Background and aims Vasopressin plays a crucial role in the endocrine stress response to a variety of diseases, including insulin resistance and diabetes. Copeptin reliably mirrors vasopressin levels and is considered a marker of acute endogenous stress and insulin resistance. Intrauterine growth restriction (IUGR) due to placental insufficiency is associated with chronic fetal hypoxia, and with a phase of enhanced fetal/early postnatal insulin sensitivity, followed by later insulin resistance.
Methods Plasma copeptin concentrations were determined by ELISA in 50 cord blood samples from well-characterised non-distressed asymmetric IUGR (n = 30) and appropriate-for-gestational-age (AGA, n = 20) singleton full-term pregnancies. Fetuses were classified as IUGR/AGA, based on customised birth-weight standards adjusted for significant determinants of fetal growth. Doppler studies were indicative of placental insufficiency.
Results Fetal copeptin concentrations were similar in IUGR cases and AGA controls. In the AGA group, fetal copeptin concentrations were elevated in cases of vaginal delivery (p = 0.003). No association was recorded between cord blood copeptin concentrations and maternal age, parity, gestational age or fetal gender in both groups.
Conclusions Cord blood copeptin concentrations are probably not affected by IUGR at term, in the absence of fetal distress, possibly due to a balance between copeptin up regulation by chronic fetal stress on the one hand, and copeptin down regulation in the presence of increased insulin sensitivity, on the other; thus, copeptin may not be a sensitive marker of perinatal chronic stress in healthy asymmetric IUGR infants. On the contrary, cord blood copeptin concentrations seem to primarily reflect perinatal stress associated with delivery mode.