Influence of intrauterine growth retardation on parameters of liver function in low birth weight infants

Boehm, Günther; Müller, Dagmar; Teichmann, B.; Krumbiegel, P.

doi:10.1007/bf02009657

Cited by 39 publications

(24 citation statements)

References 16 publications

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“…Nevertheless, IUGR piglets infused with an excess of amino acids were shown to process nitrogen more slowly due, presumably, to a lower ability to produce urea, in comparison to normal-birth-weight piglets [15] . Therefore, the rise in serum ammonia observed with early HP feeding could be due to insufficient maturation of liver enzymes in the urea cycle [17] . Moreover, the high blood urea nitrogen may be due to the failure of the immature kidney to achieve the steep osmolar gradient required to excrete a high nitrogen load [18] .…”

Section: Discussionmentioning

confidence: 99%

Fatal Effects of a Neonatal High-Protein Diet in Low-Birth-Weight Piglets Used as a Model of Intrauterine Growth Restriction

et al. 2009

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Background: Although full-term infants suffering intrauterine growth restriction (IUGR) are routinely fed high-protein (HP) formulas to ensure catch-up growth, the effects of HP intake are poorly understood. An IUGR piglet model provides an opportunity to investigate these effects. Methods and Results: Twelve IUGR piglets were artificially fed HP formulas (50% more protein in comparison to sow milk) from the 2nd day of life (d2) until d28. Unexpectedly, all HP piglets developed poor growth, severe hypotonia and polypnea between d10 and d16. One third died spontaneously. This syndrome was investigated to understand its pathophysiology and to adopt a strategy to restore health. Blood and urine biochemistry and amino acid concentrations were investigated in 10 HP piglets and 8 piglets that were fed a normal-protein (NP) formula. In comparison to NP piglets, HP piglets showed significant hypokalemia (2.7 ± 0.6 vs. 3.6 ± 0.6 mmol/l; p < 0.01), hypophosphatemia (1.5 ± 0.2 vs. 3.0 ± 0.3 mmol/l; p > 0.01), hypercalcemia (3.0 ± 0.3 vs. 2.5 ± 0.2 mmol/l; p < 0.01), hyperammonemia (365 ± 4 vs. 242 ± 15 µmol/l; p < 0.05), elevated blood urea (6.5 ± 0.4 vs. 1.3 ± 0.4 mmol/l; p < 0.01) and elevated taurine concentrations (50.2 ± 8.5 vs. 17.7 ± 2.7 µmol/l; p < 0.01). Conclusions: These altered parameters indicated inadequate potassium and phosphorus dietary supplies in HP piglets. When the HP formula was supplemented with monocalcium phosphate and monopotassium phosphate (HP-sup), serum biochemistry was normalized in piglets fed this formula (n = 8). This experimental strategy restored growth in IUGR piglets fed HP-sup, without a toxic effect. The current findings suggest that use of an HP formula without a proportional increase in its phosphorus and potassium content induces pathology similar to the refeeding syndrome in IUGR piglets.

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Section: Discussionmentioning

confidence: 99%

Fatal Effects of a Neonatal High-Protein Diet in Low-Birth-Weight Piglets Used as a Model of Intrauterine Growth Restriction

et al. 2009

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“…IUGR influences hepatocyte function (Alonso et al 2007). Compared to appropriate for gestational age (AGA) infants of similar birth weight, small for gestational age (SGA) infants show a higher rate of neonatal cholestasis (Boehm et al 1990); however, only one report has shown postnatal liver histopathological changes for SGA infants that received prolonged total parenteral nutrition (TPN) (Baserga and Sola 2004).…”

mentioning

confidence: 99%

Liver Fibrosis in an Extremely Small Infant for Gestational Age

Arai

Noguchi

Goto

et al. 2010

Tohoku J. Exp. Med.

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“…There is evidence that multiple hepatocellular functions are influenced by intrauterine growth retardation (IUGR) [9]. In infants with IUGR we found a higher urinary ammonium excretion and a lower urea excretion when compared to infants with similar postnatal age but without IUGR [10].…”

Section: Introductionmentioning

confidence: 99%

Postnatal Development of Urea Synthesis Capacity in Preterm Infants with Intrauterine Growth Retardation

Boehm¹,

Teichmann

Jung

et al. 1998

Neonatology

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The postnatal development of the urea-synthesizing capacity was studied in 21 preterm infants with intrauterine growth retardation (IUGR) and compared with results found in 12 infants without IUGR as controls. The urea-synthesizing capacity was estimated by the ratio Q of ¹⁵N abundance of ammonia and urea in 6-hour urine samples collected after enteral administration of 3 mg [¹⁵N]H₄Cl/kg body weight. The measurements were performed on the first day when a protein intake of 3.0–3.5 g/kg/day and an energy intake of 120 kcal/kg/day were tolerated (study day 1: postnatal 14–21 days) and on the day of discharge from the hospital (study day 2: postnatal age 39–56 days). The group of infants with IUGR was subdivided in one group of infants who developed catch-up growth (n = 12) and one group who did not demonstrate catch-up growth (n = 9). On study day 1, the Q values of the IUGR infants without catch-up growth were significantly higher than those of the IUGR infants with catch-up growth (13.4 ± 2.3 vs. 9.2 ± 2.2) or of the control infants without IUGR. During the time period from study day 1 to study day 2 the Q values of the IUGR infants with catch-up growth decreased significantly (9.2 ± 2.2 vs. 4.8 ± 2.0; p < 0.001) and were in the range of the control infants without IUGR. In contrast, the Q values of the IUGR infants without catch-up growth did not significantly change during the study period (13.4 ± 2.3 vs. 11.3 ± 2.8; p = 0.097). On both study days there was a significant correlation between the Q values and the degree of IUGR (study day 1: r = 0.652, p < 0.01; study day 2: r = 0.842, p < 0.001). The data indicate that the urea-synthesizing capacity of preterm infants increases during early postnatal life and that severe IUGR may impair this development. Metabolic investigations using urea as marker for evaluation of optimal quantity or quality of dietary proteins should carefully be interpreted when infants with severe IUGR are studied.

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Influence of intrauterine growth retardation on parameters of liver function in low birth weight infants

Cited by 39 publications

References 16 publications

Fatal Effects of a Neonatal High-Protein Diet in Low-Birth-Weight Piglets Used as a Model of Intrauterine Growth Restriction

Fatal Effects of a Neonatal High-Protein Diet in Low-Birth-Weight Piglets Used as a Model of Intrauterine Growth Restriction

Liver Fibrosis in an Extremely Small Infant for Gestational Age

Postnatal Development of Urea Synthesis Capacity in Preterm Infants with Intrauterine Growth Retardation

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