scholarly journals Bone Mineral Density in Children with Fanconi Anemia after Hematopoietic Cell Transplantation

2015 ◽  
Vol 21 (5) ◽  
pp. 894-899 ◽  
Author(s):  
Anna Petryk ◽  
Lynda E. Polgreen ◽  
Jessie L. Barnum ◽  
Lei Zhang ◽  
James S. Hodges ◽  
...  
Keyword(s):  
Bone Mineral Density ◽  
Cell Transplantation ◽  
Bone Mineral ◽  
Fanconi Anemia ◽  
Hematopoietic Cell Transplantation ◽  
Hematopoietic Cell ◽  
Mineral Density

Prospective Study of Changes in Bone Mineral Density and Turnover in Children after Hematopoietic Cell Transplantation.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 1115-1115
Author(s):  
Anna Petryk ◽  
Tracy L. Bergemann ◽  
Kristen M. Polga ◽  
Kami J. Ulrich ◽  
Susan K. Raatz ◽  
...  
Keyword(s):  
Bone Mineral Density ◽  
Bone Loss ◽  
Prospective Study ◽  
Cell Transplantation ◽  
Bone Mineral ◽  
Hematopoietic Cell Transplantation ◽  
Hematopoietic Cell ◽  
Standard Normal Distribution ◽  
Mineral Density ◽  
Number Of Patients

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.

Treatment of Osteopenia/Osteoporosis in Pediatric Hematopoietic Cell Transplantation.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 57-57
Author(s):  
Jean E. Sanders ◽  
Paul A. Hoffmeister ◽  
Barry E. Storer
Keyword(s):  
Bone Mineral Density ◽  
Bone Density ◽  
Bone Loss ◽  
Cell Transplantation ◽  
Bone Mineral ◽  
Hematopoietic Cell Transplantation ◽  
Chronic Gvhd ◽  
Time Interval ◽  
Z Score ◽  
Mineral Density

Abstract The bone mineral density during childhood and the teen years is an important determinate of adult bone health. Decreased bone mineral density has been found to be a relatively common complication following adult hematopoietic cell transplantation (HCT), but has not been well studied after HCT among pediatric patients. Not surprisingly, an effective therapeutic approach to decreased bone mineral density has also not been developed for children. Patients and Methods: The records of 196 children <18 years of age who received HCT between 1/97-6/03 who survived for 1 year or more after HCT were reviewed. Patients selected for analysis had decreased bone mineral density (Z-score of <-1 standard deviation (SD) corrected for patient sex and age) and 2 or more bone mineral density (DEXA) scans performed after HCT. Change in bone density was calculated as the difference in L2-4 lumbar spine SD score. Variables associated with change in bone density were analyzed. Results: Among the 143 patients who had a DEXA scan performed, 82 (57%) demonstrated bone loss defined as <-1 SD Z-score. Fifty-six (68%) of these 82 patients had two or more DEXA scans and were analyzed. These 56 patients received an HCT when they were a median 10.8 (1.1–17.9) years of age, 33 were male, and 40 had chronic GVHD treated with corticosteroids and calcinurin inhibitor therapy. Patients were grouped according to treatment received for the bone loss. Nine patients changed therapy and were analyzed twice in separate treatment categories, hence there were 65 patients in 3 groups: 16 received a bisphosphonate or calcitonin (B/C), 37 calcium supplement only, and 12 no therapy. The B/C group included patients receiving pamidronate, zometa, fosamax, or calcitonin. Baseline median Z-scores were −2.6 SD for the B/C group, −2.2 SD for calcium, and −1.4 SD for no therapy. The median length of therapy was 446 days for the B/C group and 365 days for the calcium group. For the no therapy group, the time interval between DEXA scans was 324 days. Treatment with B/C or calcium compared with no therapy was significantly associated with improved bone density (p=0.0004). Corticosteroids, length of corticosteroid therapy (months), presence of chronic GVHD, gender, TBI received in preparative regimen, and patient age at therapy were not associated with change in bone mineral density. The mean change in bone mineral density per year was +1.16 SD for the B/C group, +0.16 for calcium, and +0.52 for no therapy. Although not statistically significant (p=0.44), concomitant steroid use for more than half the time interval between DEXA scans decreased therapeutic gains in the B/C group by −0.59 SD/year and −0.38 SD/year for the calcium group. The only observed side effect was hypocalcemia in one patient receiving pamidronate. Conclusions: These data demonstrate that the greatest improvement in bone mineral density was observed in patients receiving a bisphosphonate or calcitonin. Minimal to no toxicity was observed.

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