Pitavastatin improves glycated hemoglobin in patients with poorly controlled type 2 diabetes

Abstract

Aims/introduction: To investigate the effect of pitavastatin on glucose control in patients with type 2 diabetes.

Materials and methods: Medical records of 340 patients with type 2 diabetes treated with pitavastatin or atorvastatin between 1 August 2013 and 31 May 2014 were reviewed. A total of 96 patients who had not received statins were treated with pitavastatin (N to P group). A total of 100 patients who had previously used atorvastatin were switched to pitavastatin (A to P group). A total of 144 patients continued with atorvastatin treatment. Data were collected at baseline, 3 and 6 months of treatment. Changes in glycated hemoglobin (HbA1c) level were analyzed in 222 patients who did not change their antidiabetic agent during 6 months of treatment.

Results: A negative correlation between baseline HbA1c and delta HbA1c at 6 months was found in the pitavastatin-treated patients (N to P group: ρ = -0.329, P = 0.006; A to P group: ρ = -0.480, P < 0.001). The correlation remained similar after adjusting for age, body mass index, dose of pitavastatin, estimated glomerular filtration rate and high-density lipoprotein cholesterol. After 6 months of treatment, the benefit of pitavastatin on HbA1c in the patients with poorly controlled diabetes was significant in both the N to P (8.1 vs 7.4%, P = 0.018) and A to P (9.7 vs 9.0%, P = 0.015) groups.

Conclusions: Pitavastatin decreases HbA1c in patients with type 2 diabetes with a higher baseline HbA1c level. The benefit on HbA1c was also observed in patients with previous use of atorvastatin.

Keywords: Glycemic control; Statin; Type 2 diabetes mellitus.

Figure 1

Correlations between baseline glycated hemoglobin (HbA1c) and delta HbA1c at 6 months in the three groups are shown. The baseline HbA1c and delta HbA1c of 222 patients with type 2 diabetes without adjustments for antidiabetic agents within 6 months of treatment were analyzed using Spearman's rank correlation. The plots and regression line were stratified by three groups. Negative correlations were found in (a) patients who had no medication for dyslipidemia and began pitavastatin treatment (N to P group; ρ = −0.329, P = 0.006) and (b) patients who were switched from atorvastatin to pitavastatin treatment (A to P group; ρ = −0.480, P < 0.001), (c) but not in patients who continued atorvastatin treatment (A to A group; ρ = −0.015, P = 0.895). The correlation remained significant after adjusting for age, body mass index, dose of pitavastatin, estimated glomerular filtration rate and high‐density lipoprotein cholesterol (in the N to P group: ρ = −0.358, P = 0.016; in the A to P group: ρ = −0.478, P = 0.001; in the A to A group: ρ = 0.015, P = 0.933).