Long-term use of angiotensin converting enzyme inhibitors is associated with decreased incidence of advanced adenomatous colon polyps.

BACKGROUND: The long-term use of angiotensin converting enzyme (ACE) inhibitors may reduce the risk of developing colorectal cancer (CRC). GOAL: The aim of our study was to determine how long-term use of lisinopril influences the development of advanced adenomatous polyps (APs). STUDY: We performed a retrospective study of patients who were found to have 1 or more histologically confirmed APs on an index colonoscopy, and who also had a follow-up colonoscopy 3 to 5 years later. APs found on the follow-up colonoscopy were evaluated for location, size, number, and advanced features. Patients were divided into 2 groups: (1) those who used lisinopril continuously during the interval between colonoscopies and (2) those who were lisinopril naive. Clinical factors were evaluated for their association with advanced APs in both the groups. RESULTS: A total of 4660 patients with a history of AP were identified. There were 1760 continuous lisinopril users and 2900 nonusers. Univariate analysis showed that patients with lisinopril use had fewer right-side APs (odds ratio=0.68, P<0.001) and fewer total number of APs (P<0.001). Lisinopril users had a 41% reduced incidence of advanced APs compared with the nonusers (odds ratio=0.59, P<0.001). A Mann-Whitney U test revealed that among lisinopril users, patients with advanced APs were on a lower dose of the medication compared with patients without advanced APs (mean dose=17.2 mg vs. 20.1 mg, respectively; P<0.001). Spearman correlation analyses indicated an inverse relationship between lisinopril dosage and number of polyps (P<0.001). There was also an inverse relationship between dosage and size of polyps (P<0.001); higher dosages of lisinopril were significantly associated with smaller size of polyps. The protective effect of lisinopril was significant even when adjusted for age, body mass index, aspirin/nonsteroidal anti-inflammatory drug use, and statin use. CONCLUSIONS: The use of lisinopril was associated with a 41% reduction in the incidence of advanced APs during a period of 3 to 5 years, even after adjustment for other known polyp risk factors. We speculate that long-term ACE inhibitors use may reduce the development of CRCs by reducing the development of advanced APs.

Obesity is associated with an increased prevalence of advanced adenomatous colon polyps in a male veteran population.

Obesity has been associated with an increased risk for colonic adenomatous polyps (APs) and colorectal cancers, but the influence of obesity on the development of advanced APs is not clear. The purpose of this study is to determine the influence of obesity on the prevalence of advanced APs in a male veteran population. We performed a retrospective study of patients (n = 2,903) with histologically confirmed APs on an index colonoscopy. APs were evaluated for advanced features (size > or = 1 cm in diameter and/or a villous component and/or high grade dysplasia). Patients were categorized as: normal weight (BMI > 18.5 and < 25), overweight (BMI > or = 25 and < 30), and obese (BMI > or = 30). An association between clinical factors and advanced APs was sought by Kruskal-Wallis test and Pearson Chi-square. Multiple logistic regression analysis was used to determine independent predictors for advanced APs. We identified 2,903 male patients with APs (mean age 64 + 1.1(SE) years; 770 (27%) normal weight, 1,029 (35%) overweight, 1,104 (38%) obese. By univariate analysis, obese patients had a greater prevalence of advanced APs than the overweight and normal weight patients (28 vs. 23 vs. 24%, p = 0.025). Multiple logistic regression analysis confirmed the association of obesity and advanced APs (OR = 1.01, CI = 1-1.02, p = 0.04). For every one-unit increase in BMI above 30, there was a corresponding 1% increase in the frequency of finding advanced APs. Obesity in male veteran patients is associated with the finding of advanced APs on colonoscopy. We speculate that obesity may increase the risk for CRC by promoting the development of advanced APs.

Correlation between beta-lipoprotein levels and outcome of hepatitis C treatment.

The low-density lipoprotein receptor (LDLR) has been proposed as a candidate receptor for the hepatitis C virus (HCV). Competitive inhibition of HCV binding to the LDLR by low-density lipoprotein (LDL) has been shown in vitro. If similar inhibition occurs in vivo, an elevated serum concentration of beta-lipoproteins may reduce the efficiency of infecting hepatocytes with HCV by competitively inhibiting HCV viral receptor binding. We investigated the role of baseline lipid values in influencing the outcome of HCV treatment. We conducted a retrospective chart review of patients treated with an interferon-based regimen at our liver and gastroenterology clinics between 1998 and 2004. Of 99 patients enrolled in the study, 49 (49.5%) had HCV genotype 1 (LDL 100.2 +/- 30.2 mg/dL [mean +/- SD]), and 50 patients (50.5%) had genotype 2 or 3 (LDL 110.1 +/- 40 mg/dL) infection. Early viral response (EVR), end-of-treatment response (ETR), and sustained viral response (SVR) were documented in 99, 88, and 77 patients, respectively. LDL and cholesterol levels prior to treatment were found to be higher in patients with positive EVR, ETR, and SVR. This difference remained significant independent of age. Multivariate analysis controlling for genotype and age showed that the higher the cholesterol and LDL levels prior to treatment, the greater the odds of responding to treatment. In conclusion, having higher serum LDL and cholesterol levels before treatment may be significant prognostic indicators for treatment outcome of those with chronic hepatitis C infection, particularly in genotypes 1 and 2.