Prevalence and Risk Factors of Gallbladder Polypoid Lesions in a Healthy Population

PURPOSE: To determine the prevalence of and investigate the risk factors for gallbladder (GB) polypoid lesions in a healthy population. MATERIALS AND METHODS: A total of 23827 subjects who underwent abdominal ultrasonography in conjunction with health screening examinations were retrospectively analyzed. The prevalence of risk factors for GB polypoid lesions were evaluated. In addition, risk factors according to the number of polypoid lesions and the presence of stones with polypoid lesions were investigated. To analyze these risk factors, a control group was established with a 1:2 ratio matched for age and sex. RESULTS: The prevalence of GB polypoid lesions was identified as 9.96%. On multivariate analysis, chronic hepatitis B infection (CHB) and the presence of metabolic syndrome (MS) were risk factors for GB polypoid lesions. CHB and MS were also significant independent risk factors for multiple GB polypoid lesions when compared with solitary GB polypoid lesions. In addition, gastric Helicobacter pylori infection and MS were significant risk factors for GB polypoid lesions with stones when compared with GB polypoid lesions without stones. CONCLUSION: The prevalence of GB polypoid lesions in a healthy Korean population was 9.96%. Patients with CHB and MS need to be carefully examined for such lesions.

Fenofibrate Reduces C-Reactive Protein Levels in Hypertriglyceridemic Patients With High Risks for Cardiovascular Diseases

BACKGROUND AND OBJECTIVES: The effects of fenofibrate on C-reactive protein (CRP) are under debate. We investigated the effect of fenofibrate on CRP levels and the variables determining changes. SUBJECTS AND METHODS: This case-control study enrolled 280 hypertriglyceridemic patients who were managed either with 200 mg of fenofibrate (Fenofibrate group, n=140) or with standard treatment (comparison group, n=140). CRP levels were measured before and after management for 2 months. RESULTS: CRP levels decreased in both the fenofibrate (p=0.003) and comparison (p=0.048) groups. Changes in CRP levels were not significantly different between the two groups (p=0.27) and were negatively associated with baseline CRP levels (r=-0.47, p or =1 mg/L, CRP levels also decreased in both groups (p=0.000 and p=0.001 respectively), however, more in the fenofibrate group than in the comparison group (p=0.025). The reduction of CRP was associated with higher baseline CRP levels (r=-0.29, p=0.001), lower body mass index (BMI, r=0.23, p=0.007), and fenofibrate therapy (r=0.19, p=0.025). CRP levels decreased more in the fenofibrate group than in the comparison group in patients with a BMI < or =26 kg/m2 with borderline significance (-1.21+/-1.82 mg/L vs. -0.89+/-1.92 mg/L, p=0.097). In patients with a high density lipoprotein-cholesterol level <40 mg/dL, CRP levels were reduced only in the fenofibrate group (p=0.006). CONCLUSION: Fenofibrate reduced CRP levels in hypertriglyceridemic patients with high CRP and/or low high density lipoprotein-cholesterol levels and without severe overweight. This finding suggests that fenofibrate may have an anti-inflammatory effect in selected patients.

Effects of the Transition from Premenopause to Postmenopause on Lipids and Lipoproteins: Quantification and Related Parameters

BACKGROUND/AIMS: The aim of this study was to quantitatively measure changes in lipids and lipoproteins during perimenopause and to identify variables related to these changes. METHODS: Among women who had three regular health evaluations over a span of 2-4 years, 34 women remained in the premenopausal state, 34 premenopausal women transitioned to the postmenopausal state, and 36 postmenopausal women were enrolled. The menopausal state was determined not only by a history of amenorrhea but also by levels of female sex hormones. Yearly changes in lipids were calculated using a linear regression of the three measurements. RESULTS: The transition from premenopause to postmenopause was associated with increased total cholesterol and low-density lipoprotein (LDL) cholesterol levels by 7.4 +/- 8.0 mg/dL (4.2 +/- 4.9%) and 6.9 +/- 6.5 mg/dL (6.8 +/- 7.0%) over one year, resulting in an elevation of 19.6 +/- 22.6 mg/dL (10.9 +/- 13.0%) and 18.9 +/- 19.5 mg/dL (18.6 +/- 20.3%), respectively, during perimenopause. There were no changes observed in premenopausal and postmenopausal women. Body weight, blood pressure, high-density lipoprotein (HDL) cholesterol, and triglycerides did not change in any of the three groups. In all women, changes in both total cholesterol and LDL cholesterol were associated with changes in follicle stimulating hormone (r = 0.40, p < 0.001 and r = 0.38, p < 0.001, respectively). Changes in triglycerides were associated with changes in body weight (r = 0.28, p = 0.005). CONCLUSIONS: During perimenopause, total and LDL cholesterol levels increase and these changes in cholesterol are mainly dependent on changes in female sex hormones.

Effects of Ezetimibe Added to Ongoing Statin Therapy on C-Reactive Protein Levels in Hypercholesterolemic Patients

BACKGROUND AND OBJECTIVES: Ezetimibe alone does not decrease C-reactive protein (CRP) levels in hypercholesterolemic patients. However, several reports have suggested that ezetimibe might potentiate the effect of statin not only on cholesterol but also on CRP when administered together. We investigated the effect of ezetimibe on CRP levels in patients taking statins. SUBJECTS AND METHODS: Patients who had not achieved recommended low density lipoprotein-cholesterol (LDL-C) goals with statin therapy were divided into two groups, the ezetimibe group (n=60) and the control group (n=60). A third group of hypercholesterolemic patients without statin therapy was treated with statin (n=59). Patients with CRP level 10 mg/L were excluded. Lipid and CRP levels were measured before therapy commenced, and after 2 months of therapy. RESULTS: Ezetimibe decreased cholesterol and LDL-C levels by 20.2% (p=0.000) and 28.1% (p=0.000) respectively. However, ezetimibe did not reduce CRP levels (from 0.83+/-0.68 to 1.14+/-1.21 mg/dL, p=0.11). CRP levels remained unchanged in the control group (p=0.42). In contrast, statin lowered CRP levels (from 0.82+/-0.73 to 0.65+/-0.57 mg/dL, p=0.008). In patients taking statins, changes in CRP levels were not associated with changes in LDL-C (r=-0.02, p=0.87), but with baseline CRP levels (r=-0.38, p=0.000). CONCLUSION: Ezetimibe failed to reduce CRP levels in hypercholesterolemic patients taking statins despite significant reduction of LDL-C. This finding suggests that the anti-inflammatory effect of statin may not be secondary to cholesterol reduction, but via other mechanisms.