Hdl Handle:
http://hdl.handle.net/10034/197720
Title:
Increased circulating Dickkopf-1 in Paget's disease of bone
Authors:
Marshall, Michael J.; Evans, Sally F.; Sharp, Christopher A.; Powell, Diane E.; McCarthy, Helen S.; Davie, Michael W. J.
Abstract:
This article discusses Dickkopf-1 (Dkk-1), which is a secreted inhibitor of Wnt signaling which in adults regulates bone turnover. Dkk-1 over-production is implicated in osteolytic disease where it inhibits bone formation and stimulates bone breakdown. Recently it was reported that osteoblastic cells from Paget's disease of bone (PDB) over-expressed Dkk-1. This study aimed yo see if increased Dkk-1 was detected in serum from patients with PDB. The results showed that Dkk-1 and total serum alkaline phosphatase activity (tsAP) were significantly elevated in sera from PDB patients. Patients with polyostotic PDB had significantly higher levels of tsAP but not Dkk-1, than monostotic patients. TsAP but not Dkk-1, was significantly lower in sera from bisphosphonate treated versus untreated PDB patients. Dkk-1 and tsAP were not significantly correlated. Dkk-1 may be a useful biomarker of PDB and the authors speculate that Dkk-1 may play a central role in the etiology of PDB.
Affiliation:
Charles Salt Centre, Robert Jones and Agnes Hunt Orthopaedic Hospital NHS Trust in Oswestry / University of Chester ; Charles Salt Centre, Robert Jones and Agnes Hunt Orthopaedic Hospital NHS Trust in Oswestry
Citation:
Clinical Biochemistry, 42(10-11), 2009, pp. 965-969
Publisher:
Elsevier
Journal:
Clinical Biochemistry
Publication Date:
Jul-2009
URI:
http://hdl.handle.net/10034/197720
Additional Links:
http://www.journals.elsevier.com/clinical-biochemistry/
Type:
Article
Language:
en
Description:
This article is not available through ChesterRep.
ISSN:
0009-9120
Appears in Collections:
Biological Sciences

Full metadata record

DC FieldValue Language
dc.contributor.authorMarshall, Michael J.en
dc.contributor.authorEvans, Sally F.en
dc.contributor.authorSharp, Christopher A.en
dc.contributor.authorPowell, Diane E.en
dc.contributor.authorMcCarthy, Helen S.en
dc.contributor.authorDavie, Michael W. J.en
dc.date.accessioned2011-12-16T17:11:49Zen
dc.date.available2011-12-16T17:11:49Zen
dc.date.issued2009-07en
dc.identifier.citationClinical Biochemistry, 42(10-11), 2009, pp. 965-969en
dc.identifier.issn0009-9120en
dc.identifier.urihttp://hdl.handle.net/10034/197720en
dc.descriptionThis article is not available through ChesterRep.en
dc.description.abstractThis article discusses Dickkopf-1 (Dkk-1), which is a secreted inhibitor of Wnt signaling which in adults regulates bone turnover. Dkk-1 over-production is implicated in osteolytic disease where it inhibits bone formation and stimulates bone breakdown. Recently it was reported that osteoblastic cells from Paget's disease of bone (PDB) over-expressed Dkk-1. This study aimed yo see if increased Dkk-1 was detected in serum from patients with PDB. The results showed that Dkk-1 and total serum alkaline phosphatase activity (tsAP) were significantly elevated in sera from PDB patients. Patients with polyostotic PDB had significantly higher levels of tsAP but not Dkk-1, than monostotic patients. TsAP but not Dkk-1, was significantly lower in sera from bisphosphonate treated versus untreated PDB patients. Dkk-1 and tsAP were not significantly correlated. Dkk-1 may be a useful biomarker of PDB and the authors speculate that Dkk-1 may play a central role in the etiology of PDB.en
dc.language.isoenen
dc.publisherElsevieren
dc.relation.urlhttp://www.journals.elsevier.com/clinical-biochemistry/en
dc.subjectdickkopf-1en
dc.subjectserumen
dc.subjectPaget's disease of boneen
dc.subjectAlkaline phosphataseen
dc.subjectwnten
dc.subjectinhibitoren
dc.titleIncreased circulating Dickkopf-1 in Paget's disease of boneen
dc.typeArticleen
dc.contributor.departmentCharles Salt Centre, Robert Jones and Agnes Hunt Orthopaedic Hospital NHS Trust in Oswestry / University of Chester ; Charles Salt Centre, Robert Jones and Agnes Hunt Orthopaedic Hospital NHS Trust in Oswestryen
dc.identifier.journalClinical Biochemistryen
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