Serum 25-hydroxy-vitamin D in hepatobiliary disease in infancy.

Kobayashi, Akio; Kawai, Saburo; Ohkubo, Mataichi; Ohbe, Yoshiro

doi:10.1136/adc.54.5.367

Cited by 14 publications

(8 citation statements)

References 14 publications

(17 reference statements)

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“…This is the largest such study and is consistent with other previous smaller reports by Kobayashi (14 infants) and Tokita (16 infants) (4,8). We did not find a link between the severity of vitamin D deficiency with age of presentation, the variant of BA (developmental or isolated groups) or CMV IgM status, all factors which have been incriminated in previous BA studies as aetiological or impacting on severity (12).…”

Section: Discussionsupporting

confidence: 93%

Vitamin D Levels in Infants With Biliary Atresia

Paul

Wright

et al. 2016

J. pediatr. gastroenterol. nutr.

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Section: Discussionsupporting

confidence: 93%

Vitamin D Levels in Infants With Biliary Atresia

Paul

Wright

et al. 2016

J. pediatr. gastroenterol. nutr.

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“…Our findings in this study support our hypothesis that vitamin D malabsorption is not the proximate cause of the osteopenia, at least in a segment of pediatric patients with chronic liver disease. Despite several reports of low circulating levels of 25(OH)D in pediatric patients with hepatic osteodystrophy (14–16), vitamin D deficiency produces secondary hyperparathyroidism and an increase in bone turnover. In contrast, we found evidence of a low bone‐formation rate as demonstrated by low serum osteocalcin levels, and transient evidence of increased resorption in only one patient, as shown by serum ICTP levels.…”

Section: Discussionmentioning

confidence: 97%

Hepatic osteodystrophy in chronic cholestasis: Evidence for a multifactorial etiology

Klein

Soriano

Shulman

et al. 2002

Pediatric Transplantation

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Children with cholestatic liver disease have been thought to develop hepatic osteodystrophy resulting from vitamin D and calcium malabsorption, resulting in secondary hyperparathyroidism and osteomalacia or rickets. However, treatment with vitamin D has not always proven successful in improving the bone disturbance. The aim of our study was to determine the role of vitamin D deficiency in the pathogenesis of hepatic osteodystrophy. We studied five patients, three female and two male, ages 0.9-19 yr, with biopsy-proven chronic cholestatic liver disease and previously low serum levels of vitamin D despite oral intake of vitamin D preparations. Patients were admitted to the Clinical Research Center for 8 days for sunlight deprivation and ultraviolet light substitution and for determinations of serum 25-hyroxyvitamin D(25(OH)) D2 and -D3, osteocalcin, and type I collagen telopeptide (ICTP), the last two being markers of bone formation and resorption, respectively. Samples were taken on admission, at discharge, and 1 month later. Results demonstrated low serum levels of osteocalcin and normal circulating levels of ICTP. Admission serum 25(OH)D2 levels were uniformly low or undetectable and remained so. Admission levels of circulating 25(OH)D3 were normal or low and did not rise during ultraviolet light therapy or subsequent resumption of oral vitamin D therapy and remained low 1 month later. These results indicate that in the face of low-normal to low total 25(OH)D levels, the low osteocalcin and normal ICTP levels suggest that decreased bone formation and not increased bone resorption is the main determinant of bone loss in a subset of children with chronic cholestatic liver disease.

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“…If a higher cutoff were to be used, as has been suggested by others, 14 then a higher frequency of vitamin D deficiency would have been identified (Figs 1 and 2). Cross-sectional studies of cholestatic children have revealed that .50% will have biochemical evidence of insufficiency of vitamins A, D, and E. 4,15,[20][21][22][23] In the current study, the effectiveness of a standardized regimen of vitamin supplementation in achieving normal serum levels of FSV was assessed in infants with BA after HPE. Supplementation with the FSV/TPGS preparation plus additional vitamin K failed to prevent FSV insufficiency in up to 58% of infants.…”

Section: Discussionmentioning

confidence: 99%

Efficacy of Fat-Soluble Vitamin Supplementation in Infants With Biliary Atresia

Shneider

Magee²,

Bezerra

et al. 2012

Pediatrics

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WHAT'S KNOWN ON THIS SUBJECT: Cholestasis predisposes to the development of fat-soluble vitamin (FSV) deficiency. D-a tocopheryl polyethylene glycol-1000 succinate and coadministered FSVs are absorbed in spite of cholestasis. WHAT THIS STUDY ADDS:Infants with biliary atresia with total bilirubin .2 mg/dL are at risk for fat-soluble vitamin (FSV) deficiency. A multivitamin preparation containing d-a tocopheryl polyethylene glycol-1000 succinate alone is not effective in treating biochemical FSV insufficiency in cholestatic infants. abstract OBJECTIVE: Cholestasis predisposes to fat-soluble vitamin (FSV) deficiencies. A liquid multiple FSV preparation made with tocopheryl polyethylene glycol-1000 succinate (TPGS) is frequently used in infants with biliary atresia (BA) because of ease of administration and presumed efficacy. In this prospective multicenter study, we assessed the prevalence of FSV deficiency in infants with BA who received this FSV/ TPGS preparation. METHODS:Infants received FSV/TPGS coadministered with additional vitamin K as routine clinical care in a randomized double-blinded, placebocontrolled trial of corticosteroid therapy after hepatoportoenterostomy (HPE) for BA (identifier NCT 00294684). Levels of FSV, retinol binding protein, total serum lipids, and total bilirubin (TB) were measured 1, 3, and 6 months after HPE.RESULTS: Ninety-two infants with BA were enrolled in this study. Biochemical evidence of FSV insufficiency was common at all time points for vitamin A (29%-36% of patients), vitamin D (21%-37%), vitamin K (10%-22%), and vitamin E (16%-18%). Vitamin levels were inversely correlated with serum TB levels. Biochemical FSV insufficiency was much more common (15%-100% for the different vitamins) in infants whose TB was $2 mg/dL. At 3 and 6 months post HPE, only 3 of 24 and 0 of 23 infants, respectively, with TB .2 mg/dL were sufficient in all FSV.CONCLUSIONS: Biochemical FSV insufficiency is commonly observed in infants with BA and persistent cholestasis despite administration of a TPGS containing liquid multiple FSV preparation. Individual vitamin supplementation and careful monitoring are warranted in infants with BA, especially those with TB .2 mg/dL. Pediatrics 2012;130:e607-e614 AUTHORS:

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Serum 25-hydroxy-vitamin D in hepatobiliary disease in infancy.

Cited by 14 publications

References 14 publications

Vitamin D Levels in Infants With Biliary Atresia

Vitamin D Levels in Infants With Biliary Atresia

Hepatic osteodystrophy in chronic cholestasis: Evidence for a multifactorial etiology

Efficacy of Fat-Soluble Vitamin Supplementation in Infants With Biliary Atresia

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