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Mineral homeostasis and bone mass at diagnosis in children with acute lymphoblastic leukemia
J M Halton1, S A Atkinson, L Fraher
1Department of Pediatrics, McMaster University, Hamilton, Ontario, Canada.
Insights
Children with acute lymphoblastic leukemia (ALL) often show bone issues at diagnosis. These findings suggest that the leukemia itself, not just treatment, causes defective bone mineralization and reduced bone mass in pediatric patients.
Area of Science:
- Pediatric Oncology
- Pediatric Endocrinology
- Bone Metabolism
Background:
- Children with acute lymphoblastic leukemia (ALL) can experience osteopenia and fractures.
- The cause of these bone abnormalities in ALL patients is debated, with potential links to disease or treatment.
Purpose of the Study:
- To investigate whether osteopenia and fractures in children with ALL are associated with the leukemia itself or its treatment.
- To assess bone and mineral status in children newly diagnosed with ALL.
Main Methods:
- Prospective study of 40 children with ALL before therapy initiation.
- Biochemical markers (minerals, vitamin D), bone mass (radiography, dual-photon absorptiometry), and bone turnover markers were assessed.
- Correlations between clinical, leukemia, and bone parameters were analyzed.
Main Results:
- Musculoskeletal pain occurred in 36% of patients at diagnosis.
- Osteopenia and fractures were observed in 13% and 10% of children, respectively.
- Low plasma osteocalcin and 1,25-dihydroxyvitamin D3 levels were noted, with hypercalciuria in 64%; bone biopsy revealed mineralization defects in 3/9 children.
Conclusions:
- Children with ALL exhibit bone metabolism and bone mass alterations at diagnosis.
- Defective mineralization appears to be the mechanism behind reduced bone mass in these patients.
- The leukemic process is implicated as the causative factor for bone abnormalities in children with ALL.
Objective:
To determine whether the osteopenia and unusual fractures observed in children with acute lymphoblastic leukemia (ALL) were related to the disease rather than to its treatment.
Design:
Prospective analysis of the bone and mineral status in 40 consecutive children with ALL seen in a pediatric tertiary-care referral center.
Methods:
Biochemical indicators of mineral, endocrine, and vitamin D status were measured before initiation of therapy. Bone mass was determined radiographically and by dual-photon absorptiometry of the lumbar region of the spine (L2-L4). Correlations between clinical observations, leukemia variables, bone mass, and biochemical assessment were determined.
Results:
At the time of diagnosis musculoskeletal pain was present in 36% of patients and was more common in children with CD10-positive leukemia and leukocyte counts less than 20 x 10(9) cells/L. Radiographic evidence of osteopenia and fractures was observed in 13% and 10% of children, respectively. The mean bone mineral content was normal. Bone mass measurement z scores correlated with plasma 1,25-dihydroxyvitamin D3 concentrations (r = 0.43, p < 0.05). Plasma calcium, magnesium, phosphorus, and 25-hydroxyvitamin D3 levels were normal. Low plasma osteocalcin (mean +/- SD, 1.6 +/- 1.6 nmol/L) and 1,25-dihydroxyvitamin D3 (33.4 +/- 26.4 pmol/L) values were observed. Parathyroid hormone levels were low in 14% of children. Hypercalciuria was detected in 64% of children. Urinary deoxypyridinoline was lower (p < 0.01) than in age-matched control subjects. Histomorphometric measurements of iliac bone showed abnormalities in mineralization in the biopsy specimens from three of nine children.
Conclusion:
Most children with ALL have alterations in bone metabolism and bone mass when first examined. These data suggest defective mineralization as the mechanism for decreased bone mass and implicate the leukemic process as causative.