Effects of switching pravastatin to cerivastatin on C-reactive protein, butyrylcholinesterase, and lipids.

OBJECTIVE: C-reactive protein (CRP) concentrations, butyrylcholinesterase (BChE) activity, total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL), and triglycerides (TG) were evaluated in patients switched from pravastatin to cerivastatin. The purpose of this study was to determine whether a more potent statin (cerivastatin) would further affect CRP, whether a relation ship between CRP and BChE existed, and if there were any relationships between CRP or BChE and lipids. In view of the withdrawal of cerivastatin from the market, studies considering the effects of conversion of patients from one statin to another are warranted.

RESEARCH DESIGN AND METHODS: Thirty-seven patients actively taking pravastatin (10 mg-40 mg) were switched to cerivastatin (0.2 mg-0.8 mg) at the initial visit in the Lipid Clinic at David Grant Medical Center, Travis Air Force Base. Samples were collected before the conversion (pravastatin phase) and at 6 weeks and 12 weeks post-conversion. Patients were excluded from the study if they were taking gemfibrozil concomitantly. Patients were counseled on the adverse effects of cerivastatin, including rhabdomyolsis.

RESULTS: Median CRP levels at the pravastatin phase, 6 weeks of cerivastatin, and 12 weeks of cerivastatin, were 0.380 mg/dL, 0.403 mg/dL, and 0.364 mg/dL (p = 0.772), respectively. Median BChE activity at the pravastatin phase, 6 weeks of cerivastatin, and 12 weeks of cerivastatin were 0.338 micromol/mL/min, 0.332 micromol/mL/min, 0.33 micromol/mL/min (p = 0.746), respectively. A negative correlation was observed between CRP and BChE at baseline only (r = -0.353, p = 0.032). There was a significant decline in mean TC (p < 0.001) and median LDL (p < 0.001) and a significant increase in mean HDL (p = 0.017) over the three time points. Numerically TG declined, but it was not statistically significant (p = 0.649). No correlations were observed between CRP or BChE and any of the lipids. Gender, aspirin use, and the presence of CHD or diabetes did not affect CRP levels or BChE activity.

CONCLUSION: Median CRP remained stable with pravastatin and cerivastatin use, although TC and LDL decreased. The further decline observed with LDL, but not CRP suggests differing effects of statins on LDL and CRP. Limitations include no serum levels prior to statin use and small sample size; thus, future studies are needed to address the relationship between cholesterol and CRP and the mechanism of action of statins on CRP.