Changes in RANKL, OPG, and 25(OH)D Levels in Children with Leukemia from Diagnosis to Remission

白血病儿童从诊断到缓解期间 RANKL、OPG 和 25(OH)D 水平的变化

阅读:7
作者:Salvador Atilano-Miguel, Lourdes Barbosa-Cortés, Rocío Ortiz-Muñiz, Jorge Maldonado-Hernández, Jorge A Martin-Trejo, Maricela Rodríguez-Cruz, Lourdes Balcázar-Hernández, Karina A Solís-Labastida, Benito A Bautista-Martínez, Azalia Juárez-Moya, Zayra Hernández-Piñón, Raeline A Galindo-Rodríguez, Adri

Background

The receptor activator of the nuclear factor-kB (RANK)/RANK ligand (RANKL)/osteoprotegerin (OPG) pathway is a determining pathway in the balance between bone formation and resorption, and disruptions in this complex can affect bone metabolism.

Conclusions

we suggest that the RANKL/OPG ratio could serve as a bone remodeling marker in ALL patients.

Methods

This study analyzes the changes in RANKL, OPG, and 25(OH)D levels; the RANKL/OPG ratio; and other bone turnover markers (BTMs) from diagnosis to complete remission in children with acute lymphoblastic leukemia (ALL). This is a prospective observational cohort study, carried out at the Instituto Mexicano del Seguro Social, Mexico City, including 33 patients (4-17 years) with newly diagnosed B-cell ALL. The patients were treated with the HP09 chemotherapy protocol. Children who had previously been treated with corticosteroids were excluded. A peripheral blood sample at diagnosis and remission was collected to determine the 25(OH)D and BTM concentrations.

Results

Increased RANKL (p = 0.001) and osteocalcin (p < 0.001) levels and RANKL/OPG ratio (<0.001) and a decreased OPG level (p = 0.005) were observed at remission, predominantly in the high-risk (HR) relapse and vitamin D deficiency groups. A negative association between RANKL and OPG (r = -0.454, p = 0.008) was observed. Conclusions: we suggest that the RANKL/OPG ratio could serve as a bone remodeling marker in ALL patients.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。