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

Fifteen newborn infants developed roentgenographic evidence of rickets while on long-term intravenous hyperalimentation. In each instance, the initial diagnosis of rickets was suggested on the chest roentgenogram, where characteristic cupped and frayed upper humeral metaphyses were noted; subsequent knee and wrist roentgenograms substantiated these findings. Factors which may have predisposed to the development of rickets include inadequate doses of vitamin D, prematurity and a rapid change in body weight during hyperalimentation therapy.
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PMID:Rickets as a complication of intravenous hyperalimentation in infants. 10 70

In premature infants calcium and phosphate supplementation should be continued until the infants weigh more than 2000 g, because osteopenia of prematurity has been described after discontinuation of the supplements at body weights of < 1800 g. Premature infants generally receive substantially more vitamin D than their daily requirements (> 400 IU), but then are no studies on the side effects of high vitamin D intake (hypercalciuria?). The extremely high calzitriol concentrations in plasma of premature infants who receive Ca/P supplements indicate that maximal stimulation of Ca/P absorption is necessary and present supplementation could still be inadequate. The daily vitamin D requirements of term infants are between 100 and 400 IU and no supplements are necessary if the infants are fed vitamin-D-fortified formulas. The high prevalence of rickets in infants on macrobiotic or vegetarian diets indicates that those infants should receive calcium and vitamin D supplements.
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PMID:[Calcium, phosphorus and vitamin D administration in infancy. Unsolved questions]. 143 21

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

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

In a study of children with chronic disorders of calcium and phosphate homeostasis, enamel hypoplasia was found in hereditary vitamin D-dependency rickets and in hypoparathyroidism, conditions characterized by hypocalcemia, and was not found in X-linked hypophosphatemic rickets, a condition in which the plasma calcium concentration is normal. The occurrence of enamel hypoplasia bore no relation to the plasma phosphate concentration. Enamel hypoplasia has also been reported in other pediatric disorders in which hypocalcemia is a major sign (for example, vitamin D deficiency, prematurity, and neonatal tetany). The existence of enamel hypoplasia in a hypoparathyroid or rachitic patient, when correlated with the chronology of enamel mineralization, helps to establish the time of onset of hypocalcemia. The observations led us to the hypothesis that a low serum calcium concentration during enamel formation is a specific determinant of enamel hypoplasia. This hypothesis may be relevant to the etiology of linear enamel hypoplasia, an endemic lesion of primary teeth in children of many Third World countries that predisposes the teeth to dental caries. The hypothesis may therefore be relevant also in explaining the prevalence of caries in the primary teeth of children in many underdeveloped countries.
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PMID:The etiology of enamel hypoplasia: a unifying concept. 626 72

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

Three cases of neonatal hyperparathyroidism are reported: 2 children born to a mother with idiopathic hypoparathyroidism and a boy born to a mother with pseudohypoparathyroidism. Severe demineralization, decreased plasma calcium levels and very low phosphorus levels were seen in all three cases. The PTH level was high in the two cases in which is was measured. In the second of these, the lack of vitamin D administration since birth led to very severe rickets lesions at the age of 7 weeks. This is an argument for the role of hyperparathyroidism-induced vitamin depletion in the lesions observed and in the maintenance of secondary hyperparathyroidism. Analysis of 10 previously reported cases reveals the severity of the calcium deficiency induced in the fetus in this manner, the frequency of prematurity, of dysmaturity. With calcium and vitamin treatment, biological and radiological findings become normal.
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PMID:[Neonatal hyperparathyroidism secondary to maternal hypoparathyroidism (author's transl)]. 746 5

