Premium
Bortezomib reduces serum dickkopf‐1 and receptor activator of nuclear factor‐ κ B ligand concentrations and normalises indices of bone remodelling in patients with relapsed multiple myeloma
Author(s) -
Terpos Evangelos,
Heath Deborah J.,
Rahemtulla Amin,
Zervas Kostas,
Chantry Andrew,
Anagnostopoulos Athanasios,
Pouli Anastasia,
Katodritou Eirini,
Verrou Evgenia,
Vervessou ElisavetChristine,
Dimopoulos MeletiosAthanassios,
Croucher Peter I.
Publication year - 2006
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.2006.06356.x
Subject(s) - bortezomib , osteoprotegerin , n terminal telopeptide , osteocalcin , endocrinology , medicine , bone remodeling , bone resorption , rankl , chemistry , multiple myeloma , alkaline phosphatase , osteopontin , activator (genetics) , receptor , biochemistry , enzyme
Summary The effect of bortezomib on bone remodelling was evaluated in 34 relapsed myeloma patients. At baseline, patients had increased serum concentrations of dickkopf‐1 (DKK‐1), soluble receptor activator of nuclear factor‐ κ B ligand (sRANKL), sRANKL/osteoprotegerin ratio, C‐telopeptide of type‐I collagen (CTX) and tartrate‐resistant acid phosphatase isoform‐5b (TRACP‐5b); bone‐alkaline phosphatase and osteocalcin were reduced. Serum DKK‐1 correlated with CTX and severe bone disease. Bortezomib administration significantly reduced serum DKK‐1, sRANKL, CTX, and TRACP‐5b after four cycles, and dramatically increased bone‐alkaline phosphatase and osteocalcin, irrespective of treatment response. This is the first study showing that bortezomib reduces DKK‐1 and RANKL serum levels, leading to the normalisation of bone remodelling in relapsed myeloma.