The spectrum of metabolic bone disease in lymphoblastic leukemia

✍ Scribed by Susan L. Cohn; Elaine R. Morgan; Lawrence E. Mallette

• Publisher: John Wiley and Sons
• Year: 1987
• Tongue: English
• Weight: 490 KB
• Volume: 59
• Category: Article
• ISSN: 0008-543X
• DOI: 10.1002/1097-0142(19870115)59:2<346::aid-cncr2820590230>3.0.co;2-i

✦ Synopsis

Eight patients with childhood acute lymphoblastic leukemia (ALL) and hypercalcemia, osteopenia, or vertebral compression fractures seen at our institution during the last 12 years were evaluated for biochemical evidence of bone disease. Five patients were hypercalcemic, three had abnormal phosphorous levels, and four had elevated alkaline phosphatase values. Parathyroid hormone (PTH) was measured by a polyvalent radioimmunoassay in five patients and these levels were abnormally high in three patients. Four of these five patients also had PTH measured by a midregion-specific radioimmunoassay. One patient had a high PTH value. Two patients had low levels and one patient had a normal PTH level. Although these studies suggest diverse biochemical mechanisms may be contributing to the bone changes and hypercalcemia seen in childhood ALL, ectopic PTH production as well as ectopically produced fragments of PTH may have a role in mediating bone resorption and hypercalcemia.

Cancer 59:346-350, 1987.

KELETAL ABNORMALITIES demonstrated by plain S radiographs may occur in children with newly diagnosed acute lymphoblastic leukemia (ALL). Radiolucent metaphyseal bands, osteolytic and osteosclerotic lesions, periosteal new bone formation, generalized osteoporosis and vertebral compression fractures have been reported. 1-6 Although many investigators have attributed the bony lesions to cortical and periosteal tumor invasion: the precise etiologies of the bony changes are controveIsial. Biochemical findings of altered mineral metabolism appear to be uncommon, but hypercalcemia has been documented occasionally in childhood ALL associated with osteolytic lesions or limited areas of osteoporosis.' Osteoclast-activating facto1.8 and prostaglandin E9 have been