The goal of this analysis was to evaluate the ability of insulin resistance, identified
by the presence of prediabetes mellitus (PreDM) combined with either an elevated triglyceride
(TG >1.7 mmol/l) or body mass index (BMI ≥27.0 kg/m2), to identify increased risk of statin-associated type 2 diabetes mellitus (T2DM).
Consequently, a retrospective analysis of data from subjects without diabetes in the
Treating to New Targets and the Stroke Prevention by Aggressive Reduction in Cholesterol
Levels randomized controlled trials was performed, subdividing participants into 4
experimental groups: (1) normal fasting glucose (NFG) and TG ≤1.7 mmol/l (42%); (2)
NFG and TG >1.7 mmol/l (22%); (3) PreDM and TG ≤1.7 mmol/l (20%); and (4) PreDM and
TG >1.7 mmol/l (15%). Comparable groupings were created substituting BMI values (kg/m2 <27.0 and ≥27.0) for TG concentrations. Patients received atorvastatin or placebo
for a median duration of 4.9 years. Incident T2DM, defined by developing at least
2 fasting plasma glucose (FPG) concentrations ≥126 mg/dl, an increase in FPG ≥37 mg/dl,
or a clinical diagnosis of T2DM, was observed in 8.2% of the total population. T2DM
event rates (statin or placebo) varied from a low of 2.8%/3.2% (NFG and TG ≤1.7 mmol/l)
to a high of 22.8%/7.6% (PreDM and TG >1.7 mmol/l) with intermediate values for only
an elevated TG >1.7 mmol/l (5.2%/4.3%) or only PreDM (12.8%/7.6%). Comparable differences
were observed when BMI values were substituted for TG concentrations. In conclusion,
these data suggest that (1) the diabetogenic impact of statin treatment is relatively
modest in general; (2) the diabetogenic impact is accentuated relatively dramatically
as FPG and TG concentrations and BMI increase; and (3) PreDM, TG concentrations, and
BMI identify people at highest risk of statin-associated T2DM.
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Article info
Publication history
Published online: August 12, 2016
Accepted:
July 28,
2016
Received in revised form:
July 28,
2016
Received:
June 9,
2016
Footnotes
Drs. Kohli and Knowles contributed equally to this work.
See page 1280 for disclosure information.
Identification
Copyright
© 2016 Elsevier Inc. All rights reserved.