Bone and mineral abnormalities in childhood acute lymphoblastic leukemia: Influence of disease, drugs and nutrition

摘要: In children with acute lymphoblastic leukemia (ALL), abnormalities in mineral homeostasis and bone mass were first reported by our group the late 1980s. Prospective longitudinal cohort studies 40 consecutive patients receiving treatment according to Dana-Farber Cancer Institute (DFCI) protocol 87-001 16 DFCI 91-001 afforded us opportunity explore various etiologies of observed metabolism, specifically leukemic disease process chemotherapeutic drugs such as steroids aminoglycoside antibiotics. At diagnosis ALL, >70% had abnormally low plasma 1,25-dihydroxyvitamin D, 73% osteocalcin 64% hypercalciuria, indicating an effect on vitamin D metabolism turnover. During remission induction, high-dose steroid (prednisone or dexamethasone) resulted further reduction elevated parathyroid hormone levels. 24 months chemotherapy-maintained remission, content (BMC), measured Z-scores, occurred children, most severely affecting those >11 years age. A BMC during 6 a positive predictive value for subsequent fracture. By end 2 therapy, fractures 39% radiographic evidence osteopenia was found 83% entire study group. Investigations biochemical basis revealed that hypomagnesemia developed 84% (of whom 52% hypermagnesuric) remained 70%. Altered magnesium status attributed renal wastage following cyclical prednisone therapy antibiotics amikacin fever accompanying neutropenia. Dietary intake absorption normal. 10 treated supplemental up 16–20 weeks, normalized only 50% subjects. Int. J. Supplement 11:35–39, 1998. © 1998 Wiley-Liss, Inc.