title: Cerebral glucose metabolism in survivors of childhood acute lymphoblastic leukemia.
abstract: BACKGROUND
  Cranial radiation therapy (CRT) has been suggested to be a principal factor responsible for long term neurocognitive deficits in survivors of acute lymphoblastic leukemia (ALL). However, neither reduction of the irradiation dose nor the elimination of irradiation entirely appear to have abolished neurocognitive impairment in long term ALL survivors. Positron emission tomography (PET) and [(18)F]-fluorodeoxyglucose (FDG) can be used to quantitate cerebral glucose metabolism, a potential indicator of treatment-induced adverse central nervous system (CNS) effects. The purpose of this study was to assess whether CRT is associated with defects in cerebral glucose metabolism in long term ALL survivors. The authors also studied whether chemotherapy and/or the severity of disease have deleterious effects on glucose metabolism.
  
  
  METHODS
  Forty long-term survivors of childhood ALL were studied using FDG PET. All subjects went through an elaborate neurocognitive assessment. In 20 of these children, the prophylactic treatment of the CNS had been CRT combined with methotrexate (MTX), and it was MTX only in the remaining 20 children.
  
  
  RESULTS
  No major differences were found in the regional cerebral glucose utilization or in neurocognitive performance between the irradiated and nonirradiated groups. A high leukocyte count at the time of diagnosis was found to be associated inversely with cerebral glucose utilization.
  
  
  CONCLUSIONS
  CRT does not appear to affect cerebral glucose metabolism in long term survivors of ALL. By contrast, the association between the leukocyte count and glucose utilization implies that disease severity may be partly responsible for adverse CNS effects in long term survivors of childhood ALL.
authors.affiliation: Turku Positron Emission Tomography Center, University of Turku, Turku, Finland.
authors.forename: M
authors.initials: M
authors.lastname: Kähkönen
authors.forename: L
authors.initials: L
authors.lastname: Metsähonkala
authors.forename: H
authors.initials: H
authors.lastname: Minn
authors.forename: T
authors.initials: T
authors.lastname: Utriainen
authors.forename: T
authors.initials: T
authors.lastname: Korhonen
authors.forename: M K
authors.initials: MK
authors.lastname: Norvasuo-Heilä
authors.forename: A
authors.initials: A
authors.lastname: Harila-Saari
authors.forename: T
authors.initials: T
authors.lastname: Aärimaa
authors.forename: H
authors.initials: H
authors.lastname: Suhonen-Polvi
authors.forename: U
authors.initials: U
authors.lastname: Ruotsalainen
authors.forename: O
authors.initials: O
authors.lastname: Solin
authors.forename: T T
authors.initials: TT
authors.lastname: Salmi
mesh_terms: D000293:Adolescent; D000367:Age Factors; D000964:Antimetabolites, Antineoplastic / Q000627:therapeutic use; D001288:Attention / Q000528:radiation effects; D001921:Brain / Q000378:metabolism* / Q000528:radiation effects; D001927:Brain Diseases / Q000209:etiology; D001932:Brain Neoplasms / Q000517:prevention & control; D002648:Child; D016371:Cranial Irradiation / Q000009:adverse effects; D005260:Female; D019788:Fluorodeoxyglucose F18; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D007958:Leukocyte Count; D008297:Male; D008606:Mental Processes / Q000528:radiation effects; D008727:Methotrexate / Q000627:therapeutic use; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000188:drug therapy / Q000378:metabolism / Q000532:radiotherapy*; D011597:Psychomotor Performance / Q000528:radiation effects; D011832:Radiation Injuries / Q000209:etiology; D019275:Radiopharmaceuticals; D011879:Radiotherapy Dosage; D017741:Survivors; D014055:Tomography, Emission-Computed
chemical_list: D000964:Antimetabolites, Antineoplastic; D019275:Radiopharmaceuticals; D019788:Fluorodeoxyglucose F18; D005947:Glucose; D008727:Methotrexate