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Bone mass and body composition after cessation of therapy for childhood cancer
Author(s) -
Nysom Karsten,
Mølgaard Christian,
Holm Kirsten,
Hertz Henrik,
Fleischer Michaelsen Kim
Publication year - 1998
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(1998)78:11+<40::aid-ijc12>3.0.co;2-h
Subject(s) - medicine , body mass index , cancer , childhood leukaemia , endocrinology , pediatrics
Our aim was to review current information on body composition and bone mass after cessation of therapy for childhood cancer and to present preliminary data on body composition and bone mass in a group of Danish survivors of childhood leukaemia or lymphoma. Elevated body‐mass index (weight/height 2 ; BMI) is frequent after treatment for childhood acute lymphoblastic leukaemia. BMI increases during therapy or within the first year after therapy and remains abnormal thereafter. Treatment with corticosteroids, abnormal growth‐hormone secretion after treatment with cranial irradiation (CI) or corticosteroids, younger age at diagnosis, or female gender were risk factors for elevated BMI in earlier studies. We evaluated 185 survivors of childhood leukaemia or lymphoma by dual‐energy X‐ray absorptiometry scanning. We found elevated whole‐body relative fat mass, which was associated with CI. Other studies found reduced bone mass in the radius, the lumbar spine and the whole body after treatment for childhood cancer. Growth‐hormone deficiency that is not adequately corrected, CI, reduced height or reduced weight were risk factors for reduced bone mass. In our 185 participants, the whole‐body bone mass was also reduced significantly compared with reference values. CI and older age at follow‐up were risk factors for reduced bone mass. We conclude that the elevated relative fat mass and reduced bone mass seen after treatment for childhood leukaemia or lymphoma is associated mainly with CI. Int. J. Cancer Supplement 11: 40–43, 1998. © 1998 Wiley‐Liss, Inc.