The role of genomic or gametic imprinting and its association with growth has become an exciting research area during the last 10 years. Studies in both man and mouse have implicated chromosomal regions and specific genes that are imprinted such that the expression of the same gene is different depending on its parental origin. When the normal imprinted pattern of genes in some of these regions is altered through deletions, uniparental disomy or localized mutations affecting specific gene expression, specific growth disorders are observed.

Intrauterine growth retardation

Intrauterine growth retardation (IUGR) is one of the three major causes of perinatal and childhood morbidity (Dobson, Abell & Beischer, 1981). Only prematurity and major malformations numerically outrank it. In many cases the aetiology is unknown, making management and prognosis difficult. IUGR can be divided broadly into three aetiological groups: cases associated with pre-eclampsia or vascular disorders; those found to have syndromes associated with chromosomal abnormalities; and a heterogeneous ‘idiopathic’ group.

The pattern of intrauterine growth that defines IUGR occurs when a fetus is observed to be small for gestational age (SGA) and growing slowly as defined by ultra-sound evidence. The post-natal characteristics have traditionally been a SGA baby with a fairly typical clinical appearance suggesting poor intrauterine nutrition. The prevalence of IUGR is difficult to assess and depends heavily on how the limits to the growth parameters are defined. It is defined generally by birthweight below the 10th percentile in accordance with the gestational age for infants born in the same community (Kitchen, 1968). However about 75% of these show catch-up growth during the first four years of life (Fancourt et al., 1976).