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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
6
|
| pubmed:dateCreated |
1994-7-6
|
| pubmed:abstractText |
We examined two siblings who had severe rickets at ages 2 and 7 years, respectively, despite a history of adequate vitamin D intake. The patients' sera had calcium concentrations at the lower limits of normal, low phosphate concentrations, elevated alkaline phosphatase activity, and low levels of 25-hydroxyvitamin D. Treatment with high doses of vitamin D2 resulted in resolution of the biochemical abnormalities and radiographic deformities; pharmacologic doses of vitamin D2 were required to maintain normal concentrations of 25-hydroxyvitamin D in the serum even though vitamin D absorption was normal. These children may have a genetic defect of the 25-hydroxylation step in vitamin D activation.
|
| pubmed:grant | |
| pubmed:commentsCorrections | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jun
|
| pubmed:issn |
0022-3476
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
124
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
929-32
|
| pubmed:dateRevised |
2007-11-14
|
| pubmed:meshHeading | |
| pubmed:year |
1994
|
| pubmed:articleTitle |
A possible genetic defect in 25-hydroxylation as a cause of rickets.
|
| pubmed:affiliation |
Division of Pediatric Endocrinology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Case Reports,
Research Support, Non-U.S. Gov't
|