4.7 Article

Metabolic bone disease in children with intestinal failure is not associated with the level of parenteral nutrition dependency

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CLINICAL NUTRITION
卷 40, 期 4, 页码 1974-1982

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CHURCHILL LIVINGSTONE
DOI: 10.1016/j.clnu.2020.09.014

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Children; Intestinal failure; Home parenteral nutrition; Bone mineral density; Growth

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All children on long-term HPN are at risk of low BMD. High dependency on HPN (PNDI 120%) and very long-term HPN (>10 years) do not appear to increase the risk of growth failure or MBD. PN-related bone fractures were rare. Close follow-up remains mandatory.
Background & aims: Children on long-term home parenteral nutrition (HPN) are at increased risk of suboptimal growth and metabolic bone disease (MBD) i.e. decreased bone mineral density (BMD). The aims of this cross-sectional study were to assess growth and bone health in children on long term HPN and to identify risk factors for MBD. Methods: Children above the age of 5 years, stable on HPN for more than 2 years were included. Medical files were reviewed retrospectively and included demographics, gestational age, birth weight and height, indication for PN, age at PN start, duration of PN, number of weekly PN infusions, weight-for-age and height-for-age (SD), body mass index (BMI, kg/m2) as well as blood and urine analyses at the time of Dual X-ray absorptiometry (DXA) measurements. All BMD values were adjusted to statural age which corresponds to the 50th percentile of height. Growth failure (height-for-age < -2SD) and MBD (at least one BMD measurement < -2SD) were analyzed according to the indication of PN, duration of PN and PN dependency index (PNDI) by comparing means and performing logistic regression analysis. PNDI is the ratio of non-protein energy intake in HPN to resting energy expenditure using Schofield equations. Results: Forty children were assessed at 12.4 ? 4.5 years of age. Mean age at PN start was 1.1 ? 3.6 y (median 0.5). The indications for PN were short bowel syndrome (SBS, n = 21), chronic intestinal pseudoobstruction syndrome (CIPOS, n = 10) and congenital enteropathies (CE, n = 9). The mean number of PN perfusions was 6 ? 1/week. PNDI was 110 ? 30%. The mean serum level of 25-OHD3 was suboptimal at 26.5 ? 9.1 ng/mL (66.2 ? 22.8 nmol/L). The mean concentrations of calcium, phosphorus, and parathyroid hormone (PTH) were in the normal ranges. Eight children (20%) had PTH levels above normal with low 25-OHD3 levels. The mean weight-for-age and height-for-age Z-scores SDS were 0.4 ? 0.9 and -0.5 ? 1.1 respectively. The actual height was lower than genetic target height (p 0.001). The BMD Z-scores, adjusted to the 50th percentile of height, of the spine, the left femur and the whole body were: -1.1 ? 1.7, -1.2 ? 1.5 and -1.5 ? 1.8 SDS respectively. Children with CE had significantly lower BMD values than those with SBS and CIPOS (p = 0.01). Only two children had bone fractures after a mild trauma (5%). Conclusions: All children on long-term PN, are at risk of low BMD. High dependency on PN (PNDI 120%) and very long-term PN (>10 years) do not appear to increase the risk of growth failure nor MBD. PNrelated bone fractures were rare. Close follow-up remains mandatory. 0 2020 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.

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