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To assess the effect of computer-aided detection (CAD) as a second reader on the sensitivity and specificity of computed tomographic (CT) colonography in detecting 6-9-mm colorectal cancer (CRC) lesions.Individuals with clinical indications for colonoscopy--either for symptoms or as part of participating in a surveillance program or CRC screening--were prospectively enrolled at one of 10 academic centers between July 2007 and May 2009. Institutional review board approval was obtained at each clinical site, and all participants provided written informed consent. All participants underwent CT colonography and colonoscopy on the same day. Experienced readers interpreted the CT colonography images unassisted and then reviewed all colorectal lesion-like structures pinpointed by the CAD algorithm. Segmental unblinding of CT colonoscopy findings at colonoscopy was utilized. The sensitivity and specificity of unassisted and CAD-assisted reading in identifying individuals with 6-9-mm lesions were calculated and compared by means of pairwise analysis.A total of 618 participants (mean age, 57.9 years; 54.5% male) were included in the final analysis. Of these participants, 464 (75.1%) had no lesions 6 mm or larger, and 52 (8.4%) had 6-9-mm lesions. The sensitivity of CT colonography with unassisted reading and that with CAD-assisted reading in identifying individuals with 6-9-mm lesions was 65.4% (95% confidence interval [CI]: 50.9%, 78.0%) and 76.9% (95% CI: 63.2%, 87.5%; P = .016), respectively. No significant change in specificity was observed: The specificity of CT colonography with unassisted and that with CAD-assisted reading was 91.8% (95% CI: 88.9%, 94.1%) and 90.9% (95% CI: 88.0%, 93.4%; P = .063), respectively. Evaluation of CAD candidates required an additional 1.6 minutes (25th-75th percentile: 1.0 minute to 3.4 minutes).The addition of CAD to reading performed by experienced readers resulted in a significant benefit in the detection of 6-9-mm polyps at CT colonography in this cohort.http://radiology.rsna.org/lookup/suppl/doi:10.1148/radiol.12120376/-/DC1.

We report the results of an Italian multicenter study aimed at measuring retrospectively the lifetime amount and duration of alcohol consumption in non-selected consecutive patients with chronic liver disease. We used a standardized, reproducible questionnaire for measuring the lifetime daily alcohol intake (globally and separately for wine, beer and spirits), total alcohol intake and duration of alcohol consumption in 1,258 patients recruited from 17 medical centers. Wine intake contributed to the total alcohol intake in a proportion ranging from 44% to 85% throughout the centers. Spirits and beer intake contributed in smaller proportions (15% to 56%; and 3% to 27%, respectively). Males showed higher alcohol intake: those from northern-central Italy showed significantly higher intake than their southern-insular counterparts; of these, younger patients also showed a higher alcohol intake, due to a higher beer and spirit intake. Older patients showed higher intakes in southern-insular Italy, whereas the opposite was found in northern-central Italy. In this area, a longer duration of alcohol consumption was found, reflecting an earlier start in the use of alcohol. In conclusion, we believe that measuring alcohol intake on a wide series of patients in a multicenter study is feasible. This should stimulate gastroenterologists to approach the relationship between alcohol and liver disease using standardized and epidemiologically correct methods, and form the basis for well-designed case-control studies on a large scale, aimed at clarifying the risk of both hepatic and extrahepatic diseases associated with alcohol intake.

In order to assess the inter-relationship between nutritional intake and alcohol consumption on the risk of liver cirrhosis we performed a hospital-based retrospective case-control study. We enrolled 115 cases admitted to hospital for liver decompensation at their first diagnosis of liver cirrhosis and 167 hospital controls without evidence of liver disease admitted for acute diseases unrelated to alcohol intake. Daily alcohol intake and average nutrient intake were measured throughout the patient's life, using a reproducible questionnaire. No dose-effect relationship was found between nutrient intake and risk of cirrhosis using classical association statistical methods. We then corrected the intake of each nutrient for the total caloric intake and this energy-adjusted nutrient intake was used in a logistic regression model together with alcohol intake, viral B and C hepatitis markers, age and gender. Using this approach, carbohydrates intake were shown to have a protective effect on the risk of cirrhosis, whereas saturated lipid intake had a significant multiplicative effect on the risk associated with alcohol consumption. By comparison with the teetotalers category who had an average daily intake of saturated fatty acids lower than 40.3 g (reference category; OR = 1), drinkers of more than 100 g ethanol per day showed ORs ranging from 14.2 (95% confidence interval 2.0-101.0) for consumers of less than 40.3 g fatty acid per day, to 39.0 (95% confidence interval 5.0-305.1) for consumers of more than 40.4 g fatty acid per day. In conclusion we give additional evidence on the relationship between diet and risk of cirrhosis, whereby saturated lipid intake multiplies the risk associated with alcohol intake. However, caution should be used to interpret such results, since they seem to suggest that diet but not a particular nutrient can modify the effect of alcohol on the risk of cirrhosis. The present lack of agreement on the mechanisms and the nutrients involved in the pathogenesis of alcoholic liver injury should stimulate wider epidemiological studies using modern nutritional techniques.

