Open AccessSerum Dickkopf-1 is increased and correlates with reduced bone mineral density in patients with thalassemia-induced osteoporosis. Reduction post-zoledronic acid administration
Author(s) -
Ersi Voskaridou,
Dimitrios Christoulas,
Charoula Xirakia,
Konstantinos Varvagiannis,
Georgios Boutsikas,
Antonios Bilalis,
Efstathios Kastritis,
Αθανάσιος Παπαθεοδώρου,
Evangelos Terpos
Publication year - 2009
Publication title -
haematologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.782
H-Index - 142
eISSN - 1592-8721
pISSN - 0390-6078
DOI - 10.3324/haema-tol.2008.000893
Subject(s) - zoledronic acid , osteoporosis , medicine , bone mineral , bone remodeling , bone resorption , endocrinology , thalassemia , dkk1 , gastroenterology , wnt signaling pathway , chemistry , biochemistry , gene
Dickkopf-1 is an inhibitor of Wnt signaling, which is crucial for osteoblast differentiation. We evaluated serum levels of Dickkopf-1 in 66 patients with thalassemia-induced osteoporosis who received therapy with zoledronic acid in a placebo-controlled, randomized trial. At baseline, thalassemia patients had increased serum levels of Dickkopf-1 that correlated with reduced bone mineral density of the lumbar spine and the distal radius. High Dickkopf-1 also correlated with increased bone resorption and reduced bone formation markers. Zoledronic acid produced a reduction in serum Dickkopf-1, which was associated with bone mineral density increase after 12 months of therapy. On the contrary, placebo group showed a borderline increase of Dickkopf-1, which was higher in patients who showed deterioration in pain scores. These results suggest that Dickkopf-1 is implicated in the pathogenesis of osteoporosis in thalassemia and reveal Dickkopf-1 as a possible target for the development of novel agents for the management of thalassemia-induced osteoporosis.