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Clinical endocrinology · 2015

Differential effects of low birthweight and intrauterine growth restriction on umbilical cord blood insulin-like growth factor concentrations.

СтатьяМногоцентровое исследованиеПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Tzschoppe Anja, Riedel Christina, von Kries Rüdiger, Struwe Ellen, Rascher Wolfgang, Dörr Helmuth G, Beckmann Matthias W, Schild Ralf L, Goecke Tamme W, Flyvbjerg Allan, Frystyk Jan, Dötsch Jörg

Аннотация

OBJECTIVE: Alterations in the growth hormone-insulin-like growth factor (IGF) axis have been considered as a causal factor for intrauterine growth restriction (IUGR) and for the increased risk of metabolic disease in later life. We compared members of the IGF axis in umbilical cord blood between IUGR neonates, small for gestational age without foetal restriction (SGA) and appropriate for gestational age (AGA) neonates.

DESIGN: Prospective controlled multicenter study.

PATIENTS: Sixteen ultrasound-proven IUGR, 8 SGA and 40 AGA neonates.

MEASUREMENTS: Concentrations of total IGF-I and total IGF-II by immunoassays, bioactive IGF by cell-based bioassay and IGFBP-I in mixed venous and arterial umbilical cord blood samples at birth. Auxological parameters at birth.

RESULTS: IGF-I concentrations in IUGR [17·7 μg/l (CI 13·8;21·6)] were clearly below those in AGA [48·3 μg/l (CI 43·7;52·9)] and SGA neonates [36·0 μg/l (CI 26·6;45·4)]. IGF-II levels were significantly reduced in IUGR [201·4 μg/l (CI 190·2;212·6)] compared to AGA neonates [231·2 μg/l (CI 220·6;241·9)]. A trend for lower IGF-II concentrations was observed in IUGR when compared to SGA neonates [232·0 μg/l (CI 207·2;256·8)]. These differences could not be explained by confounding. For IGFBP-1, a trend towards higher values in IUGR was observed.

CONCLUSIONS: Low IGF-I cord blood concentrations in hypotrophic neonates after IUGR might not only result from low birthweight per se, but also reflect prenatal placental environment. Alterations of the IGF axis could be in the causal pathway of IUGR and thus constitute a potential surrogate marker for IUGR in the assessment of foetal programming.

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