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Query: UMLS:C0728731 (prematurity)
 7,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During the last trimester of pregnancy, there is a sixfold increase in fetal calcium and phosphorus accumulation. Unsupplemented human breast milk may not provide sufficient calcium and phosphorus for the rapidly growing preterm infant to match the accumulation that should have taken place in utero and to permit normal bone mineralization. Rickets of prematurity may present clinically between the 6th and 12th postnatal week. The clinical diagnosis may be confirmed using simple biochemical tests. Inadequate mineral substrate intake, particularly of phosphorus, is the most common cause, although a delay in the maturation of the renal enzyme, 1-alpha hydroxylase, with low plasma concentrations of 1,25-dihydroxyvitamin D, may also occur. The biochemical response to treatment can be determined by documenting a fall in plasma alkaline phosphatase activity and a rise in plasma phosphate concentration and urinary phosphate excretion.
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PMID:Calcium and phosphorus metabolism in the premature infant. 177 18

Calcium and phosphorus are, respectively, the fifth and sixth most abundant elements in the body; both play vital roles in a multitude of physiologic systems. Because the great bulk of these elements is found in the skeleton, a large part of the discussion of calcium and phosphorus metabolism focuses on skeletal disorders, the impact of which falls heavily on young children. This article reviews the physiology of calcium and phosphorus, the skeletal and systemic consequences of disorders of vitamin D nutrition and metabolism, and the metabolic bone disease of prematurity.
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PMID:Disorders of calcium and phosphorus homeostasis. 225 48

To assess the effects of increasing the mineral content of parenteral nutrition solutions on the biochemical and radiological indicators of metabolic bone disease of prematurity 27 neonates who required parenteral nutrition were sequentially allocated to receive either a standard solution (group 1) or one with an increased mineral content (group 2). The 13 patients in group 1 received 0.68 mmol/kg/day of calcium and 0.61 mmol/kg/day of phosphorus, and the 14 in group 2 received 1.25 and 1.20 mmol/kg/day, respectively. The two groups did not differ significantly in the severity of their illness measured by birth weight, gestational age, duration of parenteral nutrition or ventilation, or the amount of supplementary oxygen required. In patients in group 2 the median plasma phosphate concentration was higher, the plasma alkaline phosphatase activity was lower, and there was less radiological evidence of rickets. There were no complications caused by excess calcium and phosphorus, and the rate of growth was similar in both groups. We conclude that an increased mineral content in parenteral nutrition solutions reduces the severity of metabolic bone disease in sick infants who require this form of nutrition.
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PMID:Association of mineral composition of neonatal intravenous feeding solutions and metabolic bone disease of prematurity. 249 71

The bone mineral status of very low birthweight (VLBW) infants fed exclusively their own mother's milk (group I) was compared with that of VLBW infants fed mother's milk in the initial 4 weeks followed by a 1:1 mixture of mother's milk and preterm formula containing high phosphorus (P) and calcium (Ca) (group II). In both groups, most infants showed a biochemical picture characteristic of phosphorus deficiency syndrome by the fourth week. Thereafter, serum alkaline phosphatase activity (ALP) decreased and serum P increased in all group II infants. Conversely, serum ALP rose and hypophosphatemia persisted in most group I infants. Group II had a significantly higher serum P at weeks 8 and 12 and a significantly lower ALP at week 12 than group I. Furthermore, group II had a lower incidence of severe radiographic abnormalities than group I at week 12. We confirmed previous observations that VLBW infants fed exclusively human milk require P and Ca supplementation to prevent metabolic bone disease of prematurity.
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PMID:Improved bone mineral status in very low birthweight infants fed human milk mixed with preterm formula. 250 28

In summary the following can be stated: (1) The comparable large number of premature and low birth weight infants leads in many countries to a public health problem. (2) Prematurity is an unphysiological state which causes some peculiarities in digestive and metabolic functions which in turn have implications on nutrition. (3) Under normal circumstances an intake of about 115-130 kcal/kg b.w./day meets the energy requirements. (4) For the so-called healthy low birth weight infant with a birth weight of 1.5 kg or more 2.9 to g protein/kg b.w./day seem to be adequate. Small for gestational age infants tolerate higher, severely ill low or very low birth weight infants only much smaller amounts or protein. (5) Quality of gain in weight has become a central issue in neonatal nutrition. Data available so far indicate the key role of energy and protein intake. (6) Due to the high requirements for growth the premature and low birth weight infant has greater needs for almost all other nutrients compared to term infants. (7) If human milk is fed - whether from the infant's own mother or pooled - it should at least be supplemented with protein, calcium, phosphorus and sodium as otherwise the high requirements could not be covered. (8) The scientific work done over the last decade has made available so-called premature formulas. (9) Only a very few bodies have issued guidelines on the nutrition of low birth weight infants, the most comprehensive one which has just been published by the ESPGAN. (10) Clinical trials with a premature formula which was formulated according to those guidelines confirmed the theoretical considerations of ESPGAN. (11) Final goals for nutrition of premature and low birth weight infants remain to be clarified by future scientific work. There is, however, considerable evidence that the diet fed to premature or low birth weight infants influences their future quality of life.
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PMID:New perspectives in the nutrition of premature and low birth weight infants. 268 68

