25-Hydroxylation of Vitamin D in Primary Biliary Cirrhosis

Skinner, R.K.; Sherlock, Sheila; Long, Richard; Wills, M. R.

doi:10.1016/s0140-6736(77)92166-3

Cited by 97 publications

(22 citation statements)

References 5 publications

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“…One mechanism for the higher prevalence of vitamin D deficiency in cirrhotics is impairment in the 25-hydroxylation of vitamin D [2,10,12,21], which occurs in cholestatic forms of liver disease and alcoholic cirrhosis and leads to low serum levels of 25(OH)D in relation to the degree of liver dysfunction. In one study [22], deficient hepatic hydroxylation was observed only in patients with advanced CLD, whereas others found no impediment to the production of vitamin D metabolites even in the advanced stages of liver disease [23,24]. The fact that cirrhosis was an independent risk factor for vitamin D deficiency in our study raises the question of whether impaired synthetic function of liver was responsible for low levels of vitamin D in some of our patients.…”

Section: Discussioncontrasting

confidence: 43%

Prevalence of Vitamin D Deficiency in Chronic Liver Disease

2009

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Section: Discussioncontrasting

confidence: 43%

Prevalence of Vitamin D Deficiency in Chronic Liver Disease

2009

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“…It proved to be almost normal except in biliary atresia (Seino et al 1978;Daum et al 1976) and in some patients with biliary cirrhosis (Wagonfeld et al 1976;Skinner et al 1977;Krawitt et al 1977), where results con¬ sistent both with vitamin D malabsorption and impaired 25-hydroxylation were obtained.…”

Section: Discussionmentioning

confidence: 95%

“…25-hydroxylation of vitamin D has been esti¬ mated in primary biliary cirrhosis (Wagonfeld et al 1976;Skinner et al 1977;Krawitt et al 1977), biliary atresia (Seino et al 1978;Daum et al 1976), alcoholic liver disease (Posner et al 1978), neonatal hepatitis (Seino et al 1978) and acute and chronic hepatitis (Imawari et al 1979). It proved to be almost normal except in biliary atresia (Seino et al 1978;Daum et al 1976) and in some patients with biliary cirrhosis (Wagonfeld et al 1976;Skinner et al 1977;Krawitt et al 1977), where results con¬ sistent both with vitamin D malabsorption and impaired 25-hydroxylation were obtained.…”

Section: Discussionmentioning

confidence: 99%

Hypoparathyroidism and liver disease – evidence for a vitamin D hydroxylation defect A case report

Gustafsson

Holmberg

Hardell

et al. 1984

Acta Endocrinologica

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The case history of a 4 year old girl with primary hypoparathyroidism is reported. Treatment with oral 1\g=a\-hydroxyvitaminD3 did not result in normal calcium and phosphate levels, whereas treatment with oral 1\g=a\,25-dihydroxyvitaminD3 did. During the treatment period, the patient developed signs of severe liver disease and died in a picture of increased intracranial pressure. Post-mortem examination revealed a giant cell hepatitis and severe cirrhosis. The clinical course is consistent with a liver vitamin D3 hydroxylation defect.Several clinically important diseases are associated with derangements of calcium and vitamin D meta¬ bolism. The availability of hydroxylated vitamin D metabolites has become important in treatment of such conditions (DeLuca 1982). A number of stud¬ ies (Haussler & Brickman 1982;Lund et al. 1980) has shown that the hypocalcaemia associated with hypoparathyroidism can be readily adjusted with small doses of lcx-hydroxyvitamin D3 or let,25-dihydroxyvitamin D3. The rapid turnover of these metabolites makes them preferable to vitamin D (Tojo et al. 1982).The use of vitamin D or monohydroxylated vitamin D metabolites requires renal and/or hepa¬ tic hydroxylations in the formation of the metabolically active form, lot,25-dihydroxvvitamin D

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“…Jaundiced patients should be given calcium supplements and intramuscular vitamin D, 100,000 units monthly, which will restore intestinal absorption of calcium to normal (68).…”

Section: Steatorrhoeamentioning

confidence: 99%