Abstract

Allogenic hematopoietic stem cell transplantation (allogenic HSCT) is employed to treat benign and malignanthematologic disorders. Increased use of allogenic HSCT has improved outcomes and patient survival, but has led to increased complications. Bone complications following HSCT include osteopenia, osteoporosis, avascular necrosis (AVN) and fracture. These complications decrease patient quality of life and increase morbidity. Allogenic HSCTassociated bone loss is linked to multiple factors including pre-transplant physiologic risk, myeloablative regimens, total-body irradiation, graft-versus-host disease (GVHD), immunosuppressive regimens, secondary hypogonadism, intestinal malabsorption and renal dysfunction. However, the precise molecular causes of HSCT-associated bone loss remain to be determined. Herein, we summarize the epidemiology, risk factors, and pathophysiology of allogenic HSCT-related bone loss and fracture. Also, review is made of the current modalities for prevention and treatment of these complications.

Highlights

  • Allogenic hematopoietic stem cell transplantation has become a standard treatment for numerous benign and malignant hematologic disorders

  • Allogenic HSCT-associated bone loss is linked to several factors including pre-transplant physiologic risk, myeloablative regimens, total-body irradiation, graft-versus-host disease (GVHD), immunosuppressive regimens, secondary hypogonadism, intestinal malabsorption and renal dysfunction

  • Likewise, coexisting secondary causes of bone loss should be comprehensively evaluated in HSCT patients including measurement of calcium, phosphate, TSH, ALP, creatinine, 5-hydroxy vitamin D, parathyroid hormone (PTH), FSH, and LH and testosterone levels as many of these may be amenable to modification

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Summary

Introduction

Allogenic hematopoietic stem cell transplantation (allogenic HSCT) has become a standard treatment for numerous benign and malignant hematologic disorders. The incidence of AVN is higher in patients undergoing allogenic, as opposed to autologous, HSCT, due, in part, to the increased risk of chronic GVHD and the accompanying high-dose corticosteroid use [3]. We summarize the epidemiology, risk factors, and pathophysiology of allogenic HSCT-related bone loss and fracture and review the current modalities for prevention and treatment of these complications.

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