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High Body Mass Index Increases the Risk for Osteonecrosis in Children With Acute Lymphoblastic Leukemia

Riitta A. Niinimäki, Arja H. Harila-Saari, Airi E. Jartti, Raija M. Seuri, Pekka V. Riikonen, Eija L. Pääkkö, Merja I. Möttönen, Marjatta Lanning

From the Departments of Pediatrics and Radiology, Oulu University Hospital, Oulu; and the Departments of Radiology and Pediatrics, Kuopio University Hospital, Kuopio, Finland

Address reprint requests to Riitta A. Niinimäki, MD, Department of Pediatrics, Oulu University Hospital, Box 23, 90029 Oulu, Finland; e-mail: rsalonen{at}paju.oulu.fi

Purpose The aim of the study was to determine the incidence of and clinical risk factors for radiographic osteonecrosis (ON) in children treated for acute lymphoblastic leukemia (ALL) using the Nordic ALL protocols.

Patients and Methods Ninety-seven consecutive patients with childhood ALL were studied prospectively by magnetic resonance imaging (MRI) of the lower extremities at the end of the treatment.

Results Twenty-three (24%) of the 97 patients had ON. Seven of the patients (30%) were symptomatic, and three patients (13%) required surgical interventions. Multiple logistic regression analysis showed that high body mass index (BMI; P = .04), female sex (P = .01), older age at diagnosis (P < .001), and higher cumulative dexamethasone dose (P = .03) were independent risk factors for radiographic ON. The cumulative prednisone dose did not differ significantly between the patients with and without ON. The incidence of radiographic ON decreased significantly, from 36% to 7%, when the duration of dexamethasone exposure during the delayed-intensification phase was shortened from 3 to 4 weeks to 2 weeks with a taper (P = .001).

Conclusion ON as determined by MRI was found to be a common complication in children and adolescents after treatment with the Nordic ALL protocols. Revision of the ALL protocols by shortening the single exposure to dexamethasone has diminished the risk for ON remarkably. High BMI was identified as a new significant risk factor for ON.

Supported by grants from the Nona and Kullervo Väre Foundation, Finland.

Presented at the 23rd Annual Meeting of the Nordic Society for Paediatric Haematology and Oncology, May 8-11, 2005, Lillehammer, Norway, and at the 38th Congress of the International Society of Paediatric Oncology, September 17-21, 2006, Geneva, Switzerland.

Authors’ disclosures of potential conflicts of interest and author contributions are found at the end of this article.

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