Neonatal pattern of adrenergic metabolites in urine of small for gestational age and preterm infants

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Neonatal hypoglycemia is particularly dangerous for the brain when it is symptomatic or/and recurrent. In order to avoid symptomatic hypoglycemia a compensatory production of ketone bodies is required since they are actively taken up by the neonatal brain. Recurrent hypoglycemia can be avoided by stimulation of neonatal gluconeogenesis which is limited by glucose infusion and/or insulin secretion. Lipid administration induces a hyperglycemic response which is explained by a stimulation of gluconeogenesis. It also results in ketogenesis which provides the compensatory factors of hypoglycemia and which seems to be linked to gluconeogenesis. We therefore suggest that the best way to prevent neonatal hypoglycemia is achieved by supplementing the neonate with lipids and especially medium chain triglycerides.

Section: Lipids and Glueoneogenesismentioning

confidence: 99%

Neonatal Hypoglycemia

Sann¹

1990

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“…Although the CAT response has been ex amined at term gestation both in humans and animals, only a few studies have measured CAT release in the preterm human infant [6][7][8], However, these studies have included a mixed group of infants mostly greater than 29 weeks gestation, and have included acidotic and asphyxiated newborns [6][7][8]. The pur pose of the present study was to examine the ability of the very premature infants to mount a CAT response at birth in the absence of asphyxia and to compare their response with that observed in near-term healthy newborn infants.…”

Section: Introductionmentioning

confidence: 99%

Catecholamine Response at Birth in Preterm Newborns

Mehandru¹,

Assel²,

Nuamah³

et al. 1993

We compared the extrauterine adaptation of preterm with term newborn infants, by sequentially measuring plasma catecholamine (CAT) levels at birth and during the first 24 h of life. Twenty-seven preterm appropriate-for-gestational-age (AGA) infants, less than 35 weeks gestation, were compared with 26 healthy near-term AGA infants. Modes of delivery and umbilical arterial pH (mean 7.28) did not differ. Infants with asphyxia, presumed sepsis or hypoglycemia were excluded. CAT (norepinephrine, epinephrine, dopamine) levels were measured by radioenzymatic assay in blood samples from maternal vein, cord vein, cord artery and blood samples obtained at 1, 2 and 24 h of postnatal age. At birth, the cord arterial CAT levels were significantly higher than maternal venous CAT levels in both groups of neonates. Plasma epinephrine levels (mean ± SD) at 1 and 2 h of postnatal age were significantly higher in preterm than in near-term newborns (0.98 ± 0.82 nmol/l vs. 0.30 ± 0.21 nmol/l at 1 h; 0.98 ± 0.68 nmol/l vs. 0.28 ± 0.29 nmol/l at 2 h; p < 0.05). The norepinephrine and dopamine measurements did not differ between the two groups studied at birth, 1, 2 and 24 h of postnatal age. These data indicate that the preterm infants (25-35 weeks gestation) are capable of mounting a catecholamine response at birth similar to near-term newborns. The persistent elevation of epinephrine in preterm infants at 1 and 2 h of life may be attributed to either slower clearance of epinephrine or continued stimulation during clinical care in the NICU.

“…This find ing may indicate relatively high dopamine and NE turnover in preterm infants, but the high plasma levels of DOPAC and DHPG may as well relate to a low urinary excretion 299 rate of the metabolites. Previous data rather support the latter explanation: high plasma levels of catecholamine metabolites in pre term infants have been documented [16], but the urinary excretion rate of DOPAC has been found to be low [ 13]. Moreover, preterm infants have immature renal function both with respect to glomerular and tubular func tion [27,28], which could lead to a low clear ance rate of catecholamine metabolites.…”

Section: Discussionmentioning

confidence: 73%

“…Preterm infants tend to have lower cord blood E and NE levels than term infants [3,5], and they have responded with less catechol amine secretion during asphyxia compared with term infants [3], suggesting that the sym- pathoadrenal system might not be completely developed before term [9], Studies on cate cholamine metabolism after birth have mainly measured urinary excretion of cate cholamines [10][11][12][13][14], Studies of plasma cate cholamines and their metabolites during the early postnatal period are quite limited [1,…”

Section: Introductionmentioning

confidence: 99%

Sympathoadrenal Activity in Preterm Infants during the First Five Days of Life

Ekblad

Kero²,

Korvenranta³

et al. 1992

We measured plasma concentrations of epinephrine (E), norepinephrine (NE), 3,4-dihydroxyphenylacetic acid (DOPAC), and 3,4-dihydroxyphenylglycol (DHPG) as well as urinary concentrations of metanephrine (M), normetanephrine (NM) and 3-methoxy-4-hydroxymandelie acid (MOMA) on day 2 and day 5 in preterm infants; gestational age < 30 weeks (G < 30; n = 16) and gestational age 30-34 weeks (G 30–34; n = 19). Concentrations of E (0.00-2.28 nmol/l) and NE (0.6-9.1 nmol/l) in plasma were much lower than those previously reported during preterm and term delivery. The E:NE ratio decreased from 1:10 on day 2 to 1:30 on day 5, and the M:NM ratio decreased from 1:4 on day 2 to 1:8 on day 5, indicating relatively higher catecholamine secretion from the adrenals than from the sympathetic nerve terminals in preterm infants during postnatal adaptation. Plasma concentrations of DOPAC and DHPG were significantly higher in G < 30 than in G 30–34 (DOPAC, p = 0.0494; DHPG, p = 0.0092), probably relating to a low urinary excretion rate of catecholamine metabolites in infants in G < 30. Plasma and urinary concentrations of catecholamines and their metabolites varied considerably, and no significant correlations to postnatal events could be demonstrated.