Genetic variability in serotonin receptor and transporter genes may influence risk for tardive dyskinesia in chronic schizophrenia

Hsieh, Chia-Sheng; Chen, Yen‐Ching; Lai, Mei‐Shu; Chien, Kuo–Liong

doi:10.1016/j.psychres.2010.10.006

Cited by 16 publications

(12 citation statements)

References 5 publications

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“… 135 A meta-analysis combining the subjects from these studies by Lerer et al confirmed the T102C polymorphism conferred a small risk towards TD (OR =1.64, 95% CI =1.17–2.32, P =0.002), 137 whereas the T/C genotype or T allele is associated with non-TD group in Chinese cohorts. 138 , 139 The −1438G/A polymorphism is associated with TD in two case-control studies, 77 , 135 but this may be explained by its complete linkage equilibrium with T102C polymorphism. 135 In studies on Indian, Russian, and African-Caribbean cohorts, no association between 5-HT2A receptor gene polymorphisms and TD has been found.…”

Section: Resultsmentioning

confidence: 98%

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Clinical significance of pharmacogenomic studies in tardive dyskinesia associated with patients with psychiatric disorders

Chang

Fung

2014

PGPM

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Pharmacogenomics is the study of the effects of genetic polymorphisms on medication pharmacokinetics and pharmacodynamics. It offers advantages in predicting drug efficacy and/or toxicity and has already changed clinical practice in many fields of medicine. Tardive dyskinesia (TD) is a movement disorder that rarely remits and poses significant social stigma and physical discomfort for the patient. Pharmacokinetic studies show an association between cytochrome P450 enzyme-determined poor metabolizer status and elevated serum antipsychotic and metabolite levels. However, few prospective studies have shown this to correlate with the occurrence of TD. Many retrospective, case-control and cross-sectional studies have examined the association of cytochrome P450 enzyme, dopamine (receptor, metabolizer and transporter), serotonin (receptor and transporter), and oxidative stress enzyme gene polymorphisms with the occurrence and severity of TD. These studies have produced conflicting and confusing results secondary to heterogeneous inclusion criteria and other patient characteristics that also act as confounding factors. This paper aims to review and summarize the pharmacogenetic findings in antipsychotic-associated TD and assess its clinical significance for psychiatry patients. In addition, we hope to provide insight into areas that need further research.

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Section: Resultsmentioning

confidence: 98%

“… 146 Similarly, no association between serotonin transporter gene polymorphism and TD has been found. 126 , 139 , 147 …”

Section: Resultsmentioning

confidence: 99%

Clinical significance of pharmacogenomic studies in tardive dyskinesia associated with patients with psychiatric disorders

Chang

Fung

2014

PGPM

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“…Proceeding to HTR2C, ser-allele of polymorphism rs6318, located in this gene, was found to be more common in patients with TD [112], but also rs6318 indicated no statistical significance in two other studies [102,119]. Further, rs3813929 indicated no association, and rs518147 was more frequent in patient with TD than those without [102,122].…”

Section: Pharmacogenomics Of Drug-induced Dystoniamentioning

confidence: 93%

“…According to some studies, there was no association between TD development and rs6313, rs6311, and rs6314 [102,111,118]. Nevertheless, a study of 2011 regarding rs6313 showed a relation between T allele and TD development [119], whereas a study of 2001 found higher frequencies of T homozygotes in patients without TD and also allelic differences between patients with and without TD [120]. Segman and his group indicated that patients with TD had higher frequencies of 102C (rs6313) and 1438G (rs6311) alleles and also that CC (rs6313) and GG (rs6311) were associated with higher AIMS scores [121].…”

Section: Pharmacogenomics Of Drug-induced Dystoniamentioning

confidence: 99%

Tardive Dystonia due to D2 Antagonists and Other Agents

Σκώκου¹,

Tsermpini²,

Giamarelou³

et al. 2018

Dystonia - Different Prospects

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Tardive dystonia due to D2 antagonists or other agents is a potentially severe extrapyramidal side effect emerging after long-term drug treatment, prevalent but not limited to psychiatric populations. Its course is often deteriorating, and available treatments are frequently far from satisfying. It presents with sustained muscle contractions, abnormal postures, and repetitive twisting movements and leads to increased psychiatric morbidity, mortality, and decline of quality of life. Inadequate clinical skill and awareness of tardive dystonia can lead to neglect or misdiagnoses, considered as conversion symptoms or of psychogenic origin. Since the syndrome is persistent and often treatment resistant, prevention should be a mainstay of clinical care. Emerging evidence supports positive effects of atypical antipsychotics, particularly quetiapine and clozapine. Therapies such as tetrabenazine, valbenazine, deutetrabenazine, anticholinergics, baclofen, benzodiazepines, vitamin E, or non-pharmacologic interventions, namely botulinum toxin A, deep-brain stimulation, have been found to be helpful in some cases of tardive dystonia. This chapter comprehensively illustrates multiple aspects of this entity, including recent advances on etiology, pathophysiology, clinical presentation, epidemiology, pharmacogenomics, and treatment, aiming to enhance and deepen clinicians' and researchers' awareness of tardive dystonia, with the final goal of ameliorating patients' prognosis and quality of life.

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“…Patients presenting CYP2D6 PM alleles and D2 variants associated with lower receptor expression, resulting in higher receptor occupancy, are at higher risk of developing TD [25,62,63]. 5-HT2C and 5-HT2A low expression variants have also been associated with TD development, especially when considering the age of the patient, probably reflecting an indirect influence on dopamine regulation [64][65][66].…”

Section: Pharmacogenetics Of Antipsychotic-induced Side-effectsmentioning

confidence: 99%

Pharmacogenetic Applications and Pharmacogenomic Approaches in Schizophrenia

Arranz

Pérez

et al. 2013

Curr Genet Med Rep

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Several genetic factors have been identified that, in combination with clinical and environmental factors, contribute to the variability in response to treatment with antipsychotic drugs. Functional polymorphisms in genes coding for cytochrome-P450 (CYP) enzymes, responsible for the metabolism of over 85 % of drugs, have been associated with the development of drug-induced side-effects, and functional polymorphisms in dopamine and serotonin genes may be associated with adverse reactions and treatment efficacy. Recent estimations have suggested that selecting the drug and clinical dose according to the patient's genetic profile may result in a significant improvement of treatment efficacy (10-15 %) and safety (15-20 %). This information has prompted the development of commercial kits to facilitate the clinical application of pharmacogenetic information. However, prospective studies confirming the clinical and economical benefits of these tests are required before their widespread implementation in clinical practice.

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Genetic variability in serotonin receptor and transporter genes may influence risk for tardive dyskinesia in chronic schizophrenia

Cited by 16 publications

References 5 publications

Clinical significance of pharmacogenomic studies in tardive dyskinesia associated with patients with psychiatric disorders

Clinical significance of pharmacogenomic studies in tardive dyskinesia associated with patients with psychiatric disorders

Tardive Dystonia due to D2 Antagonists and Other Agents

Pharmacogenetic Applications and Pharmacogenomic Approaches in Schizophrenia

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