Several patient characteristics were significantly associated with colonic preparation quality independent of preparation type, compliance with preparation instructions, and procedure starting time. This information may help to identify patients at an increased risk for inadequate colonic preparation for whom alternative preparation protocols would be appropriate.

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Patients with primary sclerosing cholangitis (PSC) have a significantly increased risk of developing cholangiocarcinoma (CCA). Risk factors for developing such a complication are not well defined. We conducted a multicenter, case-control study to determine the risk factors and possible predictors for CCA in patients with PSC. The demographic, clinical, and laboratory features of 26 PSC patients with CCA diagnosed over a 7-year period at eight academic centers were compared with 87 patients with PSC but no CCA (controls). There was no statistically significant difference in demographics, smoking, signs or symptoms or complications of PSC, indices of disease severity (Mayo Risk score or Child-Pugh score), frequency or duration or complications of inflammatory bowel disease (IBD), frequency of biliary surgery, or therapeutic endoscopy between the two groups. Alcohol consumption was significantly associated with CCA in patients with PSC (odds ratio: 2.95; 95% CI: 1.04-8.3). Serum carbohydrate antigen 19-9 (CA 19-9) was significantly higher in patients with CCA than those without (177 ؎ 89 and 61 ؎ 58 U/mL, respectively; P ‫؍‬ .002). A serum CA 19-9 level G 100 U/mL had 75% sensitivity and 80% specificity in identifying PSC patients with CCA. In conclusion, alcohol consumption was a risk factor for having CCA in PSC patients. The indices of severity of liver disease were not associated with CCA in patients with PSC. Serum CA 19-9 appeared to have good ability to discriminate PSC patients with and without CCA. (HEPATOLOGY 2000;31:7-11.)Primary sclerosing cholangitis (PSC) is a chronic cholestatic liver disorder that is characterized by multiple fibrotic strictures of the intra-and extrahepatic biliary tree. It is a progressive disorder in which approximately 50% of symptomatic patients eventually develop cirrhosis and liver failure. 1

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From the Insulin Resistance Atherosclerosis Study (IRAS), 1173 men and women of African-American, non-Hispanic white, and Hispanic ethnicity with no history of diabetes were included in an evaluation of the cross-sectional relation of habitual dietary fat intake with insulin sensitivity (SI) as assessed by minimal-model analysis of a 12-sample, insulin-modified frequently sampled intravenous-glucose-tolerance test. Dietary intake was measured by a food-frequency interview modified to enhance sensitivity to food choices within the three ethnic groups. Percentage of energy from total fat was associated with rank of SI (SI(rank); r = -0.06, P = 0.03), with log fasting insulin (r = 0.10, P < 0.001), and with BMI (r = 0.10, P < 0.001). Multiple-linear-regression models included SI(rank) as the dependent variable, dietary fat (g/d) as the primary independent variable adjusted sequentially for total energy, other covariates, body mass index, and waist-hip circumference ratio (WHR). For all subjects combined, total fat intake was inversely related to SI(rank), but this association was not significant (P = 0.14) and was attenuated by adjustment for body mass index and WHR (P = 0.44). The association of total fat (g/d) with SI(rank) differed significantly (P < 0.01) for obese compared with nonobese individuals. Higher fat intake was associated with lower SI(rank) among obese (beta = -1.40, P = 0.03) but not among nonobese persons (beta = 0.16, P = 0.80). Among the obese (body mass index < or = 63), adjustment for body mass index largely accounted for the observed association of dietary fat with SI(rank). These findings were generally consistent for monounsaturated, polyunsaturated, and saturated fats. Among individuals already at increased risk for non-insulin-dependent diabetes mellitus because of obesity, high intake of dietary fat may worsen insulin sensitivity. This effect may be mediated by the relation of dietary fat to obesity.