Mechanisms of growth in small preterm infants and early life origins of adult cardiovascular disease
Year: 2003
Type: dissertation
Study design: Observational Study
Abstract: Background. The improved prognosis of early preterm birth has created a generation of surviving small preterm infants whose health needs in adulthood are poorly known. Epidemiological studies in subjects born at term have repeatedly shown an association between small size at birth and increased risk of adult cardiovascular disease. While considerable variation in this risk is already related to small differences within the normal range of size at birth, small preterm infants frequently exhibit severe postnatal or prenatal growth retardation, or both, and are often exposed to growth-inhibiting treatments such as glucocorticoids. There is thus reason for serious concern about increased cardiovascular risk when surviving small preterm infants become older. Endocrine programming – lifelong effects of early nutrition and hormonal milieu on endocrine systems such as the insulin-like growth factor (IGF) system and the hypothalamic-pituitary-adrenal axis (HPAA) – is likely to play a major role in linking size at birth with adult disease. Because direct assessment of late-life health in small preterm infants would require decades of follow-up, we studied endocrine mechanisms of growth in two distant parts of the life span: in small preterm infants and in 65to 75-year-old adults with birth and childhood measurements recorded. Our secondary aim was to find a biochemical indicator of growth velocity for small preterm infants. Subjects and methods. Cord vein IGFs and IGF-binding proteins (IGFBPs) as well as markers of collagen turnover were studied in 98 infants born at <32 weeks’ gestation. Fortyeight infants with birthweight < 1500 g underwent a 9-week follow-up with repeated determinations of these factors and a rigorous protocol of frequent, accurate weight and lower leg length measurements (knemometry). In 107 infants of <32 weeks’ gestation, placental 11β-HSD2 activity [enzyme converting active cortisol (F) to inactive cortisone (E)] was measured together with cord vein F and E concentrations.
Source: Työväentutkimus Vuosikirja
Author: Eero Kajantie
Language: English
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W1528063133