scholarly journals Accelerated Bone Mineral Density Loss Occurs with Similar Incidence and Severity, But with Different Risk Factors, after Autologous versus Allogeneic Hematopoietic Cell Transplantation

2010 ◽  
Vol 16 (8) ◽  
pp. 1130-1137 ◽  
Author(s):  
Song Yao ◽  
Shannon L. Smiley ◽  
Kathleen West ◽  
Dominick Lamonica ◽  
Minoo Battiwalla ◽  
...  
2015 ◽  
Vol 21 (5) ◽  
pp. 894-899 ◽  
Author(s):  
Anna Petryk ◽  
Lynda E. Polgreen ◽  
Jessie L. Barnum ◽  
Lei Zhang ◽  
James S. Hodges ◽  
...  

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 1115-1115
Author(s):  
Anna Petryk ◽  
Tracy L. Bergemann ◽  
Kristen M. Polga ◽  
Kami J. Ulrich ◽  
Susan K. Raatz ◽  
...  

Abstract Osteoporosis is common in adults after hematopoietic cell transplantation (HCT). The data on bone mineral density (BMD) in children after HCT are limited. The goals of this prospective study were to determine the incidence, timing, magnitude and possible predictors of bone loss in children following HCT. The study population included 49 patients (age 5–18 years) who were eligible to receive HCT at the University of Minnesota. The patients were evaluated at baseline, 100 days, 6 months, and 1 year after HCT. Lumbar BMD (BMDL) was assessed by dual-energy x-ray absorptiometry. The number of patients with osteopenia increased from 18% at baseline to 33% one year after HCT, and with osteoporosis from 16% to 19%. Mean areal BMDL z-score decreased from −0.56 to −1.1 by 6 months and at 1 year was −0.94, which was significant compared to standard normal distribution (p=0.004 and p=0.022, respectively). The absolute loss of bone mineral corresponded to 5.3% reduction in areal BMDL and 4.8% reduction in volumetric BMDL. The level of bone-specific alkaline phosphatase decreased by 30% by day 100 (p=0.009), followed by recovery toward baseline by 6 months. The level of osteocalcin >6.5 ng/mL at day 100 predicted recovery from the initial bone loss by 1 year. A reduction in BMDL at 6 months correlated with a cumulative dose of glucocorticoids. In conclusion, this study demonstrates that bone loss is common in children after HCT and is primarily due to suppression of bone formation. Further studies are necessary to validate osteocalcin as a predictive biomarker.


2020 ◽  
Vol 21 (24) ◽  
pp. 9768
Author(s):  
Eleni Gavriilaki ◽  
Ioanna Sakellari ◽  
Panagiota Anyfanti ◽  
Ioannis Batsis ◽  
Anna Vardi ◽  
...  

(1) Background: survivors of allogeneic hematopoietic cell transplantation (alloHCT) suffer from morbidity and mortality due to cardiovascular events. We hypothesized that vascular injury and pro-coagulant activity are evident in alloHCT survivors without existing alloHCT complications or relapse. (2) Methods: we enrolled consecutive adult alloHCT survivors without established cardiovascular disease and control individuals matched for traditional cardiovascular risk factors (January–December 2019). Circulating microvesicles (MVs) of different cellular origins (platelet, erythrocyte, and endothelial) were measured by a standardized flow cytometry protocol as novel markers of vascular injury and pro-coagulant activity. (3) Results: we recruited 45 survivors after a median of 2.3 (range 1.1–13.2) years from alloHCT, and 45 controls. The majority of patients suffered from acute (44%) and/or chronic (66%) graft-versus-host disease (GVHD). Although the two groups were matched for traditional cardiovascular risk factors, alloHCT survivors showed significantly increased platelet and erythrocyte MVs compared to controls. Within alloHCT survivors, erythrocyte MVs were significantly increased in patients with a previous history of thrombotic microangiopathy. Interestingly, endothelial MVs were significantly increased only in alloHCT recipients of a myeloablative conditioning. Furthermore, MVs of different origins showed a positive association with each other. (4) Conclusions: endothelial dysfunction and increased thrombotic risk are evident in alloHCT recipients long after alloHCT, independently of traditional cardiovascular risk factors. An apparent synergism of these pathophysiological processes may be strongly involved in the subsequent establishment of cardiovascular disease.


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