The Plasma Levels of 25‐hydroxyvitamin D in Patients With Various Liver Diseases and the Response of 25‐hydroxyvitamin D to Vitamin D Treatment

Seino, Yoshiki; Shimotsuji, Tsunesuke; Kai, Hiroshi; Ikehara, Chiiko; Yabuuchi, Hyakuji

doi:10.1111/j.1651-2227.1978.tb16274.x

Cited by 25 publications

(16 citation statements)

References 9 publications

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“…Rickets is a common complication and is found in 59% of surgically unrepaired infants with EHBA in a series by Kobayashi et al (6) and 1211 8 infants with cholestatic liver disease by Roberts et al (22). The findings of reduced concentrations of serum 25-OH vitamin D and response to massive parenteral doses of vitamin D have led investigators to believe that severe intestinal malabsorption of vitamin D is responsible for production of rickets and bone disease in infants and children with hepatobiliary disease (23)(24)(25)(26)(27).…”

Section: -Oh Vitamin Dmentioning

confidence: 99%

Bone Disease in Chronic Childhood Cholestasis II. Better Absorption of 25-OH Vitamin D than Vitamin D in Extrahepatic Biliary Atresia

1990

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ABSTRACT. Infants with extrahepatic biliary atresia (EHBA) commonly develop rickets in infancy, whereas long-term survivors with EHBA commonly develop osteopenia with increasing age. We evaluated baseline vitamin D (Dz and D3), 25-OH vitamin D2 and D,, 1,25(0H)2 vitamin D, bone mineral content, and vitamin D2 and 25-OH vitamin D3 absorption in six infants and children (age 4-22 mo) with EHBA whose portoenterostomy failed to produce bile flow (group 1) and five infants and children (age 10112 to 8-4/12 y) with EHBA whose portoenterostomy repair led to good postoperative bile flow (group 2). Baseline serum vitamin Dz and DJ were undetectable in all subjects in group 1 despite supplements of 2500-5000 IU/ day, whereas all group 2 subjects given supplements (doses 400-5000 IU/d) had measurable levels. Baseline serum 25-OH vitamin D was less than 15 ng/mL in five of six (three with rickets) in group 1, whereas only one in group 2 had concentrations less than 15 ng/mL. A significantly blunted rise of vitamin D2 above baseline and reduced area under the absorption curve after 1000 IU/kg vitamin DZ were found in group 1 patients compared to group 2 (both p < 0.01), and five pediatric controls (both p < 0.01). The peak change and area under the absorption curve for serum 25-OH vitamin D3 from baseline after 10 pg/kg 25-OH vitamin D3 were significantly reduced for group 1 (both at least p < 0.05) and group 2 compared to controls (both p < 0.05). Malabsorption of supplemental doses of vitamin D compromises their efficacy to prevent rickets in infants with EHBA with poor bile flow after portoenterostomy. Despite severe malabsorption of vitamin D, we suggest that oral 25-OH vitamin D may be absorbed sufficiently to prevent rickets. (Pediatr Res 27:26-31, 1990) Abbreviations EHBA, extrahepatic biliary atresia PTH, parathyroid hormone EHBA accounts for approximately 25% of cases of neonatal cholestasis (1). Operable forms with atresia limited to the distal portions of the biliary tract account for 10-15% of the cases. In

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Section: -Oh Vitamin Dmentioning

confidence: 99%

Bone Disease in Chronic Childhood Cholestasis II. Better Absorption of 25-OH Vitamin D than Vitamin D in Extrahepatic Biliary Atresia

1990

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“…Regular diet was resumed 2 h later. Serum vitamin D3 levels were determined serially at 0, 4,8,12, and 24 h as outlined by Lo et al (14). On the next day, after another overnight fast, a mixture of the same dose of vitamin D3 and TPGS (Liqui-E; Twin Laboratories, Ronkonkoma, NY) 25 IU/kg was administered orally.…”

Section: Methodsmentioning

confidence: 99%

“…Regular diet was again resumed 2 h after dosing. Serial measurements of serum vitamin D3 and vitamin E levels were obtained at 0, 4,8,12,24, and 48 h.…”

