Genetic susceptibility to Tardive Dyskinesia in chronic schizophrenia subjects: V. Association of CYP1A2 1545 C&gt;T polymorphism

Tiwari, Arun; Deshpande, Smita N.; Lerer, Bernard; Nimgaonkar, Vishwajit L.; Thelma, B.K.

doi:10.1038/sj.tpj.6500415

Cited by 40 publications

(31 citation statements)

References 25 publications

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“…The CYP450 family of genes modified only the severity (CYP1A2*1C and CYP2D6*4; Tiwari et al 2005aTiwari et al , 2005bTiwari et al , 2006 and genes from the serotonergic pathway are not involved in either the development or severity of TD (Deshpande et al 2005). In the present study, the antioxidant genes investigated are not associated with the genesis of TD but influence the severity of the phenotype (NOS3 27bp duplication and NQO1 Pro187Ser).…”

Section: Nih Public Accesscontrasting

confidence: 46%

Genetic susceptibility to Tardive Dyskinesia in chronic schizophrenia subjects: Role of oxidative stress pathway genes

Thelma

Tiwari

Deshpande³

et al. 2007

Schizophrenia Research

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Keywordsnorth India; Tardive Dyskinesia; oxidative stress; NOS3; NQO1; Single nucleotide polymorphisms; association Tardive Dyskinesia (TD) is a severe debilitating movement disorder with a potentially irreversible course developing in schizophrenia patients under long term treatment with classical neuroleptics. Its development in a subset of patients (~20-25%), familial nature, and concordance amongst twins indicate a possible genetic basis (for review see Muller et al. 2004). In addition to the classical dopaminergic pathway genes, oxidative stress mediated neurotoxic damage is also an important hypothesis proposed to explain the development of TD. Considerable support to OS hypothesis comes from the observations of increased lipid peroxidation in cerebrospinal fluid in patients with TD and antioxidants such as vitamin E alleviate TD symptoms (Adler et al. 1999; for review see Lohr, 2003). Recently a novel antioxidant AD4 has been reported to reduce haloperidol induced vacuous chewing moments in rats (Sadan et al. 2005).In this study, genes involved in the maintenance of cellular redox balance namely, superoxide dismutase 2 (SOD2; MnSOD; Ala9Val), Uncoupling protein 2 (UCP2; 45bp del/ins), neuronal nitric oxide synthase (nNOS; NOS1; His902His, rs2682826), endothelial NOS (eNOS; NOS3; 27bp ins/del), glutathione S transferase (GST; GSTMI, TI; Presence/Null; GSTPI, Ile105Val) and NADPH: quinone oxidoreductase 1 (NQO1, Pro187Ser) were analysed. Schizophrenia patients with TD (n=96) and without TD (n=239) were recruited for the study. SNPs were genotyped using PCR-RFLP and allelic, genotypic and haplotypic association was tested using χ 2 test. Further, to test whether severity of TD was influenced by genotype, mean AIMS score was compared across the genotypic categories for each of the polymorphism using Kruskal Wallis H test.

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Section: Nih Public Accesscontrasting

confidence: 46%

Genetic susceptibility to Tardive Dyskinesia in chronic schizophrenia subjects: Role of oxidative stress pathway genes

Thelma

Tiwari

Deshpande³

et al. 2007

Schizophrenia Research

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“…No study mentioned conducting specific tests for population stratification even though six 57,60,87,96,102,103 were known to include patients with different ethnic backgrounds. A minority (21/51) of studies [59][60][61][62]66,67,70,72,74,[76][77][78][79]81,82,[85][86][87][88]96,100 reported testing for Hardy-Weinberg equilibrium.…”

Section: Clinical Validitymentioning

confidence: 99%

Cytochrome P450 testing for prescribing antipsychotics in adults with schizophrenia: systematic review and meta-analyses

et al. 2010

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There is wide variability in the response of individuals to standard doses of antipsychotic drugs. It has been suggested that this may be partly explained by differences in the cytochrome P450 (CYP450) enzyme system responsible for metabolizing the drugs. We conducted a systematic review and metaanalyses to consider whether testing for CYP450 single nucleotide polymorphisms in adults starting antipsychotic treatment for schizophrenia predicts and leads to improvements in clinical outcomes. High analytic validity in terms of sensitivity and specificity was seen in studies reporting P450 testing. However, there was limited evidence of the role of CYP2D6 polymorphisms in antipsychotic efficacy, although there was an association between CYP2D6 genotype and extrapyramidal adverse effects. No studies reported on the prospective use of CYP2D6 genotyping tests in clinical practice. In conclusion, evidence of clinical validity and utility of CYP2D6 testing in patients being prescribed antipsychotics is lacking, and thus, routine pharmacogenetic testing prior to antipsychotic prescription cannot be supported at present. Further research is required to improve the evidence base and to generate data on clinical validity and clinical utility.

