Serum Levels of Vitamin D Metabolites in Children Receiving Total Parenteral Nutrition

Kimura, Shunta; Nose, Osamu; Harada, Tokuzo; Maki, Ichiro; Kanaya, S.; Tajiri, Hitoshi; Shimizu, Kazuo; Yamaoka, Kanji; Seino, Yoshiki; Yabuuchi, Hyakuji; Itakura, Takeo; Takagi, Yasuaki; Okada, Akira

doi:10.1177/0148607186010002191

Cited by 7 publications

(5 citation statements)

References 25 publications

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“…In Shils et al's 1985 study, 16 the average 25(OH)D level was 55.7 nmol/L, which is insufficient by current definitions, on once‐daily multivitamin infusions of MVI providing 200 IU (5 mcg) vitamin D 16 . In a study of pediatric patients, 25(OH)D levels were normal in all pediatric patients receiving between 200 IU (5 mcg) and 360 IU (9 mcg) vitamin D per day 14 . Therefore, while the daily requirement of parenteral vitamin D is unknown, it may be greater than what was once thought.…”

Section: Discussionmentioning

confidence: 99%

“…1,5,11 In studies from the 1980s and early 1990s, vitamin D deficiency was considered to be very uncommon. [12][13][14][15][16] One of the major reasons is that the definition of vitamin D deficiency has changed over time, as recently there has been increasing awareness of the importance of maintaining higher levels of 25(OH)D. 1 Vitamin D receptors are located in the bones, kidneys, intestines, brain, prostate, breasts, colon, and immune cells. Data have suggested a role for vitamin D at the cellular level in regulation of cellular proliferation and immune modulation and linked this role to various cancers as well as diseases of the autoimmune, endocrine, and cardiovascular systems.…”

Section: Discussionmentioning

confidence: 99%

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Vitamin D Deficiency in Patients Receiving Home Parenteral Nutrition

Thomson¹

2011

J Parenter Enteral Nutr

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Background: In addition to its role in bone metabolism, vitamin D has important immunomodulatory and antineoplastic effects. Patients on home parenteral nutrition (HPN) receive most of their vitamin D from intravenous (IV) supplementation. Vitamin D deficiency is common in the general population, and the adequacy of vitamin D supplementation in HPN patients is unclear. The purpose of this study is to determine the vitamin D status of patients on HPN. Methods: Consecutive patients seen in a regional home nutrition program had their oral and IV vitamin D intakes determined. Plasma 25‐hydroxyvitamin D levels were measured in all patients. Intake of calcium, magnesium, and phosphate were also determined. Results: The mean 25‐hydroxyvitamin D level in 22 patients receiving HPN for a mean of 33.5 months (range, 1–177) was 42 nmol/L. Vitamin D deficiency was present in 15 (68%) patients and vitamin D insufficiency in 6 (27%) patients. The mean dietary vitamin D intake was 79.5 IU per day, while the mean IV supplementation was 166 IU per day. Conclusions: In this study of a regional Canadian HPN program, there was a high prevalence of vitamin D deficiency/insufficiency affecting virtually all patients. All patients receiving HPN should be supplemented with vitamin D and have their 25‐hydroxyvitamin D levels monitored. Further studies are required to determine optimal methods and dosing of vitamin D replacement using oral supplements or ultraviolet light therapy.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Vitamin D Deficiency in Patients Receiving Home Parenteral Nutrition

Thomson¹

2011

J Parenter Enteral Nutr

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“…The introduction of breast milk fortifiers, which contain 30-40 mg/kg/day of phosphate, for these infants has all but eliminated this problem. By contrast, a far more common cause of phosphate depletion is from inappropriately supplemented parenteral nutrition (8, 9). Hypophosphatemia suppresses circulating levels of fibroblast growth factor 23 (FGF23), a phosphate-regulating hormone or “phosphatonin,” with subsequent disinhibition of calcitriol production.…”

