COQ2 polymorphisms are not associated with increased risk of statin-induced myalgia/myopathy in the Czech population
Language English Country Germany Media print
Document type Controlled Clinical Trial, Journal Article, Research Support, Non-U.S. Gov't
PubMed
29257754
DOI
10.1515/dmpt-2017-0027
PII: /j/dmdi.ahead-of-print/dmpt-2017-0027/dmpt-2017-0027.xml
Knihovny.cz E-resources
- Keywords
- COQ2, coenzyme Q10, myalgia, myopathy, polymorphism, statin,
- MeSH
- White People genetics MeSH
- Genetic Predisposition to Disease genetics MeSH
- Genotype MeSH
- Haplotypes MeSH
- Middle Aged MeSH
- Humans MeSH
- Muscular Diseases chemically induced epidemiology genetics MeSH
- Polymorphism, Genetic genetics MeSH
- Hydroxymethylglutaryl-CoA Reductase Inhibitors adverse effects MeSH
- Case-Control Studies MeSH
- Ubiquinone genetics MeSH
- Check Tag
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Controlled Clinical Trial MeSH
- Research Support, Non-U.S. Gov't MeSH
- Geographicals
- Czech Republic epidemiology MeSH
- Names of Substances
- Hydroxymethylglutaryl-CoA Reductase Inhibitors MeSH
- Ubiquinone MeSH
- Ubiquinone Q2 MeSH Browser
BACKGROUND: The gene COQ2, encoding 4-hydroxybenzoate-polyprenyltransferase (coenzyme Q2), belongs to the candidates potentially influencing statin treatment tolerability. This enzyme is involved in the biosynthesis of coenzyme Q10 (CoQ10), in which depletion induced by statin treatment is implicated in the development of statin-associated muscle symptoms (SAMS). Thus, polymorphisms in the COQ2 gene might explain susceptibility to SAMS. METHODS: Adult patients with SAMS (on low doses of atorvastatin and simvastatin)-induced myalgia/myopathy (n=278), patients on statins but without SAMS (n=293) and population (part of the post-MONICA [Multinational MONItoring of trends and determinants in CArdiovascular disease] study) controls (n=561) were genotyped (polymerase chain reaction-restriction fragment length polymorphism [PCR-RFLP] assay) for rs6535454 and rs4693075 polymorphisms within the COQ2 gene loci. RESULTS: Distribution of rs6535454 in patients with SAMS (GG=51.1%, GA=40.0%, AA=8.9%) did not significantly differ (p=0.33; respectively 0.32 for codominant models of the analysis) from that in the population controls (GG=48.1%, GA=45.0%, AA=6.9%) or the SAMS-unaffected patients (GG=49.8%, GA=40.3%, AA=9.7%). Similarly, neither rs4693075 was associated with SAMS (CC=36.8%, CG=48.2%, GG=15.0% in patients suffering SAMS vs. CC=36.6%, CG=47.5%, GG=15.9 in controls and CC=35.8%, CG=48.2%, GG=15.9% in symptom-free patients, p=0.94 and 0.95 for codominant models of the analysis). Also, the haplotype distributions were not significantly different between the groups analyzed. CONCLUSIONS: The polymorphisms of the COQ2 gene do not associate with SAMS in the Czech patients treated with low doses of statins. This is another clue that the coenzyme Q10 pathway is not the most important for the development of SAMS.
3rd Department of Internal Medicine 1st Faculty of Medicine Charles University Prague Czech Republic
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