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Accelerated Bone Mass Senescence After Hematopoietic Stem Cell Transplantation
Osteoporosis and avascular necrosis (AVN) are long-lasting and debilitating complications of hematopoietic stem cell transplantation (HSCT). We describe the magnitude of bone loss, AVN and impairment in osteogenic cell compartment following autologous (auto) and allogeneic (allo) HSCT, through the r...
Autores principales: | , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Università di Salerno
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3728811/ https://www.ncbi.nlm.nih.gov/pubmed/23905076 |
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author | Serio, B Pezzullo, L Fontana, R Annunziata, S Rosamilio, R Sessa, M Giudice, V Ferrara, I Rocco, M De Rosa, G Ricci, P Tauchmanovà, L Montuori, N Selleri, C. |
author_facet | Serio, B Pezzullo, L Fontana, R Annunziata, S Rosamilio, R Sessa, M Giudice, V Ferrara, I Rocco, M De Rosa, G Ricci, P Tauchmanovà, L Montuori, N Selleri, C. |
author_sort | Serio, B |
collection | PubMed |
description | Osteoporosis and avascular necrosis (AVN) are long-lasting and debilitating complications of hematopoietic stem cell transplantation (HSCT). We describe the magnitude of bone loss, AVN and impairment in osteogenic cell compartment following autologous (auto) and allogeneic (allo) HSCT, through the retrospective bone damage revaluation of 100 (50 auto- and 50 allo-HSCT) long-term survivors up to 15 years after transplant. Current treatment options for the management of these complications are also outlined. We found that auto- and allo-HSCT recipients show accelerated bone mineral loss and micro-architectural deterioration during the first years after transplant. Bone mass density (BMD) at the lumbar spine, but not at the femur neck, may improve in some patients after HSCT, suggesting more prolonged bone damage in cortical bone. Phalangeal BMD values remained low for even more years, suggesting persistent bone micro-architectural alterations after transplant. The incidence of AVN was higher in allo-HSCT recipients compared to auto-HSCT recipients. Steroid treatment length, but not its cumulative dose was associated with a higher incidence of bone loss. Allo-HSCT recipients affected by chronic graft versus host disease seem to be at greater risk of continuous bone loss and AVN development. Reduced BMD and higher incidence of AVN was partly related to a reduced regenerating capacity of the normal marrow osteogenic cell compartment. Our results suggest that all patients after auto-HSCT and allo-HSCT should be evaluated for their bone status and treated with anti-resorptive therapy as soon as abnormalities are detected. |
format | Online Article Text |
id | pubmed-3728811 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Università di Salerno |
record_format | MEDLINE/PubMed |
spelling | pubmed-37288112013-07-31 Accelerated Bone Mass Senescence After Hematopoietic Stem Cell Transplantation Serio, B Pezzullo, L Fontana, R Annunziata, S Rosamilio, R Sessa, M Giudice, V Ferrara, I Rocco, M De Rosa, G Ricci, P Tauchmanovà, L Montuori, N Selleri, C. Transl Med UniSa Articles Osteoporosis and avascular necrosis (AVN) are long-lasting and debilitating complications of hematopoietic stem cell transplantation (HSCT). We describe the magnitude of bone loss, AVN and impairment in osteogenic cell compartment following autologous (auto) and allogeneic (allo) HSCT, through the retrospective bone damage revaluation of 100 (50 auto- and 50 allo-HSCT) long-term survivors up to 15 years after transplant. Current treatment options for the management of these complications are also outlined. We found that auto- and allo-HSCT recipients show accelerated bone mineral loss and micro-architectural deterioration during the first years after transplant. Bone mass density (BMD) at the lumbar spine, but not at the femur neck, may improve in some patients after HSCT, suggesting more prolonged bone damage in cortical bone. Phalangeal BMD values remained low for even more years, suggesting persistent bone micro-architectural alterations after transplant. The incidence of AVN was higher in allo-HSCT recipients compared to auto-HSCT recipients. Steroid treatment length, but not its cumulative dose was associated with a higher incidence of bone loss. Allo-HSCT recipients affected by chronic graft versus host disease seem to be at greater risk of continuous bone loss and AVN development. Reduced BMD and higher incidence of AVN was partly related to a reduced regenerating capacity of the normal marrow osteogenic cell compartment. Our results suggest that all patients after auto-HSCT and allo-HSCT should be evaluated for their bone status and treated with anti-resorptive therapy as soon as abnormalities are detected. Università di Salerno 2013-01-04 /pmc/articles/PMC3728811/ /pubmed/23905076 Text en http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Articles Serio, B Pezzullo, L Fontana, R Annunziata, S Rosamilio, R Sessa, M Giudice, V Ferrara, I Rocco, M De Rosa, G Ricci, P Tauchmanovà, L Montuori, N Selleri, C. Accelerated Bone Mass Senescence After Hematopoietic Stem Cell Transplantation |
title | Accelerated Bone Mass Senescence After Hematopoietic Stem Cell Transplantation |
title_full | Accelerated Bone Mass Senescence After Hematopoietic Stem Cell Transplantation |
title_fullStr | Accelerated Bone Mass Senescence After Hematopoietic Stem Cell Transplantation |
title_full_unstemmed | Accelerated Bone Mass Senescence After Hematopoietic Stem Cell Transplantation |
title_short | Accelerated Bone Mass Senescence After Hematopoietic Stem Cell Transplantation |
title_sort | accelerated bone mass senescence after hematopoietic stem cell transplantation |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3728811/ https://www.ncbi.nlm.nih.gov/pubmed/23905076 |
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