Abstract：
OBJECTIVE:Hypophosphatasia (HP; MIM 241510) is an inborn error of bone metabolism, characterized by a genetic defect in the gene of the tissue-non-specific alkaline phosphatase TNSALP. Long-term data on bone mineral density measurements are not available. METHODS:We have analyzed changes of bone mineral density (pQCT and DXA) prospectively during 4years of follow-up in a cohort of 6 patients with childhood HP. RESULTS:At diagnosis hypermineralization of the trabecular bone in the metaphyseal area of long bones in affected children was noted. During 4 years of follow-up a gradual, significant decrease of mineralization was noted in the radial metaphyses. In contrast, BMC by DXA and total body DXA values were stable in comparison to healthy controls. During follow-up a systemic hyperprostaglandinism was documented in the majority of the patients. Non-steroidal anti-inflammatory drug treatment was evaluated by measuring prostaglandin excretion in the urine. CONCLUSIONS:Metaphyseal hypermineralization in childhood HP, which might be a compensation for a mechanically incompetent bony structure, decreased over time. There might be a pathophysiological link to continually elevated systemic prostaglandins.
journal_name
Joint Bone Spinejournal_title
Joint bone spineauthors
Girschick HJ,Haubitz I,Hiort O,Schneider Pdoi
10.1016/j.jbspin.2006.06.017subject
Has Abstractpub_date
2007-05-01 00:00:00pages
263-9issue
3eissn
1297-319Xissn
1778-7254pii
S1297-319X(07)00106-6journal_volume
74pub_type
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