Molecular Diagnosis & Therapy

, Volume 17, Issue 4, pp 233–237 | Cite as

UGT1A1*28 is Associated with Decreased Systemic Exposure of Atorvastatin Lactone

  • Camilla StormoEmail author
  • Martin P. Bogsrud
  • Monica Hermann
  • Anders Åsberg
  • Armin P. Piehler
  • Kjetil Retterstøl
  • Marianne K. Kringen
Short Communication



Atorvastatin is commonly used to reduce cholesterol. Atorvastatin acid is converted to its corresponding lactone form spontaneously or via glucuronidation mediated by uridine diphosphate glucuronosyltransferase (UGT) 1A1 and 1A3. Atorvastatin lactone is pharmacologically inactive, but is suspected to be muscle toxic and cause statin-induced myopathy (SIM). A several fold increase in systemic exposure of atorvastatin lactone has previously been observed in patients with SIM compared with healthy control subjects. In this study we aimed to investigate the association between polymorphisms in the UGT1A gene locus and plasma atorvastatin lactone levels.


DNA was extracted from whole blood obtained from a previous pharmacokinetic study of patients carefully diagnosed as having true SIM (n = 13) and healthy control subjects (n = 15). The UGT1A1*28(TA) 7 , UGT1A3*2, UGT1A3*3, and UGT1A3*6 polymorphisms were detected by pyrosequencing.


Carriers of the low-expression allele UGT1A1*28(TA) 7 tended to have lower levels of atorvastatin lactone (p < 0.05) than carriers with the normal-activity allele (TA) 6 .


The low-expression UGT1A1*28(TA) 7 allele seems to be associated with decreased systemic exposure of the suspected muscle-toxic metabolite atorvastatin lactone.


Statin Atorvastatin Systemic Exposure Uridine Diphosphate Glucuronosyltransferase Pyrosequencing Assay 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.



This work was funded by the Division of Diagnostics and Intervention, Oslo University Hospital, Norway and South-Eastern Norway Regional Health Authority. The authors have no conflict of interest that are relevant to the content of this article.


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Copyright information

© Springer International Publishing Switzerland 2013

Authors and Affiliations

  • Camilla Stormo
    • 1
    Email author
  • Martin P. Bogsrud
    • 2
    • 3
  • Monica Hermann
    • 4
  • Anders Åsberg
    • 4
  • Armin P. Piehler
    • 5
  • Kjetil Retterstøl
    • 3
  • Marianne K. Kringen
    • 6
  1. 1.Department of Medical BiochemistryOslo University Hospital, University of OsloOsloNorway
  2. 2.Helse Møre and Romsdal Health Trust, Department of Internal Medicine Ålesund and University of Oslo Ålesund HospitalÅlesundNorway
  3. 3.Lipid ClinicOslo University HospitalOsloNorway
  4. 4.School of PharmacyUniversity of OsloOsloNorway
  5. 5.Fürst Medical LaboratoryOsloNorway
  6. 6.Department of PharmacologyOslo University HospitalOsloNorway

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