Vitamin D and the Parenteral Nutrition Patient

DeLuca, Hector F.

doi:10.1053/j.gastro.2009.07.075

Cited by 23 publications

(20 citation statements)

References 90 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…42,43 These patients can have malabsorption of fat-soluble vitamins and can often develop vitamin D deficiency. 44,45 Chronic steroid therapy (eg, for inflammatory bowel disease or other conditions) can impair bone mineralization, decrease Ca absorption, and increase renal Ca excretion. Patients with IF or SBS may require supplemental Ca to prevent oxalate kidney stone formation.…”

Section: P and Ca Considerations In Specific Conditionsmentioning

confidence: 99%

Phosphorus and Calcium

Kraft

2014

Nut in Clin Prac

View full text Add to dashboard Cite

Phosphorus (P) and calcium (Ca) serve vital roles in the human body and are essential components of nutrition support therapy. Regulation of P and regulation of Ca in the body are closely interrelated, and P and Ca homeostasis can be affected by several factors, including disease states, clinical condition, severity of illness, and medications. Nutrition support clinicians must understand these factors to prevent and treat P and Ca disorders in patients receiving nutrition support therapy. This review provides an overview of P and Ca for the adult nutrition support clinician, with some emphasis on the hospitalized inpatient.

show abstract

Section: P and Ca Considerations In Specific Conditionsmentioning

confidence: 99%

Phosphorus and Calcium

Kraft

2014

Nut in Clin Prac

View full text Add to dashboard Cite

show abstract

“…Because frank toxicity of VD in humans has been associated with circulating 25(OH)D levels of 300 ng/ml, mice in the excess 25(OH)D 3 group seemed to be intoxicated with VD. 31,32 Although all mice were fed a high calcium/phosphate diet, serum calcium and phosphate levels remained low in the vehicle and sufficiency 25(OH)D 3 groups, whereas they were normal in the excess 25(OH)D 3 group (Table 1). As the serum calcium and phosphate levels in the excess 25(OH)D 3 group were comparable to those of wild-type mice (calcium 8.47 ± 0.36 mg/100 ml and phosphate 9.99 ± 1.42 mg/100 ml), no renal calcification was observed in the three groups (Supplementary Figure S1 online).…”

Section: Excess 25(oh)d 3 Exacerbated Tubulointerstitial Injury In Uumentioning

confidence: 91%

Excess 25-hydroxyvitamin D3 exacerbates tubulointerstitial injury in mice by modulating macrophage phenotype

Kusunoki

Matsui

Hamano

et al. 2015

Kidney International

View full text Add to dashboard Cite

Vitamin D hydroxylated at carbon 25 (25(OH)D) is generally recognized as a precursor of active vitamin D. Despite its low affinity for the vitamin D receptor (VDR), both deficient and excessive 25(OH)D levels are associated with poor clinical outcomes. Here we studied direct effects of 25(OH)D3 on the kidney using 25(OH)D-1α-hydroxylase (CYP27B1) knockout mice. The effects of 25(OH)D3 on unilateral ureteral obstruction were analyzed as proximal tubular cells and macrophages are two major cell types that take up 25(OH)D and contribute to the pathogenesis of kidney injury. Excess 25(OH)D3 in obstructed mice worsened oxidative stress and tubulointerstitial fibrosis, whereas moderate levels of 25(OH)D3 had no effects. The exacerbating effects of excess 25(OH)D3 were abolished in CYP27B1/VDR double-knockout mice and in macrophage-depleted CYP27B1 knockout mice. Excess 25(OH)D3 upregulated both M1 marker (TNF-α) and M2 marker (TGF-β1) levels of kidney-infiltrating macrophages. In vitro analyses verified that excess 25(OH)D3 directly upregulated TNF-α and TGF-β1 in cultured macrophages but not in tubular cells. TNF-α and 25(OH)D3 cooperatively induced oxidative stress by upregulating iNOS in tubular cells. Aggravated tubulointerstitial fibrosis in mice with excess 25(OH)D3 indicated that macrophage-derived TGF-β1 also had a key role in the pathogenesis of surplus 25(OH)D3. Thus, excess 25(OH)D3 worsens tubulointerstitial injury by modulating macrophage phenotype.

show abstract

“…The vitamin D level that may offer protection against disease is still undetermined, but many believe that serum 25OHD should be at least 75 nmol/L to provide adequate immunomodulatory effects 8 , 19 . ‐ 20 Until recently, little was known about vitamin D levels in patients receiving PN.…”

Section: Discussionmentioning

confidence: 99%

Prevalence of Vitamin D Deficiency and Response to Oral Vitamin D Supplementation in Patients Receiving Home Parenteral Nutrition

Kumar

Fenton

Shaheen

et al. 2012

J Parenter Enteral Nutr

View full text Add to dashboard Cite

Most patients receiving HPN had insufficient vitamin D status. When prescribed high doses of oral vitamin D, patients did not consistently achieve appropriate 25OHD levels. Alternate routes of vitamin D supplementation in patients receiving HPN should be considered. Large multicenter prospective studies are needed to best characterize the relationship between vitamin D dosing for HPN patients and vitamin D status.

show abstract

Vitamin D and the Parenteral Nutrition Patient

Cited by 23 publications

References 90 publications

Phosphorus and Calcium

Phosphorus and Calcium

Excess 25-hydroxyvitamin D3 exacerbates tubulointerstitial injury in mice by modulating macrophage phenotype

Prevalence of Vitamin D Deficiency and Response to Oral Vitamin D Supplementation in Patients Receiving Home Parenteral Nutrition

Contact Info

Product

Resources

About