Osteopenia of preterm newborns is a condition of undermineralization which arises during the first years of life in very low birth-weight infants. The pathogenesis of disease is multifactorial, even if its main mechanism is the inadequate mineral intake (overall the inadequate phosphorus intake). A wide spectrum of signs and symptoms may be observed ranging from overt rickets to asymptomatic conditions. Diagnosis is usually based on either photon or biochemical findings (hypophosphoremia, hyper calciuria, hypophosphaturia). There is not agreement about the prevention and the treatment and about the benefit of any form of mineral supplementation. The aim of our study is a review of the recent studies concerning the osteopenia of prematurity to focus this new problem.
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PMID:[Osteopenia in premature children: an emerging problem]. 268 53

Thirty six preterm infants (20 boys) of 25 to 32 weeks' gestation were observed from birth to around 40 weeks' postconception. When oral feeding became possible, nine received mother's own breast milk (group B), 15 formula feed (group F), and 12 formula feed supplemented with calcium (5 ml 10% calcium gluconate/100 ml feed) and phosphorus (0.5 ml 17% potassium phosphate similarly) (group S). All received a daily supplement of 400 IU vitamin D. Intakes of calcium, phosphorus, vitamin D, energy, and fluid volume were recorded. When oral feeding started, and near 40 weeks' postconception, bone mineral content of the forearm was measured by photon absorptiometry; weight and crown-heel length were also measured. After logarithmic transformation of the measurements, there were no significant intergroup differences between the mean rate constants for weight or crown-heel length describing growth during the observation period. The mean rate constant for mineral accretion (M) was significantly higher in group S than in both the others. Pooling all data, M was significantly correlated with calcium intake but not with any other variable. Mineral supplementation of feed can reduce but not cure osteopenia of prematurity.
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PMID:Bone mineral accretion rate and calcium intake in preterm infants. 277 32

Serum immunoreactive parathyroid hormone (iPTH), calcium, magnesium, and phosphorus levels were measured in 13 premature infants during the first 96 hours of life. Hypocalcemia at 12-24 hours of age was associated with a markedly elevated mean serum iPTH level. Six of the hypocalcemic infants received a continuous infusion of calcium while seven were not treated. In the untreated infants, the mean serum calcium remained in the hypocalcemic range while the serum iPTH progressively increased. By contrast, the mean serum calcium in the treated infants increased to 2.35 mmol/l at 96 hours of age and was accompanied by a decline in serum iPTH. At 72 and 96 hours, the mean serum iPTH was twofold greater in the untreated than in the treated infants. The results indicate that the parathyroid glands of premature infants respond to calcium signals and that a factor(s), other than parathyroid insufficiency, plays an etiologic role in the hypocalcemia of prematurity.
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PMID:Circulating immunoreactive parathyroid hormone levels in premature infants and the response to calcium therapy. 405 Apr 12

The major physiologic control of bone mineralization in infancy involves calcium and phosphorus. Ca and P metabolism in turn is affected by endogenous stores at birth and the ability to deliver and absorb exogenous sources of these minerals. Calciotropic hormones (parathyroid hormone, calcitonin and 1,25 dihydroxyvitamin D) modulate the response of major end organs - intestine, kidney and bone - to balance the need to maintain a relatively stable extracellular biochemical environment with the need for adequate mineralization of the bone. Many other factors such as glucocorticoids under pathological circumstances may disturb bone mineralization; however, the mechanisms by which they control bone mineralization in infancy under physiologic circumstances is ill understood. Clinical bone demineralization occurs primarily in infants born with extreme prematurity. In the presence of conventional vitamin D supplementation, deficiency of calcium and phosphorus appears to play a major role in its causation.
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PMID:Bone mineralization in infants. 639 16

Formulas designed for feeding of premature infants contain minerals added by the manufacturer. Although it is known that these minerals may be poorly suspended in the formula, little is known about concentrations of minerals in formula delivered to the infant under conditions prevailing in premature infant nurseries. In partially empty bottles of Similac Special Care, concentrations of calcium and phosphorus of this residual formula were found to be substantially greater than concentrations in full bottles. Presumably, concentrations of calcium and phosphorus in formula delivered to the infants was relatively low. Enfamil Premature and SMA Preemie infant formulas contain lesser quantities of added calcium and demonstrated less tendency to sedimentation. Substantial decrease in concentration of calcium was observed with all three formulas during continuous infusion, but the decrease was greatest with Similac Special Care. Little or no change in concentrations of calcium and phosphorus were observed with simulated bolus feeding by gavage.
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PMID:Formulas for premature infants: fate of the calcium and phosphorus. 640 94


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