Physio-somatic symptoms in schizophrenia: association with depression, anxiety, neurocognitive deficits and the tryptophan catabolite pathway.
Identifieur interne : 000752 ( PubMed/Corpus ); précédent : 000751; suivant : 000753Physio-somatic symptoms in schizophrenia: association with depression, anxiety, neurocognitive deficits and the tryptophan catabolite pathway.
Auteurs : Buranee Kanchanatawan ; Sunee Sirivichayakul ; Supaksorn Thika ; Kiat Ruxrungtham ; André F. Carvalho ; Michel Geffard ; George Anderson ; Cristiano Noto ; Rada Ivanova ; Michael MaesSource :
- Metabolic brain disease [ 1573-7365 ] ; 2017.
Abstract
To investigate the frequency of physio-somatic symptoms (PS) symptoms in schizophrenia and their relation to positive, negative and affective symptoms; neurocognitive deficits and impairments in the tryptophan catabolite (TRYCAT) pathway. Eighty four patients with schizophrenia and 40 healthy controls were assessed using the 12 item Fibromyalgia and Chronic Fatigue Syndrome Rating scale (FF) and scales for negative and positive symptoms, depression and anxiety. Cognitive functioning was tested using the Cambridge Neuropsychological Test Automated Battery (CANTAB). Other assessments included: immunoglobulin (Ig)A and IgM responses to tryptophan catabolites (TRYCATs), namely quinolinic (QA), 3-OH-kynurenine (3HK), picolinic (PA), xanthurenic (XA) and kynurenic acid (KA) and anthranilic acid (AA). More than 50% of the patients studied had elevated levels of physio-somatic (PS) symptoms, significantly co-occurring with depression and anxiety, but not with negative or positive symptoms. PS symptoms were significantly associated with IgA/IgM responses to TRYCATs, including increased IgA responses to 3 HK, PA and XA, and lowered IgA to QA and AA. Fatigue, muscle pain and tension, autonomic and cognitive symptoms and a flu-like malaise were strongly associated with cognitive impairments in spatial planning and working memory, paired associative learning, visual sustained attention and attention set shifting. PS symptoms in schizophrenia aggregate with depression and anxiety symptoms and may be driven by TRYCAT patterning of IgA/IgM-responses, with IgA indicating mucosal-mediated changes and IgM indicating regulatory functions. As such, the patterning of IgA/IgM responses to TRYCATs may indicate differential TRYCATs regulation of neuronal and glia activity that act to regulate PS signalling in schizophrenia.
DOI: 10.1007/s11011-017-9982-7
PubMed: 28258445
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pubmed:28258445Le document en format XML
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<author><name sortKey="Sirivichayakul, Sunee" sort="Sirivichayakul, Sunee" uniqKey="Sirivichayakul S" first="Sunee" last="Sirivichayakul">Sunee Sirivichayakul</name>
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<author><name sortKey="Ruxrungtham, Kiat" sort="Ruxrungtham, Kiat" uniqKey="Ruxrungtham K" first="Kiat" last="Ruxrungtham">Kiat Ruxrungtham</name>
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<author><name sortKey="Geffard, Michel" sort="Geffard, Michel" uniqKey="Geffard M" first="Michel" last="Geffard">Michel Geffard</name>
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<author><name sortKey="Ivanova, Rada" sort="Ivanova, Rada" uniqKey="Ivanova R" first="Rada" last="Ivanova">Rada Ivanova</name>
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<front><div type="abstract" xml:lang="en">To investigate the frequency of physio-somatic symptoms (PS) symptoms in schizophrenia and their relation to positive, negative and affective symptoms; neurocognitive deficits and impairments in the tryptophan catabolite (TRYCAT) pathway. Eighty four patients with schizophrenia and 40 healthy controls were assessed using the 12 item Fibromyalgia and Chronic Fatigue Syndrome Rating scale (FF) and scales for negative and positive symptoms, depression and anxiety. Cognitive functioning was tested using the Cambridge Neuropsychological Test Automated Battery (CANTAB). Other assessments included: immunoglobulin (Ig)A and IgM responses to tryptophan catabolites (TRYCATs), namely quinolinic (QA), 3-OH-kynurenine (3HK), picolinic (PA), xanthurenic (XA) and kynurenic acid (KA) and anthranilic acid (AA). More than 50% of the patients studied had elevated levels of physio-somatic (PS) symptoms, significantly co-occurring with depression and anxiety, but not with negative or positive symptoms. PS symptoms were significantly associated with IgA/IgM responses to TRYCATs, including increased IgA responses to 3 HK, PA and XA, and lowered IgA to QA and AA. Fatigue, muscle pain and tension, autonomic and cognitive symptoms and a flu-like malaise were strongly associated with cognitive impairments in spatial planning and working memory, paired associative learning, visual sustained attention and attention set shifting. PS symptoms in schizophrenia aggregate with depression and anxiety symptoms and may be driven by TRYCAT patterning of IgA/IgM-responses, with IgA indicating mucosal-mediated changes and IgM indicating regulatory functions. As such, the patterning of IgA/IgM responses to TRYCATs may indicate differential TRYCATs regulation of neuronal and glia activity that act to regulate PS signalling in schizophrenia.</div>
