Urinary N-methylnicotinamide and ß-aminoisobutyric acid predict catch-up growth in undernourished Brazilian children.

Enteric infections, enteropathy and undernutrition in early childhood are preventable risk factors for child deaths, impaired neurodevelopment, and later life metabolic diseases. However, the mechanisms linking these exposures and outcomes remain to be elucidated, as do biomarkers for identifying children at risk. By examining the urinary metabolic phenotypes of nourished and undernourished children participating in a case-control study in Semi-Arid Brazil, we identified key differences with potential relevance to mechanisms, biomarkers and outcomes. Undernutrition was found to perturb several biochemical pathways, including choline and tryptophan metabolism, while also increasing the proteolytic activity of the gut microbiome. Furthermore, a metabolic adaptation was observed in the undernourished children to reduce energy expenditure, reflected by increased N-methylnicotinamide and reduced ß-aminoisobutyric acid excretion. Interestingly, accelerated catch-up growth was observed in those undernourished children displaying a more robust metabolic adaptation several months earlier. Hence, urinary N-methylnicotinamide and ß-aminoisobutyric acid represent promising biomarkers for predicting short-term growth outcomes in undernourished children and for identifying children destined for further growth shortfalls. These findings have important implications for understanding contributors to long-term sequelae of early undernutrition, including cognitive, growth, and metabolic functions.

Relationship between birth weight and urea kinetics in children.

OBJECTIVE: To explore the effect of birth weight on urea kinetics in young healthy children. DESIGN: Observational study. SETTING: Tertiary center for treatment of malnutrition. SUBJECTS: A total of 17 male children, 6-24 months old, who had recovered from malnutrition. INTERVENTIONS: Urea kinetics were measured using stable isotope methodology with [(15)N(15)N]-urea over 36 h. RESULTS: Birth weight was negatively related to urea hydrolysis after controlling for the intake of protein (adjusted R (2 ) = 0.91, P = 0.001) and separately for energy intake (adjusted R (2) = 0.95, P = 0.001), age (adjusted R (2) = 0.90, P = 0.001) and rate of weight gain (adjusted R (2) = 0.91, P = 0.001). There was a tendency for higher urea production in the children with lower birth weight after controlling for nitrogen intake (adjusted R (2) = 0.93, P = 0.099), and separately for age (adjusted R (2) = 0.94, P = 0.06) and rate of weight gain (adjusted (R (2) = 0.92, P = 0.096). Urea excretion was not significantly related to birth weight. CONCLUSIONS: The salvaging of urea nitrogen following urea hydrolysis contributed significantly more to the nitrogen economy in children with lower birth weight compared to those with higher birth weight. This may be as a result of reductive adaptation in the children with lower birth weight as a consequence of inappropriate prenatal nutrition and growth.

Parenteral nutrient needs of very low birth weight infants.

OBJECTIVE: To determine nitrogen and mineral needs in parenterally nourished very low birth weight infants. DESIGN: Prospective observational study. SETTING: Neonatal intensive care unit. PATIENTS: Twenty-four very low birth weight infants (< 1.2 kg) expected to receive parenteral nutrition (PN) exclusively for 3 weeks beginning 3 days after birth. INTERVENTIONS: Infants received PN solutions according to nursery protocol. Serial 24-hour balance studies were conducted twice weekly. Clinical therapies were tabulated. MAIN OUTCOME MEASURES: Intake, urinary excretion, and apparent retention of nitrogen, sodium, potassium, zinc, copper, calcium, phosphorus, and magnesium after initiation of PN. RESULTS: Although urinary K, Zn, Ca, P, and Mg excretion (but not N, Na, and Cu excretion) increased after PN therapy was begun, net nutrient retention increased significantly above baseline for all nutrients. Average weekly nutrient retention was significantly below intrauterine estimates of nutrient accretion for N, Na, Ca, P, and Cu; closely approximated estimates for Zn; and significantly exceeded those for K and Mg. Regression analysis was used to predict parenteral nutrient intakes that would support postnatal nutrient retentions equivalent to the intrauterine estimates. Postnatal therapy with dexamethasone affected N, P, and K excretion and retention. CONCLUSIONS: Soon after PN administration is begun, positive nutrient balance may be achieved early in the neonatal period. The magnitude of this effect remains uniform during PN administration. Adjustments in parenteral nutrient intake are needed to provide nutrient intakes sufficient to support postnatal retention at rates similar to those of intrauterine accretion. These data should be considered in the design of future studies to determine optimal PN needs of very low birth weight infants.

[Behavioral development and nerve conduction velocity during recovery from malnutrition]. / Evolución conductual y velocidad de la conducción nerviosa durante la recuperación de la desnutrición.

OBJECTIVES: To research if the improvement in psychomotor development observed during the treatment of malnutrition, is related to favorable changes in the speed of nerve conduction and in the excretion of hydroxy-indole acetic acid (indole). DESIGNED OF THE STUDY: Prospective, of a descriptive type, includes the follow-up of children during the first month of treatment. APPLICATION: To better know the impact which malnutrition has on mental development. PATIENTS: Nine children, ranging from three to 15 months of age, gravely undernourished. INTERVENTION: The neurological development, the speed of nerve conduction and the excretion of indole were evaluated at 10 day intervals. MEASUREMENTS AND RESULTS: Using the Gesell technique in order to evaluate the development, the measurement of conduction through the medial and external popliteal sciatic nerves and indole excreted in 24 hours, a quantitative increase of all of these variables was seen in 24 hours. At the beginning the conduction speed was slow (less than 30 m/s) and the excretion of indole was very low (0.28 mg/24 h). After the tenth day these measurements returned to normal, although the development coefficient was found to still below at the end of the study (63.9 +/- 21.0). CONCLUSIONS: Simultaneous to the neurological deficit, there is a reduced speed of conduction, which returns to normal after the tenth day without a positive correlation with motor functions and development. Neither does the disponibility of serotonin (judged by the excretion of indole) correlate with the speed of conduction.

Failure to thrive and death in early infancy associated with raised urinary homovanillic and vanillylmandelic acids.

A case of failure to thrive in an infant with persistently raised urinary levels of homovanillic and vanillylmandelic acids is descirbed. No neural crest tumour was discovered at surgical exploration or at necropsy. The relation of this biochemical abnormality and failure to thrive is unclear.