Document Detail


Risperidone-related improvement of irritability in children with autism is not associated with changes in serum of epidermal growth factor and interleukin-13.
MedLine Citation:
PMID:  22070180     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Risperidone has been shown to improve serious behavioral problems in children with autism. Here we asked whether risperidone-associated improvement was related to changes in concentrations of inflammatory molecules in the serum of these subjects. Seven molecules were identified as worthy of further assessment by performing a pilot analysis of 31 inflammatory markers in 21 medication-free subjects with autism versus 15 healthy controls: epidermal growth factor (EGF), interferon-γ (IFN-γ), interleukin (IL)-13, IL-17, monocyte chemoattractant protein-1 (MCP-1), IL-1 and IL-1-receptor antagonist. Serum concentrations of these markers were then established in a different set of subjects that participated in a double-blind, clinical trial and an expanded group of healthy subjects. In the first analysis, samples obtained from subjects with autism at baseline visits were compared to visits after 8-week treatment with placebo (n=37) or risperidone (n=40). The cytokine concentrations remained stable over the 8-week period for both risperidone and placebo groups. In the second analysis, we explored further the differences between medication-free subjects with autism (n=77) and healthy controls (recruited independently; n=19). Serum levels of EGF were elevated in subjects with autism (median=103 pg/mL, n=75) in comparison to healthy controls (75 pg/mL, n=19; p<0.05), and levels of IL-13 were decreased in autism (median=0.8 pg/mL, n=77) in comparison to controls (9.8 pg/mL, n=19; p=0.0003). These changes did not correlate with standardized measures used for a diagnosis of autism. In summary, risperidone-induced clinical improvement in subjects with autism was not associated with changes in the serum inflammatory markers measured. Whether altered levels of EGF and IL-13 play a role in the pathogenesis or phenotype of autism requires further investigation.
Authors:
Zuzana Tobiasova; Klaas H B van der Lingen; Lawrence Scahill; James F Leckman; Yan Zhang; Wookjin Chae; James T McCracken; Christopher J McDougle; Benedetto Vitiello; Elaine Tierney; Michael G Aman; L Eugene Arnold; Liliya Katsovich; Pieter J Hoekstra; Fred Volkmar; Alfred L M Bothwell; Ivana Kawikova
Publication Detail:
Type:  Controlled Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-11-09
Journal Detail:
Title:  Journal of child and adolescent psychopharmacology     Volume:  21     ISSN:  1557-8992     ISO Abbreviation:  J Child Adolesc Psychopharmacol     Publication Date:  2011 Dec 
Date Detail:
Created Date:  2011-12-26     Completed Date:  2012-04-24     Revised Date:  2013-06-27    
Medline Journal Info:
Nlm Unique ID:  9105358     Medline TA:  J Child Adolesc Psychopharmacol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  555-64     Citation Subset:  IM    
Affiliation:
Department of Immunobiology, New Haven, CT 06520, USA.
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MeSH Terms
Descriptor/Qualifier:
Adolescent
Anti-Inflammatory Agents / pharmacology
Antipsychotic Agents / pharmacology,  therapeutic use
Autistic Disorder / blood,  drug therapy*,  psychology
Biological Markers / blood
Child
Child, Preschool
Double-Blind Method
Epidermal Growth Factor / blood,  drug effects*
Female
Humans
Inflammation Mediators / blood
Interleukin-13 / blood
Irritable Mood / drug effects*,  physiology
Male
Risperidone / pharmacology*,  therapeutic use*
Grant Support
ID/Acronym/Agency:
AS1474//Autism Speaks; MH01805/MH/NIMH NIH HHS; N01MH70001/MH/NIMH NIH HHS; N01MH70009/MH/NIMH NIH HHS; N01MH70010/MH/NIMH NIH HHS; N01MH80011/MH/NIMH NIH HHS
Chemical
Reg. No./Substance:
0/Anti-Inflammatory Agents; 0/Antipsychotic Agents; 0/Biological Markers; 0/Inflammation Mediators; 0/Interleukin-13; 106266-06-2/Risperidone; 62229-50-9/Epidermal Growth Factor
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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