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Archives de pédiatrie
Volume 22, n° 6
pages 608-612 (juin 2015)
Doi : 10.1016/j.arcped.2015.03.005
Received : 25 October 2013 ;  accepted : 5 Mars 2015
Hypercalcémie menaçante révélatrice d’une leucémie aiguë lymphoblastique de l’enfant
Life-threatening hypercalcemia as the initial presentation of childhood acute lymphoblastic leukemia
 

M. Poirée a, , A. Dupont b, E. Gondon b, C. Boyer c, D. Dupont b
a Départment d’hématologie-oncologie pédiatrique, hôpital Archet 2, CHU de Nice, 151, route Saint-Antoine-de-Ginestière, 06202 Nice, France 
b Départment de réanimation pédiatrique, CHU Lenval, avenue de la Californie, 06000 Nice, France 
c Départment de radiologie pédiatrique, CHU de Nice, hôpital Archet 2, 151, route Saint-Antoine-de-Ginestières, 06202 Nice, France 

Auteur correspondant.
Résumé

L’hypercalcémie est une complication connue mais rare des leucémies aiguës lymphoblastiques de l’enfant (LAL). Nous rapportons le cas d’une LAL B dont les signes d’appel étaient une hypercalcémie sévère associée à des lésions ostéolytiques diffuses, sans anomalies hématologiques. Ce travail souligne les difficultés à établir formellement le diagnostic de LAL et la nécessité de répéter les examens (myélogrammes). Par ailleurs, certaines anomalies biologiques, cytogénétiques et moléculaires doivent être recherchées. Le dosage de la parathormone intacte (PTHi) permet d’éliminer une hyperparathyroïdie associée. La PTH-related protein (PTHrP) est souvent impliquée dans l’hypercalcémie secondaire à une pathologie maligne. La translocation t(17;19) et son transcrit de fusion E2A-HLF doivent être recherchés. Le contrôle de l’hypercalcémie doit associer le traitement de la pathologie sous-jacente à une prise en charge symptomatique associant une hyperhydratation et parfois des biphosphonates.

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Summary

Hypercalcemia in childhood acute lymphoblastic leukaemia (ALL) is a well-known but uncommon complication. Here, we report a case of B-ALL in which the first signs were life-threatening hypercalcemia associated with diffuse osteolytic lesions with no hematologic abnormalities. We draw attention to the difficulties formally establishing the ALL diagnosis. Bone marrow examinations must be repeated if necessary. Furthermore, biological, cytogenetic, and molecular aspects need to be investigated. Measurement of intact PTH can exclude hyperparathyroidism. PTHrP is possibly involved in hypercalcemia processes induced by tumor cells. The t(17;19) translocation and its E2A-HLF transcript fusion, which have been thought to be a poor prognostic factor, must be determined. Regarding severe hypercalcemia control, treatment is based on both underlying disease management and serum calcium level reduction with aggressive hydration and if necessary bisphosphonates.

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