We report the results of an Italian multicenter study aimed at measuring retrospectively the lifetime amount and duration of alcohol consumption in non-selected consecutive patients with chronic liver disease. We used a standardized, reproducible questionnaire for measuring the lifetime daily alcohol intake (globally and separately for wine, beer and spirits), total alcohol intake and duration of alcohol consumption in 1,258 patients recruited from 17 medical centers. Wine intake contributed to the total alcohol intake in a proportion ranging from 44% to 85% throughout the centers. Spirits and beer intake contributed in smaller proportions (15% to 56%; and 3% to 27%, respectively). Males showed higher alcohol intake: those from northern-central Italy showed significantly higher intake than their southern-insular counterparts; of these, younger patients also showed a higher alcohol intake, due to a higher beer and spirit intake. Older patients showed higher intakes in southern-insular Italy, whereas the opposite was found in northern-central Italy. In this area, a longer duration of alcohol consumption was found, reflecting an earlier start in the use of alcohol. In conclusion, we believe that measuring alcohol intake on a wide series of patients in a multicenter study is feasible. This should stimulate gastroenterologists to approach the relationship between alcohol and liver disease using standardized and epidemiologically correct methods, and form the basis for well-designed case-control studies on a large scale, aimed at clarifying the risk of both hepatic and extrahepatic diseases associated with alcohol intake.

In order to assess the interaction between alcohol intake, tobacco smoking and coffee consumption in determining the risk of liver cirrhosis we carried out a hospital-based case-control study involving 115 patients at their first diagnosis of cirrhosis and 167 control patients consecutively enrolled in the General Hospitals of the Province of L'Aquila (Central Italy). The mean life-time daily alcohol intake (as g ethanol consumed daily) was measured by direct patient interviews, whose reproducibility was > 0.80 and similar for cases and controls, as checked by interviewing the relatives of a sample of 50 cases and 73 controls. During the same patient's interview we also measured the mean consumption of coffee (daily number of cups of filtered coffee) and tobacco (life-time daily number of cigarettes smoked). A dose-effect relationship on the risk of cirrhosis was present both for alcohol intake--for which the risk was significantly increased above 100 g of daily intake--and for cigarette consumption. The latter did not however improve the goodness-of-fit of a logistic regression model including alcohol intake as covariate. By contrast, coffee consumption had a protective effect on the risk of cirrhosis and significantly improved the goodness-of-fit of such a model. Abstaining from coffee consumption determined both a significantly increased risk of cirrhosis, even for daily alcohol intake below 100 g, and a multiplicative effect with alcohol intake on this risk. In patients drinking > or = 101 g ethanol daily the relative risk increased from 5.5 (95% confidence interval: 1.4-22.0) for coffee consumers to 10.8 (95% confidence interval: 1.3-58.1) for coffee abstainers.(ABSTRACT TRUNCATED AT 250 WORDS)

We carried out a hospital based case-control study involving 655 patients with chronic liver disease encompassing chronic hepatitis, asymptomatic liver cirrhosis and symptomatic liver cirrhosis and 655 pair-matched control individuals in order to estimate the dose-response relationship between alcohol consumption and the occurrence of chronic liver disease. Alcohol intake was measured by a questionnaire and expressed as Daily Alcohol Intake (DAI) during the patient life. DAI estimates from patient interviews were in good agreement with those obtained by interviewing a sample of relatives. We found an exponential positive association between DAI and the risk of chronic hepatitis and cirrhosis. However, consuming less than 100g of alcohol every day did not increase the risk of developing chronic liver disease. For asymptomatic cirrhosis the risk was lower than for chronic hepatitis, especially at high DAI, probably because high consumption carried a high probability of liver decompensation. For symptomatic cirrhosis, the risk function showed a similar pattern as for chronic hepatitis. Chronic hepatitis patients were 6-7 years younger than cirrhotics. Our results suggest that the evolution towards cirrhosis once a chronic liver damage has occurred is probably time-dependent, but not or minimally dependent on alcohol intake.