Ezetimibe does not increase fasting glucose more than statins alone in non-diabetic, hypercholesterolemic patients
Ezetimibe does not increase fasting glucose levels more than statins alone in non-diabetic, hypercholesterolemic patientsPresented by: Peter Toth (Peoria, USA)
New data presented today at the 17th International Symposium on Atherosclerosis (May 23-26, 2015) in Amsterdam, The Netherlands, have shown that administration of the cholesterol absorption inhibitor, ezetimibe, to non-diabetic, hypercholesterolemic patients who are on stable statin therapy, does not increase fasting serum glucose (FSG) levels. Peter P. Toth MD, PhD, Director of Preventative Cardiology at the CGH Medical Center, Sterling, Illinois and Professor of Clinical Family and Community Medicine at the University of Illinois College of Medicine, Peoria, Illinois USA, presented the results.
Because statin therapy has been shown to be associated with a slightly increased risk of diabetes mellitus and insulin resistance in non-diabetic patients, it was of interest to evaluate FSG changes following ezetimibe coadministered with statin therapy. Previous analyses in stain-naïve, non-diabetic, hypercholesterolemic and heterozygous familial hypercholesterolemic patients showed that addition of ezetimibe to statin therapy did not increase FSG more than statin monotherapy alone during up to 96 weeks of treatment. Ezetimibe monotherapy also did not increase FSG levels compared with placebo in these patients during 12 weeks of treatment.
This study extends those observations and describes the effects of ezetimibe on FSG in patients already on stable statin therapy during 6-12 weeks of treatment. In this analysis, data were pooled from randomized, controlled clinical trials of non-diabetic, hypercholesterolemic patients on stable statin therapy. The analysis included 2 study types: “add-on” in which the administration of ezetimibe (n=1506) versus placebo (n=851) was compared, and “uptitration” in which the addition of ezetimibe (n=645) versus doubling the statin dose (n=650) was compared. Increases in FSG from baseline levels were small and ranged from 0.2 to 1.4 mg/dL (0.01 to 0.08 mmol/L) in both study types for the ezetimibe +statin combination and for statin monotherapy, and there were no significant differences between the treatments. Few patients had FSG increases ≥126 mg/dL (7.0 mmol/L) with either treatment, and elevations in FSG ≥126 mg/dL (7.0 mmol/L) occurred more often in patients who had FSG ≥100 - ≤126 mg/dL (5.6-7.0 mmol/L) at baseline. More of the patients who had elevated FSG ≥126 mg/dL (7.0 mmol/L) had metabolic syndrome and characteristics of pre-diabetes including higher BMI and baseline FSG and triglyceride levels, and somewhat lower baseline HDL-C levels at baseline; however, these factors were not related to changes in FSG. Changes from baseline in LDL-C, BMI, HDL-C, triglycerides, and Apo B also were not related to changes in FSG.
Taken together, these data indicate that ezetimibe, when administered to patients on stable statin therapy, does not further increase FSG levels beyond those observed with statins alone. The results are also consistent with the effect of combination ezetimibe +statin therapy in statin-naïve HC and HeFH patients, during up to 96 weeks of treatment. These findings are important, given that many patients with high CVD risk do not achieve adequate LDL-C lowering on high-dose statin therapy or who cannot tolerate high dose statins, may benefit from additional cholesterol lowering with combination