title: Effect of withdrawal of statin on C-reactive protein.
abstract: BACKGROUND
  C-reactive protein is considered a risk factor for coronary artery disease. In addition to its lipid-lowering properties, statin decreases the level of C-reactive protein. Abrupt cessation of statin therapy during treatment could increase the incidence of cardiac events in patients with atherosclerotic heart disease. The changes of C-reactive protein after withdrawal of statin therapy are still unknown.
  
  
  METHODS
  Twenty patients with hyperlipidemia received statin (atorvastatin, 10 mg/day) therapy for 3 months. The levels of lipid profiles and C-reactive protein were assessed before receiving the statin therapy, immediately after 3 months of therapy, and on the 3 consecutive days after withdrawal of statin treatment.
  
  
  RESULTS
  After 3 months of statin therapy, the total cholesterol, low-density lipoprotein cholesterol (LDL-chol), and C-reactive protein were significantly reduced (264.94 +/- 16.23 vs. 183.44 +/- 16.34 mg/dl, 183.17 +/- 34.56 vs. 122.00 +/- 17.66 mg/dl, and 2,309.00 +/- 437.85 vs. 1,257.95 +/- 207.99 ng/ml, respectively). The level of C-reactive protein increased on the second day after withdrawal of statin therapy (2,590.14 +/- 1,045.05 vs. 1,257.95 +/- 207.99 ng/ml); however, the total cholesterol and LDL-chol did not increase during the 3-day period after withdrawal of statin therapy.
  
  
  CONCLUSIONS
  The increase in the level of C-reactive protein after withdrawal of statin therapy may be a contributing factor to the increased incidence of cardiac events in patients who have abruptly stopped statin therapy.
authors.affiliation: Section of Cardiology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.
authors.forename: Kun-Tai
authors.initials: KT
authors.lastname: Lee
authors.forename: Wen-Ter
authors.initials: WT
authors.lastname: Lai
authors.forename: Chin-Sheng
authors.initials: CS
authors.lastname: Chu
authors.forename: Li-Yu
authors.initials: LY
authors.lastname: Tsai
authors.forename: Hsueh-Wei
authors.initials: HW
authors.lastname: Yen
authors.forename: Wen-Choi
authors.initials: WC
authors.lastname: Voon
authors.forename: Sheng-Hsiung
authors.initials: SH
authors.lastname: Sheu
mesh_terms: D000368:Aged; D000069059:Atorvastatin; D002097:C-Reactive Protein / Q000032:analysis*; D003324:Coronary Artery Disease / Q000139:chemically induced / Q000453:epidemiology; D005260:Female; D006538:Heptanoic Acids / Q000008:administration & dosage* / Q000009:adverse effects; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage* / Q000009:adverse effects; D006949:Hyperlipidemias / Q000097:blood / Q000188:drug therapy*; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D011758:Pyrroles / Q000008:administration & dosage* / Q000009:adverse effects; D012307:Risk Factors; D013375:Substance Withdrawal Syndrome / Q000097:blood / Q000503:physiopathology*
chemical_list: D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008055:Lipids; D011758:Pyrroles; D002097:C-Reactive Protein; D000069059:Atorvastatin