Inventors: Prof Zvi Laron
BACKGROUND: SGA is usually defined as a birth weight less than 2 SD below the 3rd percentile. Between 2.5% to 10% of each population meet the criteria for SGA. Fetal growth restriction may occur early or late during fetal development. Infants who demonstrate reduced fetal growth early in gestation constitute approximately 20% of all SGA infants. They are symmetrically growth retarded: head circumference, weight, and length are proportionately affected to equivalent degrees. Increasing evidence has shown that children born SGA, especially those born very small (short and underweight) suffer subsequently from neurodevelopmental retardation and abnormalities and learning difficulties when reaching school age and even at later age. Frisk et al (2002) evaluating the relationship between head growth patterns and cognitive ability at school age of SGA children concluded that poor brain growth in-utero followed by little or no catch-up head growth result in neuro-psychological impairments. A positive correlation between head circumference (HC), estimated brain weight, and neurologic development during the first years has been shown .
The presence of growth hormone receptors in the brain implies that the brain is a target for hGH.
Congenital GH deficiency or GH insensitivity (Laron syndrome) result not only in reduced birth length, but also in a small HC denoting retarded brain growth. Initiation of hGH or IGF-I replacement treatment results in a rapid catch-up growth of the brain which is much faster than that of the linear growth, denoting the high sensitivity of the brain to hGH and IGF-I in infancy.
TECHNOLOGY: Treatment of infants defined as small for gestational age (SGA) by administration of hGH or of any compound that increases blood levels of at least one of hGH and IGF-I. More specifically, the treatment of SGA infants by initiation of the hGH administration at the early age of under two years, thereby preventing irreversible future neurological and psychological damage.