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“…The number of patients genotyped in each study varied from 16 141 to 285. 170 In one study 166 genotyping 199 patients it was stated that 335 patients were included in the study but it appears that not all of them were genotyped for reasons not given.…”

Section: Cyp1a2mentioning

confidence: 99%

“…Two of these studies 166,169 also examined *1C and a further study completely sequenced the exons/exonintron boundaries of the CYP1A2 gene (1545C4T region). 170 All but one of the studies examined the relationship between ADRs and genotype/ phenotype, usually TD but also QT interval (QTc) 168 and hyperglycaemia and body weight increase; 141 the other study 171 explored efficacy (number of patients responding to treatment as measured by PANSS). …”

Section: Cyp1a2mentioning

confidence: 99%

The clinical effectiveness and cost-effectiveness of testing for cytochrome P450 polymorphisms in patients with schizophrenia treated with antipsychotics: a systematic review and economic evaluation

Fleeman

McLeod²,

Bagust³

et al. 2010

Health Technol Assess

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How to obtain copies of this and other HTA programme reports An electronic version of this title, in Adobe Acrobat format, is available for downloading free of charge for personal use from the HTA website (www.hta.ac.uk). A fully searchable DVD is also available (see below).Printed copies of HTA journal series issues cost £20 each (post and packing free in the UK) to both public and private sector purchasers from our despatch agents.Non-UK purchasers will have to pay a small fee for post and packing. For European countries the cost is £2 per issue and for the rest of the world £3 per issue. How to order:-fax (with credit card details) -post (with credit card details or cheque) -phone during office hours (credit card only).Additionally the HTA website allows you to either print out your order or download a blank order form. Contact details are as follows:Synergie UK (HTA Department) Digital House, The Loddon Centre Wade Road Basingstoke Hants RG24 8QW Email: orders@hta.ac.uk Tel: 0845 812 4000 -ask for 'HTA Payment Services' (out-of-hours answer-phone service) Fax: 0845 812 4001 -put 'HTA Order' on the fax header Payment methods Paying by chequeIf you pay by cheque, the cheque must be in pounds sterling, made payable to University of Southampton and drawn on a bank with a UK address. Paying by credit cardYou can order using your credit card by phone, fax or post. SubscriptionsNHS libraries can subscribe free of charge. Public libraries can subscribe at a reduced cost of £100 for each volume (normally comprising 40-50 titles). The commercial subscription rate is £400 per volume (addresses within the UK) and £600 per volume (addresses outside the UK). Please see our website for details. Subscriptions can be purchased only for the current or forthcoming volume. How do I get a copy of HTA on DVD?Please use the form on the HTA website (www.hta.ac.uk/htacd/index.shtml). HTA on DVD is currently free of charge worldwide.The website also provides information about the HTA programme and lists the membership of the various committees. HTA NIHR Health Technology Assessment programmeT he Health Technology Assessment (HTA) programme, part of the National Institute for Health Research (NIHR), was set up in 1993. It produces high-quality research information on the effectiveness, costs and broader impact of health technologies for those who use, manage and provide care in the NHS. 'Health technologies' are broadly defined as all interventions used to promote health, prevent and treat disease, and improve rehabilitation and long-term care. The research findings from the HTA programme directly influence decision-making bodies such as the National Institute for Health and Clinical Excellence (NICE) and the National Screening Committee (NSC). HTA findings also help to improve the quality of clinical practice in the NHS indirectly in that they form a key component of the 'National Knowledge Service'. The HTA programme is needs led in that it fills gaps in the evidence needed by the NHS. There are three routes to the start of projec...

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Genetic susceptibility to Tardive Dyskinesia in chronic schizophrenia subjects: V. Association of CYP1A2 1545 C>T polymorphism

Cited by 40 publications

References 25 publications

Genetic susceptibility to Tardive Dyskinesia in chronic schizophrenia subjects: Role of oxidative stress pathway genes

Genetic susceptibility to Tardive Dyskinesia in chronic schizophrenia subjects: Role of oxidative stress pathway genes

Cytochrome P450 testing for prescribing antipsychotics in adults with schizophrenia: systematic review and meta-analyses

The clinical effectiveness and cost-effectiveness of testing for cytochrome P450 polymorphisms in patients with schizophrenia treated with antipsychotics: a systematic review and economic evaluation

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