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Licensed Unlicensed Requires Authentication Published by De Gruyter February 8, 2018

Effect of SLCO1B1 gene polymorphisms and vitamin D on statin-induced myopathy

  • Baraa Alghalyini , Said El Shamieh EMAIL logo , Ali Salami , Sophie Visvikis Siest , Hana M. Fakhoury EMAIL logo and Rajaa Fakhoury

Abstract

Background

Statin therapy used to lower cholesterol levels results in a substantial reduction in cardiovascular complications. Previous observations in different ethnic populations showed that rs2306283A>G, p.Asn130Asp and rs4149056T>C, p.Val174Ala in solute carrier organic anion transporter 1B1 (SLCO1B1) gene encoding the organic transporter protein may be responsible for statin uptake, thus explaining the majority of statin-associated symptoms. In addition to the genetic component, vitamin D (vit D) deficiency is common in Saudi Arabia and worldwide and may cause muscle dysfunction and ache. The aim of the present study was first to reveal an effect of vit D, rs2306283A>G, and rs4149056T>C and related haplotypes on statin-associated myopathy (SAM) and then to investigate a possible interaction between low vit D levels and the above-mentioned variants.

Methods

The genomic DNA obtained from 50 individuals diagnosed with hypercholesterolemia was genotyped using light SNiP hybridization probes.

Results

Low vit D levels were associated with SAM (OR=3.6, p=0.03); however, CK levels, rs2306283A>G, and rs4149056T>C did not show any association. Interestingly, rs4149056T>C was interacting with vit D to influence SAM (p=0.02). Haplotype analysis showed that SLCO1B1 *1B and *15 were more prevalent in individuals with SAM (p=0.05). When stratified according to vit D levels, rs2306283A allele showed an increase in individuals having SAM along with low vit D (p=0.03).

Conclusions

Although preliminary, our results show an involvement of vit D and rs4149056T>C of SLCO1B1 in SAM.

Acknowledgments

The authors would like to thank the study participants.

  1. Author contributions: All the authors have accepted responsibility for the entire content of the submitted manuscript and approved submission.

  2. Research funding: The present work was funded by an internal research grant (project number 0712017) from AlFaisal University, Ryadh, Kingdom of Saudi Arabia.

  3. Employment or leadership: None declared.

  4. Honorarium: None declared.

  5. Competing interests: The funding organization(s) played no role in the study design; in the collection, analysis, and interpretation of data; in the writing of the report; or in the decision to submit the report for publication.

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Received: 2017-10-7
Accepted: 2018-1-4
Published Online: 2018-2-8
Published in Print: 2018-3-28

©2018 Walter de Gruyter GmbH, Berlin/Boston

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