</front>
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<DateCreated><Year>2017</Year>
<Month>03</Month>
<Day>04</Day>
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<DateRevised><Year>2017</Year>
<Month>07</Month>
<Day>18</Day>
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<JournalIssue CitedMedium="Internet"><Volume>32</Volume>
<Issue>4</Issue>
<PubDate><Year>2017</Year>
<Month>Aug</Month>
</PubDate>
</JournalIssue>
<Title>Metabolic brain disease</Title>
<ISOAbbreviation>Metab Brain Dis</ISOAbbreviation>
</Journal>
<ArticleTitle>Physio-somatic symptoms in schizophrenia: association with depression, anxiety, neurocognitive deficits and the tryptophan catabolite pathway.</ArticleTitle>
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<Abstract><AbstractText>To investigate the frequency of physio-somatic symptoms (PS) symptoms in schizophrenia and their relation to positive, negative and affective symptoms; neurocognitive deficits and impairments in the tryptophan catabolite (TRYCAT) pathway. Eighty four patients with schizophrenia and 40 healthy controls were assessed using the 12 item Fibromyalgia and Chronic Fatigue Syndrome Rating scale (FF) and scales for negative and positive symptoms, depression and anxiety. Cognitive functioning was tested using the Cambridge Neuropsychological Test Automated Battery (CANTAB). Other assessments included: immunoglobulin (Ig)A and IgM responses to tryptophan catabolites (TRYCATs), namely quinolinic (QA), 3-OH-kynurenine (3HK), picolinic (PA), xanthurenic (XA) and kynurenic acid (KA) and anthranilic acid (AA). More than 50% of the patients studied had elevated levels of physio-somatic (PS) symptoms, significantly co-occurring with depression and anxiety, but not with negative or positive symptoms. PS symptoms were significantly associated with IgA/IgM responses to TRYCATs, including increased IgA responses to 3 HK, PA and XA, and lowered IgA to QA and AA. Fatigue, muscle pain and tension, autonomic and cognitive symptoms and a flu-like malaise were strongly associated with cognitive impairments in spatial planning and working memory, paired associative learning, visual sustained attention and attention set shifting. PS symptoms in schizophrenia aggregate with depression and anxiety symptoms and may be driven by TRYCAT patterning of IgA/IgM-responses, with IgA indicating mucosal-mediated changes and IgM indicating regulatory functions. As such, the patterning of IgA/IgM responses to TRYCATs may indicate differential TRYCATs regulation of neuronal and glia activity that act to regulate PS signalling in schizophrenia.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kanchanatawan</LastName>
<ForeName>Buranee</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sirivichayakul</LastName>
<ForeName>Sunee</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Thika</LastName>
<ForeName>Supaksorn</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ruxrungtham</LastName>
<ForeName>Kiat</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Carvalho</LastName>
<ForeName>André F</ForeName>
<Initials>AF</Initials>
<AffiliationInfo><Affiliation>Department of Clinical Medicine and Translational Psychiatry Research Group, Faculty of Medicine, Federal University of Ceará, Fortaleza, CE, Brazil.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Geffard</LastName>
<ForeName>Michel</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Research Department, IDRPHT, Talence, France.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>GEMAC, Saint Jean d'Illac, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Anderson</LastName>
<ForeName>George</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>CRC Sotland & London, Eccleston Square, London, UK.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Noto</LastName>
<ForeName>Cristiano</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Department of Psychiatry, Universidade Federal de São Paulo (UNIFESP), Rua Pedro de Toledo, 669, 3 andar, CEP 04039-032, Sao Paulo, SP, Brazil.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ivanova</LastName>
<ForeName>Rada</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>Department of Psychiatry, Medical University of Plovdiv, Plovdiv, Bulgaria.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Maes</LastName>
<ForeName>Michael</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand. dr.michaelmaes@hotmail.com.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Psychiatry, Medical University of Plovdiv, Plovdiv, Bulgaria. dr.michaelmaes@hotmail.com.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Psychiatry, Faculty of Medicine, State University of Londrina, Londrina, Brazil. dr.michaelmaes@hotmail.com.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Revitalis, Waalre, the Netherlands. dr.michaelmaes@hotmail.com.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>IMPACT Strategic Research Center, Deakin University, Geelong, Australia. dr.michaelmaes@hotmail.com.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2017</Year>
<Month>03</Month>
<Day>03</Day>
</ArticleDate>
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<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Metab Brain Dis</MedlineTA>
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