Metabolic bone disease is recognized with increasing frequency in very-low-birth-weight infants. Radiological changes characteristic of rickets have been found in 55% of infants with a birth weight of less than 1000 g and in 23% of infants weighing less than 1500 g at birth. Twenty-four per cent of infants with a birth weight of less than 1500 g have fractures. The main aetiological factor is insufficient phosphorus supplementation. The aetiology is, however, multifactorial and also includes calcium deficiency, vitamin D deficiency, certain drugs, aluminium loading and immobilisation. The method of choice in detecting subclinical mineral bone disease of prematurity is measurement of bone mineral density, but there is as yet no single good diagnostic method available for premature infants. The optimal mineral and vitamin D requirement of the premature infant must be established so that proper recommendations can be given. The current recommended vitamin D dose in Europe (ESPGAN 800-1000 IU/day) is probably too high when extra minerals are supplied. Moreover, the duration of mineral supplementation may need to be continued until the infant has reached a body weight of 3.5 kg. This article deals with the aetiology, pathogenesis, diagnosis and future prospects of metabolic bone disease of prematurity.
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PMID:Metabolic bone disease of prematurity. 886 79

The aim of this study was to assess the long-term effects of prematurity and growth during the first year on bone mineralization in prematurely born children. The study group consisted of 38 prematurely born Finnish children (17M, 21F) examined at the age of 6-7 y. After birth, all children were fed with banked human milk until discharge from hospital. Thereafter, 27 children were partially breastfed until the age of 5-7 months. Infants with gestational age (GA) < or = 33 weeks (n = 25) received calcium 45-50 mg/100 kcal, phosphorus 40-45 mg/100 kcal, vitamin A 1000 IU/d, vitamin C 2 mg/d and vitamin D 400 IU/d until 2.5 kg. Infants born > 33 weeks received only vitamin D 400 IU/d. Bone mineral density (BMD) and bone mineral content (BMC) were measured by dual energy X-ray absorptiometry (DXA) of the lumbar spine (L2-L4) at 6-7 y of age. At examination, all children had normal height and weight. BMD values were within the confidence interval of the Finnish reference values. In regression analysis bone area, present weight, GA and weight at 1 y were the most significant factors explaining 77.1% of the variance of BMC. After adjusting for other independent variables the prematurely born children who were thinner at 1 y of age subsequently had higher BMC values when examined at the age of 6-7 y. This study shows that growth patterns during the first year of life have long-term effects on bone mineralization.
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PMID:Determinants of bone mineral density in prematurely born children aged 6-7 years. 968 58

Diseases of the parathyroid gland are uncommon in women of childbearing age. However, total serum calcium is lower in normal pregnancy, but ionized serum calcium remains within normal limits. Serum parathyroid levels are slightly decreased in the second half of pregnancy. Primary hyperparathyroidism, if unrecognized, may increase maternal and fetal morbidity, which is related to the level of serum calcium. The most common cause is a single parathyroid adenoma, accounting for about 80% of cases. Maternal complications include acute pancreatitis, hypercalcemia crisis, and toxemia. An increased incidence of prematurity and neonatal hypocalcemia has been reported when maternal hypercalcemia is significantly elevated. Other causes of hypercalcemia are rare in pregnancy. Hypoparathyroidism is seldom seen in pregnancy; the most common cause is after surgical throidectomy. The doses of vitamin D and calcium do not change during pregnancy; however, hypercalcemia may develop in the postpartum period. Serum calcium should be determined at every trimester of pregnancy and at regular intervals after delivery, and in a significant number of patients, the dose of vitamin D should be reduced. Osteoporosis has been recognized most frequently in the last few years. It appears that those patients with a family history of osteoporosis and those on heparin therapy have a tendency to develop symptoms of the disease in pregnancy. Finally, lactation is not contraindicated in women with osteoporosis; although there is a slight decrease in bone density in the few months after delivery, this is a transient event and bone densitometry returns to prepregnancy levels in most women. Recent studies indicate that there is no need for calcium therapy during lactation with few exceptions, such as lactating adolescents, mothers nursing more than one child, and mothers with closely-spaced pregnancies.
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PMID:Parathyroid disorders of pregnancy. 988 Jan 18


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