Microarchitectural parameters and bone mineral density in patients with tumour-induced osteomalacia by HR-pQCT and DXA

Objective Tumour-induced osteomalacia (TIO) is a rare paraneoplastic condition characterized by decreased tubular phosphate reabsorption. The purpose of this study was to evaluate bone mineral density (BMD) and microarchitecture in six TIO patients compared with eighteen healthy controls. Design Volumetric BMD and microarchitecture were evaluated by high-resolution peripheral quantitative computerized tomography (HR-pQCT), and areal BMD was evaluated by dual-energy X-ray absorptiometry (DXA). Differences between groups were significant for p-value All TIO subjects were healthy until development of diffuse bone pain and multiple skeletal fractures and deformities. At baseline, sPi and TmPi/GFR were low and patients were on vitamin D and phosphate replacement at the study. Measurements and Results Compared with controls, TIO patients had lower aBMD at lumbar spine and hip, and lower vBMD at trabecular, cortical and entire bone, at distal radius (R) and distal tibia (T): Dtrab (R = 118.3 x 177.1; T = 72.3 x 161.3 gHA/cm(3)); Dcomp (R = 782.3 x 866.5; T = 789.1 x 900.9 gHA/cm(3)); and Dtotal (R = 234.5 x 317; T = 167.1 x 295.8 gHA/cm(3)). Bone microarchitecture was very heterogeneous among patients and significantly different from controls: lower Ct.Th (R = 0.59 x 0.80; T = 0.90 x 1.31 mm), BV/TV (R = 0.09 x 0.14; T = 0.06 x 0.13) and Tb.N (R = 1.46 x 2.10; T = 0.93 x 1.96 mm(-1)); and also higher Tb.Sp (R = 0.70 x 0.41; T = 1.28 x 0.45 mm) and Tb.1/N.SD (R = 0.42 x 0.18; T = 0.87 x 0.20 mm). Conclusion In this original study of TIO patients, DXA and HR-pQCT evaluation identified lower areal and volumetric BMD and severely impaired microarchitecture at cortical and trabecular bones, which probably contribute to bone fragility and fractures.

Automated summary

In this study of TIO patients, lower areal and volumetric BMD were identified using DXA and HR-pQCT evaluation, as well as severely impaired microarchitecture at cortical and trabecular bones, potentially contributing to bone fragility and fractures.