pituitary GH in the maternal circulation. The rise in placental GH may explain the pregnancy-induced rise in maternal serum IGF-I levels. In the fetal compartment, IGF-I levels increase significantly in normally growing fetuses from 18 to 40 weeks of gestation, but IGF-I levels are four to five times lower than those in the maternal circulation. Thus IGF-I levels in fetal as well as in maternal circulation are thought to regulate fetal growth. Circulating levels of IGF-I are thought to be genetically controlled and several IGF-I gene polymorphisms have been described. IGF-I gene polymorphisms are associated with birth weight in some studies but not in all. Likewise, IGF-I gene polymorphisms are associated with serum IGF-I in healthy adults in some studies, although some controversy exists. Serum IGF-I decreases with increasing age in healthy adults, and this decline could hypothetically be responsible for the increased risk of IHD with ageing. A recent nested case-control study found that adults without IHD, but with low circulating IGF-I levels and high IGF binding protein-3 levels, had a significantly increased risk of developing IHD during a 15-year follow-up period. In summary, the GH/IGF-I axis is involved in the regulation of fetal growth. Furthermore, it has been suggested that low IGF-I may increase the risk of IHD in otherwise healthy subjects. Hypothetically, intrauterine programming of the GH/IGF axis may influence postnatal growth, insulin resistance and consequently the risk of cardiovascular disease. Thus IGF-I may serve as a link between fetal growth and adult-onset disease.