ArticleLaboratory medicine2016
Glutathione S-Transferase Deletion Polymorphisms in Early-Onset Psychotic and Bipolar Disorders: A Case-Control Study.
Article in Laboratory medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- Association of GSTM1, GSTT1, GSTM3, and GSTP1 Genes Polymorphisms with Susceptibility to Osteosarcoma: a Case- Control Study and Meta-AnalysisAsian Pacific journal of cancer prevention : APJCP · 2019Pooled it
- Article
- Identification and verification of the prognostic value of the glutathione S-transferase Mu genes in gastric cancer.Oncology letters · 2020Article
- Observational
- Association Between Glutathione S-Transferase (GST) Polymorphisms and Schizophrenia in a Chinese Han Population.Neuropsychiatric disease and treatment · 2020Article
- Interaction of glutathione S-transferase polymorphisms and tobacco smoking during pregnancy in susceptibility to autism spectrum disorders.Scientific reports · 2019Article
- Article
- Complex evolution of the GSTM gene family involves sharing of GSTM1 deletion polymorphism in humans and chimpanzees.BMC genomics · 2018Article
- Impaired Redox Control in Autism Spectrum Disorders: Could It Be the X in GxE?Current psychiatry reports · 2017Review
- Glial changes in schizophrenia: Genetic and epigenetic approach.Indian journal of psychiatryReview
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo examine glutathione S-transferase (GST) deletion polymorphisms in development of early-onset severe mental disorders, with the hypothesis that patients with GSTM1-null and GSTT1-null genotypes will develop psychotic disorders at a younger age.
methodsWe identified GSTM1 and GSTT1 deletion polymorphisms by multiplex polymerase chain reaction (PCR) in 93 patients with early onset severe mental disorders and 278 control individuals. The diagnoses were confirmed by Schedule for Affective Disorders and Schizophrenia for School-Age Children-Present and Lifetime Version and Schedule for Affective Disorders and Schizophrenia-Life-Time Version (K-SADS-PL) interviews.
resultsIndividuals with the GSTM1-null genotype were at 3.36-fold higher risk of developing early-onset severe mental disorders than carriers of a corresponding active genotype. The risk of those disorders was increased by 6.59-fold in patients with GSTM1-null/GSTT1-active genotype. Patients with the GSTM1-null genotype were at approximately 2-fold increased risk for developing early-onset schizophrenia-spectrum disorder (EOS), early-onset bipolar disorder (EOBD) with psychotic symptoms, or early-onset first-episode psychosis (EOFEP), compared with patients with the GSTM1-active genotype.
conclusionThe GSTM1-null genotype might be associated with higher risk for early onset severe mental disorders.
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