Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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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PMID:Increased prevalence of transglutaminase 6 antibodies in sera from schizophrenia patients. 2251 48

We propose a biochemical mechanism for celiac disease and non-celiac gluten sensitivity that may rationalize many of the extradigestive disorders not explained by the current immunogenetic model. Our hypothesis is based on the homology between the 33-mer gliadin peptide and a component of the NMDA glutamate receptor ion channel - the human GRINA protein - using BLASTP software. Based on this homology the 33-mer may act as a natural antagonist interfering with the normal interactions of GRINA and its partners. The theory is supported by numerous independent data from the literature, and provides a mechanistic link with otherwise unrelated disorders, such as cleft lip and palate, thyroid dysfunction, restless legs syndrome, depression, ataxia, hearing loss, fibromyalgia, dermatitis herpetiformis, schizophrenia, toxoplasmosis, anemia, osteopenia, Fabry disease, Barret's adenocarcinoma, neuroblastoma, urinary incontinence, recurrent miscarriage, cardiac anomalies, reduced risk of breast cancer, stiff person syndrome, etc. The hypothesis also anticipates better animal models, and has the potential to open new avenues of research.
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PMID:Extraintestinal manifestations of celiac disease: 33-mer gliadin binding to glutamate receptor GRINA as a new explanation. 2699 Feb 86

A 51-year-old male was referred to the diabetes clinic by the GP with low HbA1c (13 mmol/mol). His complaints were dizziness and intermittent palpitations for the last two years. No precipitating cause could be identified. He denied any chest pain, shortness of breath or syncope. He had a background of schizophrenia, epilepsy, coeliac disease, depression and dermatitis herpetiformis. He was on dapsone, venlafaxine, procyclidine, furosemide, diazepam, omeprazole, meloxicam and folic acid. On examination, his pulse was 82 beats per minute, blood pressure 131/74 mm of Hg, respiratory rate was 14/minute and his saturations on room air were 94%. Neurologic, cardiovascular, respiratory and abdominal examination was unremarkable. His investigations showed Hb of 121g/L (130-180) WCC 7.8*10 g/L (4-11), platelets 182*10 (150-400), MCV 83 fl (80-100), TSH 2.53 mU/L (0.4-4.0 mU/L), anti TTG 14.9 (normal). Renal, liver function, serum folate, vitamin B12 and complement levels were within normal limits with a negative ANCA and ANA. His oral glucose tolerance test was negative for diabetes with fasting and twohour post prandial blood sugar of 4.8mmol/L and 6.9 mmol/L respectively. Because of the history of chronic Dapsone use and possibility of drug induced low HbA1C, patient was investigated along those lines. The low Hba1c was attributed to haemolysis secondary to dapsone. HbA1c improved to 42 mmol/mol within three months following discontinuation of dapsone. His haemoglobin level also normalized (142 g/L). Clinicians should consider haemolysis as a possible factor falsely reducing HbA1c while interpreting results in these patients. This is of particular importance in patients with diabetes.
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PMID:Low hba1c; Is It Dapsone? 2993 42