RESUMO
To assess the influence of protein intake on renal excretion of calcium and amino acids and on bone mineralization in preterm infants, we randomly selected within weight group strata 27 infants who weighed < 1500 gm at birth (nine per group) to be fed a high-mineral (calcium, 940 mg/L; phosphorus, 470 mg/L) premature formula with one of the following protein contents: formula A, 3.0 gm/100 kcal; formula B, 2.7 gm/100 kcal; and formula C, 2.2 gm/100 kcal. Mean (+/- SD) daily weight gain was greater in infants receiving the higher protein intakes for the first 30 days (formula A, 24.8 +/- 5.1 gm; formula B, 20.5 +/- 3.8 gm; formula C, 16.2 +/- 5.9 gm (analysis of variance: p < 0.01; C < A, p < 0.05)). Bone mineral content did not differ at any time point, and all groups had a high prevalence of generalized aminoaciduria (4 weeks: formula A, 56%; formula B, 71%; formula C, 75%). Urinary calcium corrected for creatinine (in milligrams per milligram) increased as protein content decreased (2 weeks: formula A, 0.16 +/- 0.10; formula B, 0.20 +/- 013; formula C, 0.44 +/- 0.33 (C > A, C > B, p < 0.05); 4 weeks: formula A, 0.23 +/- 0.15; formula B,0.34 +/- 0.47; formula C, 0.49 +/- 0.22 (C > A, p < 0.01). We conclude that the high mineral content and other components of premature formulas result in a higher growth rate and may increase protein requirements. Failure to meet protein requirements may result in underutilization of absorbed calcium and increased renal excretion of calcium. In preterm infants, higher protein intake probably supports rather than jeopardizes bone mineral accretion, and reduces rather then increases calciuria.
Assuntos
Aminoácidos/urina , Cálcio/urina , Proteínas Alimentares/administração & dosagem , Alimentos Infantis , Recém-Nascido de Baixo Peso/urina , Minerais/administração & dosagem , Acetilglucosaminidase/metabolismo , Densidade Óssea , Humanos , Recém-Nascido de Baixo Peso/fisiologia , Recém-Nascido , Microglobulina beta-2/urinaRESUMO
We measured serum concentrations of thyroxine (T4), triiodothyronine (T3), reverse T3, free T4, thyroid-stimulating hormone, and cortisol in 62 victims of sudden infant death syndrome (SIDS) in 30 infants who died of known causes and in 15 living controls. The mean T3 value was elevated in 69% of those with SIDS. 37% of the others who died, and in no control infants. After excluding those who died of known cause who had abnormal thyroid function (abnormal postmortem concentrations of T4, free T4, or reverse T3), the T3 values were elevated in 63% of those remaining. When the data were analyzed on the basis of case histories and autopsy findings, those infants who were in good health and died suddenly of accidental causes had an elevation in mean T3 similar to that seen in SIDS victims; those who died under conditions known to alter thyroid metabolism did not. The T4, free T4, reverse T3, thyroid-stimulating hormone, and cortisol values were not useful in differentiating those with SIDS from the living controls, or those who were healthy at the time of death. We were unable to find any difference in T3 serum concentrations between the total group who had SIDS and those who had SIDS with minor infections, with petechiae on intrathoracic organs, with premature birth, or those who were resuscitated. Our data point out the importance of using appropriate controls when evaluating SIDS. The normal reverse T3 values in SIDS, as well as confirmation of the normal T4 and free T4 values, constitute evidence against chronic persistent alveolar hypoventilation or prolonged episodes of hypoxia immediately preceding death from SIDS.