Is thiopurine methyltransferase genetic polymorphism a major factor for withdrawal of azathioprine in rheumatoid arthritis patients?

Corominas, Hèctor; Domènech, Montserrat; Laíz, A.; Gich, Ignasi; Geli, C.; Díaz, César; Cuevillas, F. de; Moreno, M.; Vázquez, Guillermo; Baiget, Montserrat

doi:10.1093/rheumatology/keg028

Cited by 52 publications

(30 citation statements)

References 22 publications

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“…Corominas et al [29] observed that RA patients carrying the mutant TMPT*3A allele experienced more ADEs with AZA treatment, although this could not statistically be confirmed because of low frequency of mutant carriers.…”

Section: Genetic Overview Of Dmardsmentioning

confidence: 95%

Genetic markers of treatment response in rheumatoid arthritis

Wesoły¹,

Wessels²,

Guchelaar³

et al. 2006

Curr Rheumatol Rep

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Rheumatoid arthritis patients exhibit a considerable interindividual variability in response to drug treatment. Although many disease-related and demographic factors have been studied to predict treatment outcome, the effective disease-modifying antirheumatic drug (DMARD) therapy is not yet allocated based on factors that predict efficacy. Individual genetic characteristics are thought to play an important role in treatment response; therefore, current research aims to identify these genetic predictors for clinical response. Pharmacogenetic studies are beginning to provide results, which suggests that personalized treatment maximization of DMARD efficacy and minimization of adverse drug reactions are feasible.

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Section: Genetic Overview Of Dmardsmentioning

confidence: 95%

Genetic markers of treatment response in rheumatoid arthritis

Wesoły¹,

Wessels²,

Guchelaar³

et al. 2006

Curr Rheumatol Rep

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“…Three of the six patients who discontinued the drug due to severe gastrointestinal side effects such as nausea and vomiting were heterozygous for the TPMT n 3A allele, the remainder had the wild-type TPMT allele. Analysis of patients with and without toxicity compared to those with and without the polymorphisms showed a significant difference (P ¼ 0.018), giving a positive predictive value for a carrier of a TPMT polymorphism of 60% [Corominas et al, 2003]. …”

Section: Pharmacogenetics Of Azathioprinementioning

confidence: 99%

Pharmacogenomic approaches to therapies in rheumatic diseases

Ranganathan

Eisen

2004

Drug Development Research

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Pharmacogenomics, the study of genetic variations in drug-metabolizing enzymes and their translation to drug effects, is a rapidly evolving field. At the present time, clinicians choose drugs for patients with rheumatologic diseases based on data from population studies and at times, empirically. The application of pharmacogenomics to drugs used in the treatment of rheumatic diseases, particularly the new expensive agents, holds great promise for optimizing their use in clinical practice. In this article, we highlight some of the published literature on the pharmacogenetics of the common disease-modifying antirheumatic drugs (DMARDs) and the emerging data on the new biologic therapies. As evident from the contents of this review, this is an exciting field which is progressing productively and rapidly. Pharmacogenomic approaches are clearly the basis of the ''individualized'' therapies of the future. Drug Dev.

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“…The percentages of heterozygous carriers of the mutant allele of the TPMT gene ranged from 6.3% to 9.5%. 25 In addition to the variant alleles associated with significantly decreased levels of TPMT activity, the number of repeat elements in the polymorphic variable number of tandem repeats (VNTR) located in the 5Ј-flanking region of the TPMT promoter gene could modulate levels of enzymatic activity. In the series of Hibi et al, 1 bonemarrow suppression induced by 6-MP and azathioprine was closely related to TPMT mutation.…”

Section: Role and Toxicity Of 6-mp And Azathioprine In The Treatment mentioning

confidence: 99%