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

The absorption and retention of calcium and phosphorus in infants of 28 weeks' gestation, or less, who were fed either breast milk or a preterm formula, were determined in 22 balance studies. Breast milk contained significantly lower amounts of calcium and phosphorus than the formula milk. The percentage absorption of calcium was similar in the two groups, but the infants fed breast milk had greater urinary calcium losses and significantly lower calcium retention than the group fed formula milk. The percentage phosphate absorption was also similar in the two groups but because of the higher phosphate intake in the formula milk this group retained a significantly greater amount of phosphate. The extremely low birthweight infants fed on breast milk were phosphorus depleted, with low plasma phosphate concentrations, and seemed to retain as much phosphate as possible. The hypophosphataemia may result in reduced deposition of calcium in bone and explain the calciuria in the breast fed infants. Substrate deficiency may be an important factor in the aetiology of rickets of prematurity and, particularly if breast milk is used, preterm infants may require calcium and phosphate supplements from an early age.
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PMID:Calcium and phosphorus balance in extremely low birthweight infants in the first six weeks of life. 652 45

Rickets, hypocalcemia, hypophosphatemia, and hyperparathyroidism were found in a low-birth-weight premature infant. The concentration of plasma calcitriol (1,25-dihydroxyvitamin D) was 145 pg/mL. With additional exogenous calcitriol (37.5 ng/kg/24 hr) given for eight weeks, the biochemical abnormalities were corrected and healing of rickets was evident. Three months later, while receiving only 400 IU of ergocalciferal daily, the patient had normal levels of serum calcium, phosphate, and alkaline phosphatase with a serum calcitriol concentration of 36 pg/mL. These observations suggest that rickets of prematurity may involve a malabsorption of calcium and phosphorus with an elevated calcitriol level needed to overcome this inadequate absorption. Additional doses of calcitriol may be of benefit in these infants, although it must be given carefully. Furthermore, the role of phosphate supplementation in these infants requires consideration.
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PMID:Rickets of prematurity. Supranormal levels of serum 1,25-dihydroxyvitamin D. 696 86

Fifty-eight premature infants weighing less than 1,600 g at birth were fed a special formula. The formula contained nutrients in amounts recommended by the Committee ono Nutrition of the American Academy of Pediatrics for very low birth weight (VLBW) infants. The feeding studies were carried out at newborn nurseries in Tampa, Florida (study A, n = 25), Pittsburgh, Pennsylvania (study B, n = 20), and Oaklawn, Illinois (study C, n = 13). Study subjects were comparable in birth weight, gestational age, and in the duration of follow-up in the nurseries. All study subjects grew at rates of weight acquisition equivalent to the comparative fetal counterpart. Routine anthropometric measurements were similar to those of fetal development curves. Mean protein intake ranged from 2.3 to 3.7 g/kg/day and mean caloric intake from 105 to 150 kcal/kg/day. Late metabolic acidosis in association with prematurity was absent in all subjects studied as demonstrated by normal pH values, bicarbonate, and partial pressure of carbon dioxide. Serum sodium and serum chloride levels were normal. Serum calcium ranged from 8.3 to 10.1 mg/dl and serum phosphorus from 6.0 to 7.5 mg/dl. Total serum protein levels ranged from 4.5 to 5.1 g/dl. Blood urea nitrogen diminished progressively from 5.1 to 2 mg/dl in the course of the study. Serum glucose levels in samples taken prior to and 2 h after feeding did not demonstrate any evidence of reactive hypoglycemia.
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PMID:Results of feeding a special formula to very low birth weight infants. 718 45

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

Myopia is a frequent finding in preterm children. The close association between myopia and retinopathy of prematurity (ROP) suggested a causal relationship, but myopia of prematurity without ROP has yet to be explained. An alternative explanation is presented: myopia is caused by postnatal ellipsoid deformation of the spheric eyeball, i.e. excessive elongation of the optical, as a result of a dolichocephalic deformation of the skull with a short frontal axis. This deformation of the skull is the direct result of bone mineral deficiency frequently observed in very low birth weight infants with increasing postnatal age. This hypothesis is supported by the results of a historical comparison of very low birth weight infants without and with supplementation with calcium and phosphorus that was given in order to prevent postnatal bone mineral deficiency. In the unsupplemented group 4 of 23 children (61%) needed spectacles but only 6 out of 55 (11%) children who were supplemented as babies (questionnaire). Refraction measurements showed myopia stronger than -1 o.d. in group 1 in 5 of 14 infants, whereas in group 2 only 2 out of 22 infants were myopic (P < 0.05).
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PMID:Hypothesis: myopia of prematurity is caused by postnatal bone mineral deficiency. 775 30

Lumbar spinal bone mineral density (BMD) was measured in 40 preterm infants by dual-energy X-ray absorptiometry (DXA). During the first several months of life, their BMD was considerably lower than that of normal term infants and the osteopenia was more pronounced in the more preterm and smaller infants. Weak (inverse) correlations were found between the BMD and urinary calcium/creatinine or tubular phosphorus reabsorption ratio. Rickets-like changes in the forearm bones did not predict the greater spinal osteopenia. Follow-up study was performed in 10 preterms. In 3 of the 4 who underwent the last DXA between 8 and 12 months, BMD had improved remarkably. Our present study shows the potential of DXA for the assessment and management of osteopenia of prematurity.
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PMID:Measurement of lumbar spinal bone mineral density in preterm infants by dual-energy X-ray absorptiometry. 826 May 52

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

Rickets of prematurity is not uncommon in neonatal intensive care units. Nutritional rickets in childhood is usually caused by vitamin D deficiency, but the rickets of prematurity is mainly attributable to calcium and phosphorus deficiencies. We present a premature infant with sequelae of necrotizing enterocolitis who needed prolonged administration of total parenteral nutrition (TPN), and who sustained ricketic fracture. After high calcium-fortified TPN supplementation the fracture healed well, and serum alkaline phosphatase dropped. This finding shows (1) serum calcium and phosphorus levels are of predictive value regarding rickets, (2) regular follow-ups of alkaline phosphatase levels combined with radiography in high-risk groups of premature infants are good tools for monitoring rickets, and (3) prolonged TPN administration needs to contain higher calcium and phosphorus concentrations in prematurity than in childhood.
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PMID:Rickets of premature infants induced by calcium deficiency. A case report. 926 Mar 76

In this report, the outcome, diagnosis, management, and complications of pregnancy in dialysis patients are discussed. The advantages and disadvantages to the use of peritoneal dialysis and hemodialysis and the changes in dialysis regimen used in pregnant women are addressed. Maternal complications, particularly hypertension and anemia, are reviewed. This report looks at the approach to the management of anemia and calcium/phosphorus metabolism in the setting of limited information. The report also discusses pregnancy outcome for the mother and fetus, including the problem of prematurity and fetal loss. Special considerations in women with lupus and diabetes are noted. Pregnancy in dialysis patients remains a high-risk undertaking for both the patient and the infant. There are large gaps in our knowledge base regarding the effect of the abnormalities associated with renal failure on pregnancy. The survival of the infant and the safety of the mother depend on close cooperation among all the specialities involved, including nurses, doctors, nutritionists, and social workers from nephrology, perinatology, and neonatology.
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PMID:Management of the pregnant dialysis patient. 947 12

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


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