I. Definition.
A newborn whose birth weight and/or length is below the -2 SD or 3rd percentile of normal reference values for the same gestational age.
Incidence: 3-10% in human fetuses, 7-5% in China.
II. Etiology.
Maternal factors: such as maternal infection during pregnancy; chronic diseases (hypertension, anemia); unhealthy lifestyle (smoking, alcohol and drug abuse, etc.); malnutrition during pregnancy; other: influenced by maternal age, height, weight and race, etc.
Placental factors: placental insufficiency, infarction, placental abruption, vascular malformation.
Fetal factors: chromosomal or other genetic defect diseases (Fanconi syndrome, Bloom syndrome, Down syndrome and Turner syndrome, etc.); congenital malformations, intrauterine viral or bacterial infections, multiple births, etc.
III. Clinical features.
Catch-up growth and short stature.
Fetal to early postnatal growth (up to 1 year of age) is mainly regulated by the nutrient-insulin-insulin-like growth factor metabolic axis; growth of young children after 1 to 1.5 years of age is regulated by the growth hormone/insulin-like growth factor axis (GH/IGF), and catch-up growth in SGA is mainly regulated by the GH/IGF-I axis; most children with SGA (about 85%) have spontaneous catch-up growth after birth Most children with SGA (about 85%) have spontaneous catch-up growth after birth; catch-up growth starts immediately after birth and reaches its maximum within 6 months; most of them usually reach normal height by 2 years of age; while about 10% of children with SGA do not show catch-up growth, resulting in a height below -2 SD of the normal mean in childhood and adulthood; short stature due to SGA accounts for 20% of short stature in adults.
Metabolic abnormalities : insulin resistance and metabolic syndrome.
Insulin resistance (IR) is present during childhood in SGA.
SGA are at high risk of developing metabolic syndrome (MS) in adulthood: type 2 diabetes, hypertension, hyperlipidemia and obesity SGA have 7-10 times higher incidence of MS in adulthood than AGA.
Intellectual and psychological abnormalities.
Children with SGA are generally short and thin, with protruding faces, small jaws, small arms and legs and pelvis, and a relatively large ratio of arms and legs to body length; they may have clumsy movements, mental and skeletal age lag, cognitive impairment (such as poor academic and work performance); psychosocial dysfunction (such as lack of self-confidence, poor self-perception, social apprehension, behavioral problems, etc.).
IV. Treatment.
In 1970, SGA was first treated with growth hormone; in July 2001, the US FDA approved SGA as one of the indications for growth hormone; in March 2003, the European EMEA approved recombinant human growth hormone (rhGH) for the long-term treatment of children with SGA dwarfism who failed to achieve catch-up growth at the age of 2.
V. Recombinant Human Growth Hormone (rhGH) Objectives.
Primary goal: To promote linear growth before puberty and normalize height in early childhood.
Secondary goal: Maintain normal height in late childhood (adolescence).
Ultimate goal: to achieve normal adult height.