Effect of fenofibrate on C-reactive protein levels in hypertriglyceridemic patients.
- Author:
Sung Ho LEE
1
;
Kyung Heon LEE
;
Yeo Jin CHOI
;
Kwang Ho LEE
;
Soo Hee CHOI
;
Kyung Eun LEE
;
Kwang Je LEE
;
Tae Ho KIM
;
Hong Sook KO
;
Chee Jeong KIM
;
Wang Seong RYU
Author Information
1. Division of Cardiology, Department of Internal Medicine, College of Medicine, Chung-Ang University, Seoul, Korea. cjkim@cau.ac.kr
- Publication Type:Original Article
- Keywords:
C-reactive protein;
Fenofibric acid;
Lipid;
Lipoprotein
- MeSH:
C-Reactive Protein*;
Cardiovascular Diseases;
Diabetes Mellitus;
Fenofibrate*;
Fibric Acids;
Humans;
Hydroxymethylglutaryl CoA Reductases;
Hydroxymethylglutaryl-CoA Reductase Inhibitors;
Hypercholesterolemia;
Lipoproteins;
Triglycerides
- From:Korean Journal of Medicine
2006;70(6):656-662
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: High levels of C-reactive protein (CRP) are associated with an increased risk for cardiovascular diseases. Most reports on the effect of fibrate on CRP level have inadequate study designs and the results are inconsistent. This study was designed to evaluate the effect of fenofibrate on CRP levels in hypertriglyceridemic patients. METHODS: Patients with triglyceride (TG) level over 200 mg/dL were treated with 200 mg of fenofibrate (Fenofibrate group, n=30) or with general measures (Control group, n=30). Patients with CRP levels >10 mg/L were excluded. Patients with hypercholesterolemia were treated with HMG CoA reductase inhibitor (Statin group, n=30). Lipid and lipoprotein levels were measured before and 2 months after medication. RESULTS: Baseline characteristics were similar in Fenofibrate and Control groups. Baseline CRP levels were independently associated with the presence of diabetes mellitus. Fenofibrate therapy did not change CRP levels (1.67+/-1.60 vs 1.76+/-1.88 mg/L, p=0.79) as did Control group (p=0.46). When both Fenofibrate and Control groups were divided into three subgroups in terms of baseline CRP levels, CRP levels were increased in the lowest group (p=0.019), did not change in the middle and the highest groups (p=0.89 and p=0.47 respectively). In patients with baseline CRP level > or =3 mg/L, CRP levels were decreased (p=0.041). Changes of CRP levels were independently associated with baseline CRP levels. Statin therapy decreased CRP levels (p=0.046). CONCLUSIONS: Fenofibrate did not change CRP levels in hypertriglyceridemic patients. Cardioprotective effects of fibrates may not be associated with anti-inflammatory mechanisms in contrast to those of statins.