Section: Diagnosis Of Hypercalcemia In Neonates and Infantsmentioning

confidence: 99%

Hypercalcemia in children and adolescents

Lietman

Germain‐Lee

Levine

2010

Current Opinion in Pediatrics

115

125

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Purpose of the review-In this review we define hypercalcemia levels, common etiologies for hypercalcemia in children, and treatment in order to aid the practicing pediatrician.Recent Findings-One rare cause of hypercalcemia in the child is Familial hypocalciuric hypercalcemia (FHH) [also termed familial benign hypercalcemia (FBH)]. Mutations that inactivate the Ca 2+ -sensing receptor gene FHH have been described as an autosomal dominant disorder, but recently milder mutations in the CASR have been shown to cause hypercalcemia when homozygous.Summary-Normal serum levels of calcium are maintained through the interplay of parathyroid, renal, and skeletal factors. In this review, we have distinguished the neonate and infant from the older child and adolescent because the causes and clinical features of hypercalcemia can differ in these two age groups. However the initial approach to the medical treatment of severe or symptomatic hypercalcemia is to increase the urinary excretion of calcium in both groups. In most cases, hypercalcemia is due osteoclastic bone resorption, and agents that inhibit or destroy osteoclasts are therefore effective treatments. Parathyroid surgery, the conventional treatment for adults with symptomatic primary hyperparathyroidism, is recommended for all children with primary hyperparathyroidism.

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“…Moreover. in thi s stud y , patient KT s had a low serum level of 25-0HD, despite pare nte ra l treatment with 250 I U/day of vitamin D 1 during total parenteral nutrit ion (Table I), while a s we have reported (21) during long-term total parentcral nutrition. dail y vitamin D. , intakes of 200 to 360 IU/da y yie lded normal level s of se rum 25-0HD and 1.25-(OH)~D in children without di seases of the liver and kidne y.…”

Section: Discussionmentioning

confidence: 73%

Vitamin D Metabolism in Biliary Atresia

Kimura,

Seino,

Harada

et al. 1988

J. pediatr. gastroenterol. nutr.

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SummaryIn children with biliary atrcsia, defective intestinal absorption of vitamin D and impaired hepatic uptake and 25‐hydroxylation of vitamin D lead to a deficiency of vitamin D and rickets. We recently observed severe rickets in a 3‐year‐old boy with corrected biliary atrcsia resulting in jaundice, despite oral treatment with 1α‐hydroxyvitamin D, (1α‐OHD,) or 1,25‐dihydroxyvitamin D, [1,25‐(OH)2D3]. He had low 25‐hydroxyvitamin D (25‐OHD) and high 1.25‐(OH)2D serum levels. Intramuscular vitamin D2 administration produced radiological and biochemical evidence of recovery. Oral 1.25‐(OH)2D3 (O.1 μg/kg) and 25‐OHD3 (10 μg/kg) tolerance tests were done to assess the ability to absorb vitamin D and the effectiveness of using these drugs orally. Eleven children with corrected biliary atresia, aged 9 months to 7 years, were studied. In oral 1.25‐(OH)2D3 tolerance tests, the increments above the baseline serum levels of 1.25‐(OH)2D were 140.7 ± 27.4 pg/ml in non‐jaundiced patients (n = 5). In jaundiced patients (n ‐ 3). 1,25‐(OH)2D3 absorption in two patients with high basal 1.25–(OH)2D values was lower than that of nonjaundiced patients: however, the absorption in the third patient with a low basal value was similar to that of nonjaundiced patients. In oral 25‐OHD3 tolerance tests, the mean increase of serum 25‐OHD was 48.9 ± 30.6 ng/ml in non‐jaundiced patients (n = 5) and 23.7 ± 9.5 ng/ml in jaundiced patients (n ‐ 4), the peak serum 25‐OHD levels being reached 6–12 h after 25‐OHD3 loading. The increase of serum 25‐OHD in jaundiced patients tended to be less than that in nonjaundiced patients at 4 hours after 25‐OHD3 administration (15.1 ± 12.6 vs 48.9 ± 30.6 ng/ml), but the difference was not significant. In addition, oral treatment with 25‐OHD, (4 μg/kg/day) for 3 months resulted in marked increases in the serum 25‐OHD level and hone density in the jaundiced patients (n = 3).

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Serum Levels of Vitamin D Metabolites in Children Receiving Total Parenteral Nutrition

Cited by 7 publications

References 25 publications

Vitamin D Deficiency in Patients Receiving Home Parenteral Nutrition

Vitamin D Deficiency in Patients Receiving Home Parenteral Nutrition

Hypercalcemia in children and adolescents

Vitamin D Metabolism in Biliary Atresia

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