Sequential Serum Aluminum and Urine Aluminum: Creatinine Ratio and Tissue Aluminum Loading in Infants With Fractures/Rickets

PEDIATRICS ◽  
1992 ◽  
Vol 89 (5) ◽  
pp. 877-881
Author(s):  
Winston W.K. Koo ◽  
Susan K. Krug-Wispe ◽  
Paul Succop ◽  
Robert Bendon ◽  
Lawrence A. Kaplan

Aluminum toxicity is associated with the development of bone disorders, including fractures, osteopenia, and osteomalacia. Fifty-one infants with a mean (± SEM) birth weight of 1007 ± 34 g, gestational age of 28.5 ± 0.3 weeks, and serial radiographic documentation at 3, 6, 9, and 12 months for the presence (n = 16) or absence (n = 35) of fractures and/or rickets were studied at the same intervals to determine the serial changes in serum aluminum concentrations and urine aluminum-creatinine ratios. Autopsy bone samples were used to determine the presence of tissue aluminum. Serum aluminum concentrations from 46 infants were stable and similar between groups, with mean values between 15 and 22 µg/L. Urine aluminum-creatinine (micrograms per milligram) ratios from 14 infants were higher in infants with fractures and/or rickets (0.26 ± 0.06 vs 0.12 ± 0.04) at onset, and rate of decrease in aluminum-cratinine ratio was faster in infants without fractures and/or rickets. All but three infants were tolerating complete enteral feeding at all sampling points. One infant who received aluminum-containing antacid had marked increase in serum aluminum to 83 µg/L while urine aluminum-creatinine ratio increased from 0.09 to a peak of 8.53. Vertebrae from three infants at autopsy (full enteral feeding was tolerated for 37 and 41 days in two infants, respectively) showed aluminum deposition in the zone of provisional calcification and along the newly formed trabecula. It is concluded that in enterally fed very low birth weight infants, serum aluminum levels and urine aluminum-creatinine ratios were similar in infants with and without fractures and/or rickets, presumably in part from modulation of aluminum absorption. However, aluminum absorption can be increased as indicated by increased serum and urine aluminum concentrations from aluminum antacid therapy. Bone accumulation of aluminum is possible with currently used enteral and parenteral nutrients, but the critical level of tissue aluminum loading associated with development of fractures and/or rickets remains to be determined.

PLoS ONE ◽  
2014 ◽  
Vol 9 (3) ◽  
pp. e92235 ◽  
Author(s):  
Luigi Corvaglia ◽  
Maria Pia Fantini ◽  
Arianna Aceti ◽  
Dino Gibertoni ◽  
Paola Rucci ◽  
...  

Author(s):  
Verena Walsh ◽  
Jennifer Valeska Elli Brown ◽  
Bethany R Copperthwaite ◽  
Sam J Oddie ◽  
William McGuire

PEDIATRICS ◽  
1979 ◽  
Vol 64 (4) ◽  
pp. 550-550
Author(s):  
Richard L. Schreiner

We concur with Babson and Reynolds that the volume of feeding in the first few weeks of life in very low birth weight infants is probably an important factor in the etiology of lactobezoar formation. We would certainly agree with their policy of increasing the volume of enteral feeding very gradually, but we doubt that limiting the total volume to 150 to 160 ml/kg/day until nipple feedings are established will prevent lactobezoar formation since 13 of our 17 cases of infants with lactobezoars in the past three years were receiving less than 160 ml/kg/day.


2009 ◽  
Vol 48 (4) ◽  
pp. 464-470 ◽  
Author(s):  
Christoph Härtel ◽  
Berit Haase ◽  
Kathryn Browning-Carmo ◽  
Corinna Gebauer ◽  
Evelyn Kattner ◽  
...  

2014 ◽  
Vol 90 (5) ◽  
pp. 227-230 ◽  
Author(s):  
Emily Hamilton ◽  
Cynthia Massey ◽  
Julie Ross ◽  
Sarah Taylor

PEDIATRICS ◽  
1987 ◽  
Vol 79 (6) ◽  
pp. 894-900
Author(s):  
Harry L. Greene ◽  
Barry L. Phillips ◽  
Linda Franck ◽  
Capri Mara Fillmore ◽  
Hamid M. Said ◽  
...  

Very low birth weight infants have little storage of hepatic retinol and are, therefore, highly dependent upon an exogenous supply. The recent association between low serum retinol level and bronchopulmonary dysplasia and the persistently low serum levels of retinol during total parenteral nutrition prompted a prospective study to evaluate serial changes in serum retinol levels during 1 month of total parenteral nutrition (retinol dose 455 µg/d) and again during 1 month of total enteral feeding (retinol dose 200 to 300 µg/d) in the same infants. Infants were divided into two groups. Group 1 consisted of infants weighing less than 1,000 g (n = 24) and group 2 consisted of infants weighing 1,000 to 1,500 g (n = 17). Although initial mean levels of retinol were similar in both groups (14.8 ± 0.9 and 13.5 ± 0.7 µg/dL), there was wide variation between infants. In group 1 infants, there was a significant (P < .01) decline in retinol level by the second week of life (to 9.2 ± 1 µg/dL), which persisted during total parenteral nutrition, but increased to 13.4 ± 2 after 1 week of enthral feeding. This level was maintained throughout enteral feeding. In group 2 infants, there was no significant change in serum retinol level throughout the study. During total parenteral nutrition, several infants had retinol levels below 10 µg/dL, a level associated with signs of retinol deficiency in older children. Because losses of retinol are known to occur in smaller volume total parenteral nutrition solutions, it was speculated that losses of retinol in our patients were due to retinol losses in the total parenteral nutrition delivery system. Because lipid might prevent these losses, in vitro studies were done to compare retinol losses in total parenteral nutrition v the usual daily dose of Intralipid. Results indicated 80% loss of retinol in total parenteral nutrition compared to only 10% loss in Intralipid. Lipid stability, as monitored by light microscopy and laser light scatter, indicated no changes in the stability of the lipid particles with the addition of the vitamin.


Author(s):  
Verena Walsh ◽  
Jennifer Valeska Elli Brown ◽  
Bethany R Copperthwaite ◽  
Sam J Oddie ◽  
William McGuire

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