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• W2014594637 abstract "The 3-hydroxy-3-methyl-glutaryl coenzyme A reductase inhibitors (statins) are the most effective medications for the treatment of primary and secondary hypercholesterolemia. Rosuvastatin has been available since 2003 and is used by 12 million people worldwide. St. John's wort is an herbal supplement used for centuries for its antidepressant and anti-inflammatory properties and has been reported to interact with many common medications. A 59-year-old black man presented to his physician with hyperlipidemia. He was initially given pravastatin 80 mg/day, but high-density lipoprotein cholesterol remained low and low-density lipoprotein (LDL) cholesterol elevated despite therapy. Treatment was changed to rosuvastatin 10 mg/day with marked improvement of the lipid profile (Table). A routine lipid panel was performed 6 months later, and marked increases of total cholesterol and LDL cholesterol levels were noted. The patient confirmed that he was compliant with rosuvastatin but had begun taking St. John's wort, 2 capsules per day in June 2007, for insomnia. Each capsule contained St. John's wort 300 mg, rosemary 80 mg, and spirulina 40 mg. He was asked to stop taking the herbal supplement in October 2007, and a repeat lipid panel 4 months later showed marked improvement of all parameters.TableSerum Lipid Levels of Subject on PharmacotherapyDateMedication (Daily Dose)Total Cholesterol (mg/dL)Triglycerides (mg/dL)HDL-C (mg/dL)LDL-C (mg/dL)December 2006Pravastatin 80 mg21912038147April 2007Rosuvastatin 10 mg1651214299October 2007Rosuvastatin 10 mg & St. John's wort 2 caps/day23714941162February 2008Rosuvastatin 10 mg1631154595HDL-C=high-density lipoprotein cholesterol; LDL=low-density lipoprotein cholesterol.SI conversion factor: to convert triglyceride value to mmol/L, multiply by 0.011; to convert LDL-C, total cholesterol, and HDL-C values to mmol/L, multiply by 0.0259. Open table in a new tab HDL-C=high-density lipoprotein cholesterol; LDL=low-density lipoprotein cholesterol. SI conversion factor: to convert triglyceride value to mmol/L, multiply by 0.011; to convert LDL-C, total cholesterol, and HDL-C values to mmol/L, multiply by 0.0259. St. John's wort (Hypericum performatum), used since antiquity for depression, mood disorders, premenstrual symptoms, and wound healing, is widely available and is the second most popular herbal medication in the United States, with annual sales of $140 million.1Ernst E. The risk-benefit profile of commonly used herbal therapies: Ginkgo, St. John's Wort, Ginseng, Echinacea, Saw Palmetto, and Kava.Ann Intern Med. 2002; 136: 42-53Crossref PubMed Scopus (449) Google Scholar It contains both hyperforin, which induces cytochrome P450 3A4 (CYP3A4) and hypericin, which induces the intestinal drug transporter P-glycoprotein (P-gp). These mechanisms might significantly affect the bioavailability of half of currently marketed drugs.2Markowitz J.S. Donovan J.L. DeVane C.L. et al.Effect of St John's wort on drug metabolism by induction of cytochrome P450 3A4 enzyme.JAMA. 2003; 290: 1500-1504Crossref PubMed Scopus (330) Google Scholar Both simvastatin and atorvastatin are metabolized by CYP3A4 and are inhibitors or substrates of P-gp. Concurrent use of St. John's wort and these statin drugs has been shown to adversely affect serum lipid levels and raise LDL cholesterol levels.3Andren L. Andreasson A. Eggertsen R. Interaction between a commercially available St.John's wort product (Movina) and atorvastatin in patients with hypercholesterolemia.Eur J Clin Pharmacol. 2007; 63: 913-916Crossref PubMed Scopus (61) Google Scholar, 4Eggertsen R. Andreasson A. Andren L. Effects of treatment with a commercially available St John's Wort product (Movina) on cholesterol levels in patients with hypercholesterolemia treated with simvastatin.Scand J Prim Health Care. 2007; 25: 154-159Crossref PubMed Scopus (23) Google Scholar However, rosuvastatin is neither a substrate nor an inhibitor of CYP3A4 or P-gp. It is primarily eliminated through biliary excretion, but 10% of the parent compound is metabolized hepatically via CYP2C9 and CYP2C19. St. John's wort has been reported to induce both of these enzymes.5Xu H. Williams K.M. Liauw W.S. et al.Effects of St John's wort and CYP2C9 genotype on the pharmacokinetics and pharmacodynamics of gliclazide.Br J Pharmacol. 2008; 153: 1579-1586Crossref PubMed Scopus (86) Google Scholar One possible mechanism is that hyperforin, a major constituent of St. John's wort, is a high-affinity ligand for the pregnane X-receptor, a nuclear receptor that regulates the induction of several cytochrome P450 enzymes, including CYP2C9 and CYP2C19.5Xu H. Williams K.M. Liauw W.S. et al.Effects of St John's wort and CYP2C9 genotype on the pharmacokinetics and pharmacodynamics of gliclazide.Br J Pharmacol. 2008; 153: 1579-1586Crossref PubMed Scopus (86) Google Scholar St. John's wort's induction of these enzymes might have increased clearance of rosuvastatin in our patient and decreased its lipid-lowering effects. Based on our case, we recommend adding rosuvastatin to the list of drugs whose efficacy can be diminished by St. John's wort. Rosemary or spirulina also might have interfered with metabolism of rosuvastatin, but this is unlikely. Physicians should be cognizant of the potential interaction of St. John's wort with rosuvastatin and other statins and remember to ask patients about their use of herbal supplements, especially if LDL cholesterol levels unexpectedly increase despite compliance with a statin." @default.
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• W2014594637 title "Reduced Efficacy of Rosuvastatin by St. John's Wort" @default.
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