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.
OBJECTIVE
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.


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.


CONCLUSIONS
Our results suggest that the development of APR due to glucocorticoid therapy is measurable and correlates with hormonal reaction patterns.
St. Anna Children's Hospital, Medical University, Vienna, Austria.
Rosemarie
R
Felder-Puig
Christiane
C
Scherzer
Michaela
M
Baumgartner
Magdalena
M
Ortner
Claudia
C
Aschenbrenner
Christian
C
Bieglmayer
Till
T
Voigtländer
E Renate
ER
Panzer-Grümayer
Wim J E
WJ
Tissing
Jan W
JW
Koper
Karl
K
Steinberger
Christian
C
Nasel
Helmut
H
Gadner
Reinhard
R
Topf
Michael
M
Dworzak
D000293:Adolescent; D016923:Cell Death / Q000187:drug effects; D002648:Child; D002652:Child Behavior / Q000187:drug effects; D002675:Child, Preschool; D003907:Dexamethasone / Q000008:administration & dosage / Q000009:adverse effects; D004305:Dose-Response Relationship, Drug; D004703:Endocrine System / Q000187:drug effects / Q000378:metabolism; D005247:Feeding Behavior / Q000187:drug effects; D005260:Female; D005938:Glucocorticoids / Q000008:administration & dosage / Q000009:adverse effects*; D006689:Hodgkin Disease / Q000134:cerebrospinal fluid / Q000188:drug therapy* / Q000235:genetics / Q000523:psychology*; D006728:Hormones / Q000097:blood / Q000378:metabolism; D006801:Humans; D008297:Male; D001523:Mental Disorders / Q000139:chemically induced*; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D010865:Pilot Projects; D011110:Polymorphism, Genetic; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000134:cerebrospinal fluid / Q000188:drug therapy* / Q000235:genetics / Q000523:psychology*; D011239:Prednisolone / Q000008:administration & dosage / Q000009:adverse effects; D011446:Prospective Studies; D011965:Receptors, Glucocorticoid / Q000235:genetics
D005938:Glucocorticoids; D006728:Hormones; D011965:Receptors, Glucocorticoid; D003907:Dexamethasone; D011239:Prednisolone