The estimated incidence of SGA births, using the definition of <−2 SDs in length or weight (equivalent to the 2.3 percentile), is 1 in 43, making SGA incidence relatively high compared with other growth disorders. Within the group of SGA children, 1.5% were both underweight and short, 2.4% were short only, 1.6% were underweight only. A population-based study including 3650 healthy full-term neonates born in Sweden over a 3-year period found 5.4% (N = 198) were diagnosed SGA, defined as <−2 SDs in birth length and/or weight. The available SGA incidence and prevalence data are limited due to insufficient or inconsistent records for birth length and gestational age in national databases. Placental factors that may result in SGA include placental insufficiency, infarction, abruption, and vascular abnormalities. Fetal causes include congenital anomalies chromosomal abnormalities infection and hormone abnormalities involving insulin, leptin, thyroid hormones, and insulin-like growth factors (IGF-1 and IGF-2). Maternal factors associated with SGA include inadequate nutrition hypoxia diabetes mellitus drug use and abuse vascular, hematologic, and renal disorders infection and sociodemographic factors. Of those 60% of SGA infants where an etiology is identified, about 50% involve maternal factors, 5% involve fetal abnormalities, and less than 5% are felt to be due to placental pathology. The etiology of SGA is frequently unknown, and current estimates suggest that 40% of SGA births will have no identifiable pathology. SGA may occur alongside intrauterine growth retardation (IUGR) and/or premature birth, or may be diagnosed at term in the absence of any prenatal complications. Children born SGA comprise a heterogeneous group with a broad spectrum of clinical characteristics. SGA is typically diagnosed when birth weight and/or length are at least 2 standard deviations (SDs) below the mean for gestational age, using appropriate reference data. The importance of increasing parental and physician awareness that most children born SGA will do well developmentally and will optimally benefit from early initiation of GH treatment when short-statured is addressed, as is the need to shift the age of referral to better align with consensus recommendations.īeing small for gestational age (SGA) at birth has many causes, including fetal, placental, maternal, and environmental factors. To optimize the eventual height in short-statured SGA children who fail to manifest catch-up growth, a lowering of the average age of referral for GH therapy evaluation is needed to better align with consensus recommendations for SGA management. This review discusses the importance and associated challenges of early diagnosis of children born SGA who fail to show catch-up growth, contrasts the recommended age of referral for these patients and the average age of GH treatment initiation, and discusses studies showing the significant positive effects of early referral and treatment with GH on AHs in short-statured children born SGA. Delayed referral for GH treatment is problematic as studies show younger age at GH treatment initiation in children born SGA is an independent predictor for responses such as optimal growth acceleration, normalization of prepubertal height, and most importantly, adult height (AH). Despite treatment guidelines for children born SGA that recommend referral for growth hormone (GH) therapy evaluation and initiation by ages 2 to 4 years, the average age of GH treatment initiation is typically much later, at ages 7 to 9 years. Approximately 10% of children born small for their gestational age (SGA) fail to show catch-up growth and may remain short-statured as adults.
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