Section: Methodsmentioning

confidence: 99%

“…Affected children have reduced levels of serum 25(OH)D secondary to poor intestinal absorption of fat-soluble vitamins because of reduced intraluminal bile acids, decreased sun exposure compounded by their chronic illness and multiple hospitalizations, and impaired hepatic hydroxylation of cholecalciferol to 25-OHcholecalciferol in end-stage liver disease (1,(4)(5)(6)(7). Despite the ingestion of massive doses of oral vitamin D2 or D3, metabolic bone disease may still develop.…”

mentioning

confidence: 99%

“…Despite the ingestion of massive doses of oral vitamin D2 or D3, metabolic bone disease may still develop. Various alternative modalities of therapy, including parenteral cholecalciferol and oral calcifediol and calcitriol, have been used in an attempt to normalize serum 25(OH)D levels (3)(4)(5)(8)(9)(10).…”

mentioning

confidence: 99%

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d-α-Tocopheryl Polyethylene Glycol-1000 Succinate Enhances the Absorption of Vitamin D in Chronic Cholestatic Liver Disease of Infancy and Childhood

et al. 1992

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ABSTRACT. Rickets and osteopenia, common problems in chronic childhood cholestasis, have been attributed to vitamin D malabsorption leading to reduced serum levels of 25(0H)-vitamin D. d-a-Tocopheryl polyethylene glycol-1000 succinate (TPGS), a water-soluble form of vitamin E, forms micelles at low concentration. We evaluated the potential role of TPGS in enhancing vitamin D absorption in eight children (aged 5 mo to 19 y) with severe chronic cholestasis (three extrahepatic biliary atresia, three nonsyndromic intrahepatic cholestasis, and two Alagille syndrome). To evaluate vitamin D absorption, the subjects received vitamin D3 1000 IU/kg (maximum dose of 50 000 IU); they then received the same dose of vitamin Dg mixed with TPGS (25 IU/kg). Serial serum vitamin D3 levels and areas under the curve were measured. All patients had enhanced absorption of vitamin D when it was administered in a mixture with TPGS. Mean area under the curve for serum vitamin D3 was 403.0 -C 83.1 nmol x h/L (155.6 f 32.1 ng x h/mL), with a mean rise above baseline of 13.5 f 1.8 nmol/L (5.2 f 0.7 ng/mL) with vitamin D/TPGS compared with no rise when vitamin D was given alone (both p < 0.001). Seven patients have been followed for at least 3 mo while receiving the vitamin D/TPGS combination. Those with initially low serum 25(OH)-vitamin D levels (C37.5 nmol/L or 15 ng/mL) had normalization (range 37.5-146 nmol/L) within 1 mo, whereas those with initially normal levels remained normal. While the patients were receiving vitamin D/TPGS, serum vitamin E to total lipid ratio either normalized or remained normal. In conclusion, 1 ) TPGS enhances vitamin D absorption in infants and children with severe chronic cholestasis and 2) the enhanced absorption of both vitamins is sufficient to normalize or maintain adequate levels of serum 25(OH)-vitamin D and vitamin E to total lipid ratio. (Pediatr Res 31: 146-150,1992) Abbreviations 25(OH)D, 25-hydroxy-vitamin D TPGS, d-a-tocopheryl polyethylene glycol-1000 succinate

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Iepatic vitamin D 25-hydroxylase: Inhibition by bile duct ligation or bile salts

et al. 1981

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Bone disease and low serum levels of 25-hydroxyvitamin D are prevalent in cholestatic syndromes such as primary biliary cirrhosis and biliary atresia. Defective hydroxylation, along with malabsorption of vitamin D, could be a factor in 25-hydroxyvitamin D depletion. To assess hepatic hydroxylation during experimental cholestasis, we studied vitamin D 25-hydroxylase activity in liver homogenates of rats after 7, 14, and 21 days of bile duct ligation. We have also studied the effects of bile acids on this enzyme in vitro. Hepatic 25-hydroxylation was depressed after 7 days ligation in only 1 of 4 animals, but by 14 days, all animals showed a marked reduction with a mean decrease of 64% in specific activity. Total liver enzyme activity was reduced by 43% at 14 days. In the ligated animals, liver histology showed progressive bile stasis, focal necrosis, bile ductular proliferation, periductular and periportal inflammation, and fibrosis. Addition of bile acids to the in vitro assay in concentrations approximating those found in cholestasis produced marked inhibition of vitamin D 25-hydroxylase activity.

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The Plasma Levels of 25‐hydroxyvitamin D in Patients With Various Liver Diseases and the Response of 25‐hydroxyvitamin D to Vitamin D Treatment

Cited by 25 publications

References 9 publications

Bone Disease in Chronic Childhood Cholestasis II. Better Absorption of 25-OH Vitamin D than Vitamin D in Extrahepatic Biliary Atresia

Bone Disease in Chronic Childhood Cholestasis II. Better Absorption of 25-OH Vitamin D than Vitamin D in Extrahepatic Biliary Atresia

d-α-Tocopheryl Polyethylene Glycol-1000 Succinate Enhances the Absorption of Vitamin D in Chronic Cholestatic Liver Disease of Infancy and Childhood

Iepatic vitamin D 25-hydroxylase: Inhibition by bile duct ligation or bile salts

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