GATM gene variants and statin myopathy risk

Carr, Daniel F.; Alfirevic, Ana; Johnson, Randi K.; Chinoy, Hector; Staa, Tjeerd van

doi:10.1038/nature13628

Cited by 31 publications

(29 citation statements)

References 6 publications

(2 reference statements)

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“…Our null findings are consistent with those reported in two other recent studies by Carr et al (2014) and Floyd et al (2014). Furthermore, our analysis addressed several of the limitations that were proposed as causative for the previously failed replications.…”

Section: Discussionsupporting

confidence: 92%

“…Two replication studies by Carr et al (2014) (n = 150 SIM cases) and Floyd et al (2014) (n = 175 SIM cases) did not replicate the association reported by Mangravite et al (2013). Carr et al (2014) reported an odds ratio = 0.94 (p = 0.68) and Floyd et al (2014) reported an odds ratio = 0.84 (95% CI = 0.52–1.36; p = 0.49; excluding fibrate users) for the GATM rs9806699 A allele.…”

Section: Introductionmentioning

confidence: 83%

“…Carr et al (2014) reported an odds ratio = 0.94 (p = 0.68) and Floyd et al (2014) reported an odds ratio = 0.84 (95% CI = 0.52–1.36; p = 0.49; excluding fibrate users) for the GATM rs9806699 A allele. Fixed-effect meta-analyses by both Floyd et al (2014) and Mangravite et al (2014) both yielded null associations for rs9806699.…”

Section: Introductionmentioning

confidence: 99%

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GATM Polymorphism Associated with the Risk for Statin-Induced Myopathy Does Not Replicate in Case-Control Analysis of 715 Dyslipidemic Individuals

et al. 2015

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Summary Statin-induced myopathy (SIM) is the most common reason for discontinuation of statin therapy. A polymorphism affecting the gene encoding glycine amidinotransferase (GATM rs9806699 G>A) was previously associated with reduced risk for SIM. Our objective was to replicate the GATM association in a large, multicenter SIM case-control study. Mild and severe SIM cases and age- and gender-matched controls were enrolled. Participants were genotyped, and associations were tested (n=715) using chi-square and logistic regression with consideration for SIM severity and exclusion of subjects with potentially confounding co-medications. The minor allele (A) frequencies of GATM rs9806699 in the controls (n=106), mild SIM (n=324), and severe SIM (n=285) cases were 0.26, 0.28, and 0.29, respectively (p=0.447). The unadjusted odds ratio for the A allele for any SIM (mild or severe) was 1.14 (0.82–1.61; p=0.437), which remained non-significant in all models. Our results do not replicate the association between GATM rs9806699 and SIM.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 83%

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GATM Polymorphism Associated with the Risk for Statin-Induced Myopathy Does Not Replicate in Case-Control Analysis of 715 Dyslipidemic Individuals

et al. 2015

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“…GATM catalyses a critical step in hepatic and renal synthesis of creatine, used in muscle to form creatine phosphate, which is a major source of energy storage in muscle. However, findings from studies have been controversial and further investigation is clearly needed [31,32].…”

Section: Is Genetic Testing a Viable Option In The Future?mentioning

confidence: 94%

Statin-associated muscle symptoms EAS Consensus Panel paper focuses on this neglected patient group

Stock¹

2015

Atherosclerosis

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“…The risk of myopathy is greater per copy of the SLCO1B1*5 allele and appears to be statin specific (122). Additionally, SNPs in the GATM gene may hold promise with respect to predicting SAMS (123,124). Currently, genetic determinants of pharmacokinetics more than pharmacodynamics are likely relevant in SAMS, however, severe myopathy in the setting of genetic predilection, appears relatively uncommon.…”

Section: -Expert Opinionmentioning

confidence: 97%

Expert opinion: the therapeutic challenges faced by statin intolerance

Patel

Martin²,

Banach

2016

Expert Opinion on Pharmacotherapy

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When initiating statin therapy, attention to risk factors for statin intolerance is strongly recommended. Most patients will tolerate some degree of statin therapy; thus statin re-challenge is advisable. If alternative dosing regimens are not tolerated, non-statin medications are acceptable alternatives. To limit errors in the diagnosis of statin intolerance, improvements in clinician-patient communication about the side effects and benefits of statins should be attempted.

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GATM gene variants and statin myopathy risk

Cited by 31 publications

References 6 publications

GATM Polymorphism Associated with the Risk for Statin-Induced Myopathy Does Not Replicate in Case-Control Analysis of 715 Dyslipidemic Individuals

GATM Polymorphism Associated with the Risk for Statin-Induced Myopathy Does Not Replicate in Case-Control Analysis of 715 Dyslipidemic Individuals

Statin-associated muscle symptoms EAS Consensus Panel paper focuses on this neglected patient group

Expert opinion: the therapeutic challenges faced by statin intolerance

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