Author
Listed:
- James S. Floyd
(Cardiovascular Health Research Unit, University of Washington, 1730 Minor Avenue, Suite 1360, Seattle, Washington 98101, USA
University of Washington, 1959 Northeast Pacific Street, Box 356420, Seattle, Washington 98195-6420, USA)
- Joshua C. Bis
(Cardiovascular Health Research Unit, University of Washington, 1730 Minor Avenue, Suite 1360, Seattle, Washington 98101, USA
University of Washington, 1959 Northeast Pacific Street, Box 356420, Seattle, Washington 98195-6420, USA)
- Jennifer A. Brody
(Cardiovascular Health Research Unit, University of Washington, 1730 Minor Avenue, Suite 1360, Seattle, Washington 98101, USA
University of Washington, 1959 Northeast Pacific Street, Box 356420, Seattle, Washington 98195-6420, USA)
- Susan R. Heckbert
(Cardiovascular Health Research Unit, University of Washington, 1730 Minor Avenue, Suite 1360, Seattle, Washington 98101, USA
University of Washington, 1959 Northeast Pacific Street, Box 357236, Seattle, Washington 98195-7236, USA
Group Health Research Institute, Group Health Cooperative, 1730 Minor Avenue, Suite 1600)
- Kenneth Rice
(Cardiovascular Health Research Unit, University of Washington, 1730 Minor Avenue, Suite 1360, Seattle, Washington 98101, USA
University of Washington, 1959 Northeast Pacific Street, Box 357232, Seattle, Washington 98195-7323, USA)
- Bruce M. Psaty
(Cardiovascular Health Research Unit, University of Washington, 1730 Minor Avenue, Suite 1360, Seattle, Washington 98101, USA
University of Washington, 1959 Northeast Pacific Street, Box 356420, Seattle, Washington 98195-6420, USA
University of Washington, 1959 Northeast Pacific Street, Box 357236, Seattle, Washington 98195-7236, USA
Group Health Research Institute, Group Health Cooperative, 1730 Minor Avenue, Suite 1600)
Abstract
Arising from L. M. Mangravite et al. Nature 502, 377–380 (2013); doi:10.1038/nature12508 All HMG-CoA reductase inhibitors (statins) can cause muscle injury ranging from asymptomatic elevations in creatine kinase levels to severe muscle breakdown (rhabdomyolysis) leading to kidney failure and death1, and the genetic variants responsible for this uncommon adverse drug reaction remain largely undiscovered. Mangravite et al. reported a new locus in the gene GATM (rs9806699) that was associated with a decreased risk of muscle injury in two case-control studies of myopathy (odds ratio, 0.60)2. In a larger case-control study of statin-related rhabdomyolysis, a more severe form of muscle injury, we were unable to replicate this finding. This failure to replicate raises questions about the role of GATM in statin-related muscle injury. There is a Reply to this Brief Communication Arising by Mangravite, L. M. et al. Nature 513, http://dx.doi.org/10.1038/nature13630 (2014).
Suggested Citation
James S. Floyd & Joshua C. Bis & Jennifer A. Brody & Susan R. Heckbert & Kenneth Rice & Bruce M. Psaty, 2014.
"GATM locus does not replicate in rhabdomyolysis study,"
Nature, Nature, vol. 513(7518), pages 1-3, September.
Handle:
RePEc:nat:nature:v:513:y:2014:i:7518:d:10.1038_nature13629
DOI: 10.1038/nature13629
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