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Glucocorticoids in the Treatment of Children with Acute Lymphoblastic Leukemia and Hodgkin's Disease: A Pilot Study on the Adverse Psychological Reactions and Possible Associations with Neurobiological, Endocrine, and Genetic Markers

Authors' Affiliations: ¹ St. Anna Children's Hospital, ² Clinical Institute for Medical and Chemical Laboratory Diagnostics, ³ Institute of Neurology, ⁴ Department of Radiology, Medical University; ⁵ Children's Cancer Research Institute, Vienna, Austria; ⁶ Department of Pediatric Oncology/Hematology, Erasmus MC-Sophia Children's Hospital, ⁷ Department of Endocrinology, Erasmus MC, Rotterdam, the Netherlands; and ⁸ Department of Pediatric Oncology/Hematology, Beatrix Children's Hospital, University of Groningen and University Medical Center Groningen, Groningen, the Netherlands

Requests for reprints: Reinhard Topf, St. Anna Children's Hospital, Kinderspitalgasse 6, A-1090 Vienna, Austria, Phone: 43-1401-7070; Fax: 43-1401-7070; E-mail: reinhard.topf{at}stanna.at.

Purpose: We did a controlled study to assess adverse psychological reactions (APR) associated with high-dose glucocorticoid therapy and tried to detect somatic correlates for the observed reactions.

Patients and Methods: Our study included 37 patients with acute lymphoblastic leukemia (ALL) and 11 patients with Morbus Hodgkin (MH) disease, who were treated with high-dose glucocorticoid therapy, and 26 control patients with other types of malignancies. APRs were assessed with a standardized measure via parent-report. Patients with ALL and MH were further analyzed for signs of neuronal cell death in the cerebrospinal fluid, polymorphisms of the glucocorticoid receptor gene, as well as cortisol, adrenocorticorticotropic hormone, and dehydroepiandrosterone sulfate blood levels.

Results: Fifty-four percent of ALL, 36% of MH, and 23% of control patients developed APR in the first few weeks of therapy. Approximately 3.5 months later, the majority of patients with ALL showed no APR, similar to control patients. Patients demonstrating a higher, nonsuppressible secretion of cortisol and/or adrenocorticorticotropic hormone during glucocorticoid therapy were found to be more likely to develop APR. No sign of neuronal cell destruction and no correlation of APR with specific glucocorticoid receptor polymorphisms were found.

Conclusion: Our results suggest that the development of APR due to glucocorticoid therapy is measurable and correlates with hormonal reaction patterns.