LDL cholesterol variability in patients with Type 2 diabetes taking atorvastatin and simvastatin: a comparison of two formulae for LDL-C estimation.
BACKGROUND
A new formula was recently proposed by Cordovo et al. that was more highly correlated with low-density lipoprotein (LDL) measured directly than the Friedewald LDL formula. We conducted this prospective study to establish whether the new formula allows true variations in LDL within the same individual to be tracked more closely than that of the Friedewald formula.


METHODS
A cross-over study of biological variation of lipids in 26 patients with Type 2 diabetes (T2DM) taking either a short half-life statin, simvastatin 40 mg (n=10), or a long half-life statin, atorvastatin 10 mg. After three months on one statin, fasting lipids were measured on 10 occasions over a five-week period. The same procedure was then followed for the other statin. The LDL was measured by a direct LDL immunoassay and was compared to the LDL estimated by the Friedewald and Cordova (0.7516) × (total cholesterol [TC]-high-density lipoprotein cholesterol [HDL-C]) formulae.


RESULTS
As a group, the calculated or measured mean LDL was no different between statins. However, the biological coefficient of variation (CV) of directly measured LDL was far larger with simvastatin than atorvastatin. This difference was detected by Cordova LDL but not found with the Friedewald LDL formula.


CONCLUSIONS
In contrast to Friedewald LDL, Cordova LDL estimation revealed LDL to be much more stable in T2DM patients taking atorvastatin rather than simvastatin that was in accord with LDL when measured directly. Therefore, Cordova LDL which is a measure of non-HDL-cholesterol is the simplest, cheapest and the most convenient measurement for assessment of response to statin treatment.
Department of Endocrinology, Diabetes and Metabolism, University of Hull, Hull, UK thozhukat.sathyapalan@hyms.ac.uk.
T
T
Sathyapalan
Department of Endocrinology, Diabetes and Metabolism, University of Hull, Hull, UK.
S L
SL
Atkin
Department of Clinical Biochemistry, Hull and East Yorkshire Hospitals NHS Trust, Hull, UK.
E S
ES
Kilpatrick
D000069059:Atorvastatin; D015415:Biomarkers / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood*; D018592:Cross-Over Studies; D003627:Data Interpretation, Statistical; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000188:drug therapy*; D016903:Drug Monitoring; D006207:Half-Life; D006538:Heptanoic Acids / Q000493:pharmacokinetics / Q000627:therapeutic use*; D006801:Humans; D000960:Hypolipidemic Agents / Q000493:pharmacokinetics / Q000627:therapeutic use*; D007118:Immunoassay; D011446:Prospective Studies; D011758:Pyrroles / Q000493:pharmacokinetics / Q000627:therapeutic use*; D019821:Simvastatin / Q000493:pharmacokinetics / Q000627:therapeutic use*; D014280:Triglycerides / Q000097:blood
D015415:Biomarkers; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D006538:Heptanoic Acids; D000960:Hypolipidemic Agents; D011758:Pyrroles; D014280:Triglycerides; D000069059:Atorvastatin; D019821:Simvastatin
Lipids; clinical studies; diabetes