Increased prevalence of transglutaminase 6 antibodies in sera from schizophrenia patients

Nicola G. Cascella, Debby Santora, Patricia Gregory, Deanna L. Kelly, Alessio Fasano, William W Eaton

Research output: Contribution to journalArticle

Abstract

Gluten can cause extraintestinal manifestations with or without gastrointestinal symptoms and elevated antitissue transglutaminase 2 (tTG2) autoantibodies. Organ-specific gluten reaction involves immune response toward other transglutaminase (TG) isoforms including tTG3 (expressed in the skin, leading to dermatitis herpetiformis) and tTG6 (expressed in the brain, causing gluten ataxia). This analysis focuses on tTG6 antibodies, which have never been studied before in schizophrenia (SZ) and its relationships to tTG2 and to antigliadin antibodies. We previously showed an increased prevalence of tTG2 antibodies in gluten sensitive SZ patients compared with healthy controls (HC) that was not paralleled by an increased prevalence of antiendomysial antibody. To elucidate this discrepancy, we examined those tTG2 positive SZ patients for the presence of tTG6 antibody. We also searched for tTG6 antibodies in our sample of antigliadin (AGA) positive and AGA and tTG2 negative SZ patients. Seventy-four tTG2 positive SZ patients were compared with 148 age and gender-matched HC. Of the 74 tTG2 positive SZ patients, 16 were positive for tTG6 IgA for a prevalence of 22%. Only 4 HC were positive for tTG6 IgA for a prevalence of 2.7%. Among the AGA positive SZ patients, the prevalence of tTG6 IgA was 21.3% while 13.1% of the AGA and tTG2 negative SZ patients were positive for tTG6 IgA. The HC had a prevalence of 6%. Our results indicate a higher prevalence of tTG6 antibodies in SZ that may represent a biomarker useful to identify SZ patients who would benefit from a gluten-free diet.

Original languageEnglish (US)
Pages (from-to)867-871
Number of pages5
JournalSchizophrenia Bulletin
Volume39
Issue number4
DOIs
StatePublished - 2013

Fingerprint

Transglutaminases
Schizophrenia
Antibodies
Serum
Glutens
Immunoglobulin A
Dermatitis Herpetiformis
Gluten-Free Diet
Ataxia
Autoantibodies
Protein Isoforms
Biomarkers
Skin

Keywords

  • celiac disease
  • gluten sensitivity
  • gluten-free diet
  • schizophrenia
  • transglutaminase 6

ASJC Scopus subject areas

  • Psychiatry and Mental health

Cite this

Increased prevalence of transglutaminase 6 antibodies in sera from schizophrenia patients. / Cascella, Nicola G.; Santora, Debby; Gregory, Patricia; Kelly, Deanna L.; Fasano, Alessio; Eaton, William W.

In: Schizophrenia Bulletin, Vol. 39, No. 4, 2013, p. 867-871.

Research output: Contribution to journalArticle

Cascella, Nicola G. ; Santora, Debby ; Gregory, Patricia ; Kelly, Deanna L. ; Fasano, Alessio ; Eaton, William W. / Increased prevalence of transglutaminase 6 antibodies in sera from schizophrenia patients. In: Schizophrenia Bulletin. 2013 ; Vol. 39, No. 4. pp. 867-871.
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AB - Gluten can cause extraintestinal manifestations with or without gastrointestinal symptoms and elevated antitissue transglutaminase 2 (tTG2) autoantibodies. Organ-specific gluten reaction involves immune response toward other transglutaminase (TG) isoforms including tTG3 (expressed in the skin, leading to dermatitis herpetiformis) and tTG6 (expressed in the brain, causing gluten ataxia). This analysis focuses on tTG6 antibodies, which have never been studied before in schizophrenia (SZ) and its relationships to tTG2 and to antigliadin antibodies. We previously showed an increased prevalence of tTG2 antibodies in gluten sensitive SZ patients compared with healthy controls (HC) that was not paralleled by an increased prevalence of antiendomysial antibody. To elucidate this discrepancy, we examined those tTG2 positive SZ patients for the presence of tTG6 antibody. We also searched for tTG6 antibodies in our sample of antigliadin (AGA) positive and AGA and tTG2 negative SZ patients. Seventy-four tTG2 positive SZ patients were compared with 148 age and gender-matched HC. Of the 74 tTG2 positive SZ patients, 16 were positive for tTG6 IgA for a prevalence of 22%. Only 4 HC were positive for tTG6 IgA for a prevalence of 2.7%. Among the AGA positive SZ patients, the prevalence of tTG6 IgA was 21.3% while 13.1% of the AGA and tTG2 negative SZ patients were positive for tTG6 IgA. The HC had a prevalence of 6%. Our results indicate a higher prevalence of tTG6 antibodies in SZ that may represent a biomarker useful to identify SZ patients who would benefit from a gluten-free diet.

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