Osteoporosis in Survivors of Acute Lymphoblastic Leukemia

Abstract

Osteoporosis is currently receiving increasing attention as an important late effect in survivors of childhood cancer and its treatment because of their quality of life and its negative effect on the survivors' ability to perform developmentally appropriate activities. Survivors of childhood cancer are especially vulnerable because they are affected during childhood and adolescence, a time when peak bone mass should be achieved. This paper reviews decreased bone density in acute lymphoblastic leukemia (ALL), which is the most common childhood cancer and has a cure rate approaching 80%. Osteopenia/osteoporosis has been observed in all phases of the disease: at diagnosis, during treatment, and throughout the post-treatment period for as long as 20 years. Among the findings that have been described are musculoskeletal pain, disturbed gait, fractures, kyphosis, lordosis, and growth failure. Risk factors not specifically related to ALL include smoking, ingestion of carbonated beverages, and family history of "brittle bone" or fractures. Patients should be counseled in regard to diet, exercise, smoking cessation, and avoidance of carbonated beverages. There are a number of options for specific drug therapy; however, the administration of bisphosponates to children and adolescents must be approached with caution. Research is needed to determine how extensive the problem is and how to best prevent and treat the osteopenia/osteoporosis associated with ALL.

Urolithiasis in pediatric patients with acute lymphoblastic leukemia

“…Seven patients (35%) had a family history of urolithiasis in a firstdegree relative (Table 4). All stones analyzed biochemically were calcium stones (calcium oxalate in patients 4,5,6,8,9,17,19, and 20; calcium phosphate in patients 2 and 10; and calcium oxalate and phosphate in patient 7), and none were uric acid stones, consistent with the probable mechanism of steroidinduced hypercalciuria.…”

“…[1][2][3][4] Unfortunately, such regimens can cause complications, including bone demineralization, that can persist many years after the completion of therapy. 5,6 The underlying cause of osteopenia is thought to be a combination of direct effects of ALL on bone and demineralization induced by glucocorticoid therapy, an essential component of all treatment regimens for pediatric ALL. Other potential risk factors include ectopic parathyroid hormone production, paracrine lymphokines, reduced physical activity, use of methotrexate, cranial radiation therapy, reduced sunlight exposure, and reduced calcium intake.…”

Osteopenia and cancer in children and adolescents

“…135 The opportunity for healthcare professionals to contribute to the maintenance of bone health in young people is gaining acceptance. 136 Loss of bone mineral is clearly a common consequence to children and adolescents who receive treatment for cancer; [137][138][139] they fit the paradigm of chronic disease often attended by therapy with large cumulative doses of glucocorticosteroids. As nonpediatricians assume increasing responsibility for the long-term care of these survivors, so they will have to rise to this particular challenge, and bisphosphonates will be part of their armamentarium.…”

Bone mineral density and serum bone turnover markers in survivors of childhood acute lymphoblastic leukemia: Comparison of megadose methylprednisolone and conventional‐dose prednisolone treatments

“…To date, the negative effects of ALL and its treatment on bone mass and fracture risk are well established [19][20][21][22][23][24][25][26]. Osteopenia can occur due to therapy in patients with ALL [11][12][13][14][15].…”