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Query: UMLS:C0005940 (bone disease)
 7,459 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During pregnancy, calcium is continuously transferred directly from the maternal intestine to the fetal bone, a transfer that is mainly induced by the interrelated actions of the calcium-regulating hormones parathyroid hormone (PTH), 1,25-dihydroxyvitamin D (1,25(OH)2D) and calcitonin. It has recently been demonstrated in animals that PTH-related protein (PTHrP) is the fetal equivalent of PTH. Human PTHrP, originally described as a product of a human lung cancer cell line and implicated in the pathogenesis of humoral hypercalcemia of malignancy, is a protein with 141 amino acids, and it has biochemical actions similar to PTH. It is believed that fetal PTHrP is mainly derived from the placenta during early gestation and from the fetal parathyroid glands during further development and that this protein has the role of maintaining the maternal-fetal calcium gradient either alone or in concert with 1,25(OH)2D. With birth, the placental supply of calcium ceases abruptly, stimulating the increase of PTH and 1,25(OH)2D, which are the main regulators of postnatal calcium metabolism. Alterations in the placental calcium (and phosphate) gradient may be caused by maternal hypo- or hypercalcemia and placental insufficiency and may be followed by transient disorders of calcium metabolism in the newborn. Due to abrupt cessation of the calcium and phosphate supply after delivery at a time when mineral demands are the highest, preterm infants are especially prone to hypocalcemia and osteopathy. If bone disease of prematurity is to be prevented, the amounts of calcium and phosphate must be adequate, as demonstrated by laboratory tests, the most important being calcium and phosphate in urine and alkaline phosphatase activity in serum.
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PMID:[Perinatal calcium metabolism. Physiology and pathophysiology]. 143 20

In an extremely low birth weight infant fed expressed own mother's milk exclusively during the first 6 months of life, introduction of a human milk fortifier resulted in improvement of biochemical alterations consistent with metabolic bone disease of prematurity. Attempts to discontinue fortification at 9 weeks (discharge) and 21 weeks of age induced deterioration of biochemical parameters, demonstrating a persistent need for mineral supplementation during the whole period of breast-feeding. The effects of long-term human milk fortification are discussed.
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PMID:Biochemical evidence for the need of long-term mineral supplementation in an extremely low birth weight infant fed own mother's milk exclusively during the first 6 months of life. 222 59

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

Two separate episodes of rickets developed in a female infant of 25 weeks gestation and birthweight 690 g, who had congenital hypothyroidism and required parenteral nutrition for more than 100 days. We speculate that there is a relationship between metabolic bone disease of prematurity and the preterm infant's thyroid status.
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PMID:Hypothyroidism and unusual rickets in a very preterm infant. 260 67

Single-photon absorptiometry (SPA), developed in 1963 and adapted for infants by Steichen et al. in 1976, is an important tool to quantitate bone mineralization in infants. Studies of infants in which SPA was used include studies of fetal bone mineralization and postnatal bone mineralization in very low birth weight infants. The SPA technique has also been used as a research tool to investigate longitudinal bone mineralization and to study the effect of nutrition and disease processes such as rickets or osteopenia of prematurity. At present, it has little direct clinical application for diagnosing bone disease in single patients. The bones most often used to measure bone mineral content (BMC) are the radius, the ulna, and, less often, the humerus. The radius appears to be preferred as a suitable bone to measure BMC in infants. It is easily accessible; anatomic reference points are easily palpated and have a constant relationship to the radial mid-shaft site; soft tissue does not affect either palpation of anatomic reference points or BMC quantitation in vivo. The peripheral location of the radius minimizes body radiation exposure. Trabecular and cortical bone can be measured separately. Extensive background studies exist on radial BMC in small infants. Most important, the radius has a relatively long zone of constant BMC. Finally, SPA for BMC in the radius has a high degree of precision and accuracy.
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PMID:Bone mineral content measurement in small infants by single-photon absorptiometry: current methodologic issues. 329 50

Bone mineral content of the forearm was measured by photon absorptiometry in 17 preterm infants at a postconceptional age of 40 weeks. Radiographs of the forearm were assessed by Koo's method and plasma alkaline phosphatase activity was also measured at this time. Bone mineral content was significantly but weakly correlated with Koo score and was not significantly correlated with alkaline phosphatase activity. Neither of these two commonly used investigations accurately predicts the presence of underlying bone disease. Compared with 15 full term infants the preterm infants had significantly lower values of bone mineral content, palpated ulnar length, and crown-heel length. After adjusting for weight and ulnar length the preterm group still had a significantly lower mean value of bone mineral content than the full term group. Accurate diagnosis of osteopenia of prematurity requires photon absorptiometry, with bone mineral content assessed relative to body weight or ulnar length.
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PMID:Osteopenia of prematurity. 376 15

A total of 75 preterm infants with gestation less than 32 wk received total parenteral nutrition (TPN) using Vamin and Aminosyn as protein base lasting more than 20 days. They were monitored for signs of liver dysfunction, cholestatic jaundice, and TPN-induced metabolic bone disease (osteopenia of prematurity). It was observed that severity of TPN-induced cholestasis depends on the duration of TPN and quantity of protein infused. When used as a protein base, Vamin seemed to be superior to Aminosyn. TPN-induced metabolic bone disease was strongly correlated to the duration of TPN. We suggest close monitoring of critically ill preterm infants on TPN for quantity of protein infusate, liver dysfunction, cholestatic jaundice, and TPN-induced metabolic bone disease. Intravenous protein intake should be limited to less than 2.5 g/kg/day in preterm infants with gestation less than 32 wk.
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PMID:An evaluation of total parenteral nutrition using Vamin and Aminosyn as protein base in critically ill preterm infants. 392 17

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


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