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 HSCT. Age at transplantation of HSCT recipients ranged between 18 and 50 years (median, 30) and their post-HSCT follow-up lasted from 1 to 15 years (median, 6). Primary diseases were acute (n=44) or chronic (n=13) myeloid leukemia, Hodgkin disease (n=17), non-Hodgkin lymphoma (n=12), and multiple myeloma (n=14). Bone mass density (BMD) was measured by dual energy X-ray absorptiometry (DEXA) at lumbar spine (LS, L1-L4) and femoral neck (FN), and by quantitative phalangeal ultrasonometry. At the time of testing (mean follow-up after HSCT: 65 months; range: 1-15 years), LS (Z score mean: -0.4 and -0.9 in auto- and in allo-HSCT recipients, respectively; p<0.05), FN (-0.6 and -1.4 in autoand in allo-HSCT recipients, respectively; p<0.05) and phalanges (-1 and -1.5 in auto- and in allo-HSCT recipients, respectively; p<0.05) BMD were significantly reduced in comparison with BMD of 100 healthy controls (p<0.001 in all examined sites), suggesting more prolonged bone damage in cortical than in trabecular bone. BMD at LS, but not at FN, improved 3 years after HSCT in some patients, suggesting more prolonged bone damage in cortical than in trabecular bone. Phalangeal BMD values remained low for even more years, suggesting persistent bone micro-architectural alterations after HSCT. Eight patients developed AVN, 1 to 15 years following HSCT: 6 (12%) after allo-HSCT and 2 (4%) after auto-HSCT (p<0.05). Development of acute and chronic graft versus- host disease, was associated with both a more severe BMD reduction in all bone sites (<0.05) and with higher frequence of AVN. Reduced BMD and higher incidence of AVN was partly related to a reduced regenerating capacity of the normal marrow osteogenic cell compartment, measured by growing colony-forming units-osteogenic cells. Our results document that an accelerated bone mineral loss and micro-architectural deterioration occurs during the first years after HSCT and is more severe in the allogeneic setting, suggesting that all patients early after auto-HSCT and allo-HSCT should be evaluated for their bone status

Accelerated and persistent bone loss after autologous and allogeneic stem cell transplantation

Giudice V;SELLERI, Carmine
2013

Abstract

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 HSCT. Age at transplantation of HSCT recipients ranged between 18 and 50 years (median, 30) and their post-HSCT follow-up lasted from 1 to 15 years (median, 6). Primary diseases were acute (n=44) or chronic (n=13) myeloid leukemia, Hodgkin disease (n=17), non-Hodgkin lymphoma (n=12), and multiple myeloma (n=14). Bone mass density (BMD) was measured by dual energy X-ray absorptiometry (DEXA) at lumbar spine (LS, L1-L4) and femoral neck (FN), and by quantitative phalangeal ultrasonometry. At the time of testing (mean follow-up after HSCT: 65 months; range: 1-15 years), LS (Z score mean: -0.4 and -0.9 in auto- and in allo-HSCT recipients, respectively; p<0.05), FN (-0.6 and -1.4 in autoand in allo-HSCT recipients, respectively; p<0.05) and phalanges (-1 and -1.5 in auto- and in allo-HSCT recipients, respectively; p<0.05) BMD were significantly reduced in comparison with BMD of 100 healthy controls (p<0.001 in all examined sites), suggesting more prolonged bone damage in cortical than in trabecular bone. BMD at LS, but not at FN, improved 3 years after HSCT in some patients, suggesting more prolonged bone damage in cortical than in trabecular bone. Phalangeal BMD values remained low for even more years, suggesting persistent bone micro-architectural alterations after HSCT. Eight patients developed AVN, 1 to 15 years following HSCT: 6 (12%) after allo-HSCT and 2 (4%) after auto-HSCT (p<0.05). Development of acute and chronic graft versus- host disease, was associated with both a more severe BMD reduction in all bone sites (<0.05) and with higher frequence of AVN. Reduced BMD and higher incidence of AVN was partly related to a reduced regenerating capacity of the normal marrow osteogenic cell compartment, measured by growing colony-forming units-osteogenic cells. Our results document that an accelerated bone mineral loss and micro-architectural deterioration occurs during the first years after HSCT and is more severe in the allogeneic setting, suggesting that all patients early after auto-HSCT and allo-HSCT should be evaluated for their bone status
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11386/4207255
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