Antineuronal antibody status and phenotype analysis in Tourette's syndrome.
Identifieur interne : 001C22 ( Ncbi/Merge ); précédent : 001C21; suivant : 001C23Antineuronal antibody status and phenotype analysis in Tourette's syndrome.
Auteurs : Davide Martino [Royaume-Uni] ; Giovanni Defazio ; Andrew J. Church ; Russell C. Dale ; Gavin Giovannoni ; Mary M. Robertson ; Michael OrthSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2007.
English descriptors
- KwdEn :
- Adolescent, Adult, Antibodies (metabolism), Blotting, Western (methods), Child, Enzyme-Linked Immunosorbent Assay (methods), Female, Humans, Logistic Models, Male, Molecular Weight, Nerve Tissue Proteins (immunology), Phenotype, Retrospective Studies, Tourette Syndrome (immunology), Tourette Syndrome (pathology), Tourette Syndrome (physiopathology).
- MESH :
- chemical , immunology : Nerve Tissue Proteins.
- chemical , metabolism : Antibodies.
- immunology : Tourette Syndrome.
- methods : Blotting, Western, Enzyme-Linked Immunosorbent Assay.
- pathology : Tourette Syndrome.
- physiopathology : Tourette Syndrome.
- Adolescent, Adult, Child, Female, Humans, Logistic Models, Male, Molecular Weight, Phenotype, Retrospective Studies.
Abstract
The Gilles de la Tourette syndrome (GTS) spectrum includes psychiatric comorbidities, mainly obsessive-compulsive disorder (OCD) and attention-deficit-hyperactivity disorder (ADHD). The role of environmental factors, e.g., antineuronal antibodies (ANeA), remains unclear. We compared the clinical features of ANeA-positive and ANeA-negative patients in 53 children and 75 adults with GTS. All diagnoses were made according to DSM-IV-TR criteria. A positive ANeA Western immunoblot showed bands for at least 1 of 3 reported striatal antigens (40, 45, and 60 kDa). Twelve children (23%) and 18 adults (25%) with GTS were ANeA-positive. Disease duration, tic phenomenology and severity, frequency of echo/pali/coprophenomena, self-injurious and aggressive behavior, or frequency of OCD comorbidity did not significantly differ between ANeA-positive and negative patients. Similar findings were obtained analyzing separately the three different antibody reactivities. A comorbid diagnosis of ADHD was significantly less frequent in GTS patients positive for the anti-60 kDa antibody only. Using a multivariate logistic regression model, adjusting for age, gender, and age at disease onset, a comorbid diagnosis of ADHD remained inversely associated with anti-60 kDa antibodies (odds ratio = 0.14; P = 0.002; 95% confidence interval 0.04-0.49). ANeA status does not differentiate a specific phenotype of GTS.
DOI: 10.1002/mds.21454
PubMed: 17516471
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pubmed:17516471Le document en format XML
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<term>Child</term>
<term>Enzyme-Linked Immunosorbent Assay (methods)</term>
<term>Female</term>
<term>Humans</term>
<term>Logistic Models</term>
<term>Male</term>
<term>Molecular Weight</term>
<term>Nerve Tissue Proteins (immunology)</term>
<term>Phenotype</term>
<term>Retrospective Studies</term>
<term>Tourette Syndrome (immunology)</term>
<term>Tourette Syndrome (pathology)</term>
<term>Tourette Syndrome (physiopathology)</term>
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<term>Child</term>
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<term>Logistic Models</term>
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<front><div type="abstract" xml:lang="en">The Gilles de la Tourette syndrome (GTS) spectrum includes psychiatric comorbidities, mainly obsessive-compulsive disorder (OCD) and attention-deficit-hyperactivity disorder (ADHD). The role of environmental factors, e.g., antineuronal antibodies (ANeA), remains unclear. We compared the clinical features of ANeA-positive and ANeA-negative patients in 53 children and 75 adults with GTS. All diagnoses were made according to DSM-IV-TR criteria. A positive ANeA Western immunoblot showed bands for at least 1 of 3 reported striatal antigens (40, 45, and 60 kDa). Twelve children (23%) and 18 adults (25%) with GTS were ANeA-positive. Disease duration, tic phenomenology and severity, frequency of echo/pali/coprophenomena, self-injurious and aggressive behavior, or frequency of OCD comorbidity did not significantly differ between ANeA-positive and negative patients. Similar findings were obtained analyzing separately the three different antibody reactivities. A comorbid diagnosis of ADHD was significantly less frequent in GTS patients positive for the anti-60 kDa antibody only. Using a multivariate logistic regression model, adjusting for age, gender, and age at disease onset, a comorbid diagnosis of ADHD remained inversely associated with anti-60 kDa antibodies (odds ratio = 0.14; P = 0.002; 95% confidence interval 0.04-0.49). ANeA status does not differentiate a specific phenotype of GTS.</div>
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<Abstract><AbstractText>The Gilles de la Tourette syndrome (GTS) spectrum includes psychiatric comorbidities, mainly obsessive-compulsive disorder (OCD) and attention-deficit-hyperactivity disorder (ADHD). The role of environmental factors, e.g., antineuronal antibodies (ANeA), remains unclear. We compared the clinical features of ANeA-positive and ANeA-negative patients in 53 children and 75 adults with GTS. All diagnoses were made according to DSM-IV-TR criteria. A positive ANeA Western immunoblot showed bands for at least 1 of 3 reported striatal antigens (40, 45, and 60 kDa). Twelve children (23%) and 18 adults (25%) with GTS were ANeA-positive. Disease duration, tic phenomenology and severity, frequency of echo/pali/coprophenomena, self-injurious and aggressive behavior, or frequency of OCD comorbidity did not significantly differ between ANeA-positive and negative patients. Similar findings were obtained analyzing separately the three different antibody reactivities. A comorbid diagnosis of ADHD was significantly less frequent in GTS patients positive for the anti-60 kDa antibody only. Using a multivariate logistic regression model, adjusting for age, gender, and age at disease onset, a comorbid diagnosis of ADHD remained inversely associated with anti-60 kDa antibodies (odds ratio = 0.14; P = 0.002; 95% confidence interval 0.04-0.49). ANeA status does not differentiate a specific phenotype of GTS.</AbstractText>
<CopyrightInformation>Copyright 2007 Movement Disorder Society</CopyrightInformation>
</Abstract>
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