Affiliations: Division of Cardiology, Department of Internal
Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University,
Kaohsiung, Taiwan | Graduate Institute of Pharmaceutical Science,
Kaohsiung Medical University, Kaohsiung, Taiwan | Department of Pharmacy, Kaohsiung Medical University
Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan
Note: [] Address for correspondence: Wen-Ter Lai, MD, Division of
Cardiology, Department of Internal Medicine, Kaohsiung Medical University
Hospital, 100 Tzyou 1st Rd, Kaohsiung, 80708, Taiwan. Tel.: +886 7 312 1101
ext. 7741; Fax: +886 7 323 4845; E-mail: wtlai@cc.kmu.edu.tw
Abstract: Statin therapy can reduce the biosynthesis of both cholesterol and
coenzyme Q_{10} by blocking the common upstream mevalonate
pathway. Coenzyme Q_{10} depletion has been speculated to
play a potential role in statin-related adverse events, and withdrawal of
statin is the choice in patients developing myotoxicity or liver toxicity.
However, the effect of statin withdrawal on circulating levels of coenzyme
Q_{10} remains unknown. Twenty-six patients with
hypercholesterolemia received atorvastatin at 10 mg/day for 3 months. Serum
lipid profiles and coenzyme Q_{10} were assessed before and
immediately after 3 months and were also measured 2 and 3 days after the last
day on the statin. After 3 months' atorvastatin therapy, serum levels of total
cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and coenzyme
Q_{10} (0.43 ± 0.23 to 0.16
± 0.10 μg/mL) were all
significantly reduced (all p < 0.001). On day 2 after the
last atorvastatin, the coenzyme Q_{10} level was
significantly elevated (0.37 ±
0.16 μg/mL) and maintained the same levels on day 3
(0.39 ± 0.18 μg/mL) compared with
those on month 3 (both p< 0.001), while TC and LDL-C did not
significantly change within the same 3 days. These results suggest that statin
inhibition of coenzyme Q_{10} synthesis is less strict than
inhibition of cholesterol biosynthesis.
