Abstract/Text: The association between self-reported alcohol intake and the risk of future liver disease was studied in a large population-based prospective cohort with 12-year follow-up. Alcohol intake was assessed in 13,285 men and women aged 30 to 79 years by a self-administered questionnaire. Diagnoses indicating alcohol-induced liver disease (n = 261) or alcohol-induced cirrhosis (n = 124) were obtained from death certificates and the hospital discharge register, and data were analyzed by multiplicative Poisson regression models. The total cumulated observation time was 130,558 person-years. The overall incidence rates of alcohol-induced cirrhosis were 0.2% per year in men and 0.03% per year in women. The nadir of the estimated relative risk of developing liver disease was observed at an alcohol intake of 1 to 6 beverages per week, and above this level a steep increase in relative risk was observed. The risk function was independent of age and stable over time. The level of alcohol intake above which the relative risk was significantly greater than 1 was observed at 7 to 13 beverages per week for women and 14 to 27 beverages per week for men. Women had a significantly higher relative risk of developing alcohol-related liver disease than men for any given level of alcohol intake. We observed a dose-dependent increase in relative risk of developing alcohol-induced liver disease for both men and women, with the steepest increase among women. In the general population, self-reported current alcohol intake is a good predictor of the future risk of alcohol-induced liver disease.

Abstract/Text: INTRODUCTION: Alcoholic hepatitis is associated with a high short term mortality. We aimed to identify those factors associated with mortality and define a simple score which would predict outcome in our population.
METHODS: We identified 241 patients with alcoholic hepatitis. Clinical and laboratory data were recorded on the day of admission (day 1) and on days 6-9. Stepwise logistic regression was used to identify variables related to outcome at 28 days and 84 days after admission. These variables were included in the Glasgow alcoholic hepatitis score (GAHS) and its ability to predict outcome assessed. The GAHS was validated in a separate dataset of 195 patients.
RESULTS: The GAHS was derived from five variables independently associated with outcome: age (p = 0.001) and, from day 1 results, serum bilirubin (p<0.001), blood urea (p = 0.019) and, from day 6-9 results, serum bilirubin (p<0.001), prothrombin time (p = 0.002), and peripheral blood white blood cell count (p = 0.001). The GAHS on day 1 had an overall accuracy of 81% when predicting 28 day outcome. In contrast, the modified discriminant function had an overall accuracy of 49%. Similar results were found using information at 6-9 days and when predicting 84 day outcome. The accuracy of the GAHS was confirmed by the validation study of 195 patients The GAHS was equally accurate irrespective of the use of the international normalised ratio or prothrombin time ratio, or if the diagnosis of alcoholic hepatitis was biopsy proven or on the basis of clinical assessment.
CONCLUSIONS: Using variables associated with mortality we have derived and validated an accurate scoring system to assess outcome in alcoholic hepatitis. This score was able to identify patients at greatest risk of death throughout their admission.

Abstract/Text: Drinking excessive amounts of alcohol regularly for years is toxic to almost every tissue of the body. On the other hand, epidemiological and clinical evidence shows that light-to-moderate drinking is associated with a reduced risk of coronary heart disease, total and ischemic stroke, and mortality. In the past two decades, metabolic syndrome, the combination of obesity, hypertension, dyslipidemia and hyperglycemia, are all also recognized as major cardiovascular risk factors, has given rise to much clinical and research attention, because of its high prevalence in the world. Therefore, it is of interest to evaluate the overall associations of alcohol consumption with the development of metabolic syndrome. Recently, the protective, detrimental or J-shaped associations have been reported between alcohol consumption and metabolic syndrome. This controversy may be due to the complex mechanistic relation between alcohol consumption and each component of metabolic syndrome, and almost all studies have various limitations and problem points. Prospective studies are therefore needed to confirm the association between alcohol consumption and prevalence of metabolic syndrome, and to assess the influence of alcohol drinking patterns and other possible factors, such as smoking, physical activity, socioeconomic status, education, occupation, diet and exercise. This article reviews the relation of alcohol consumption and components of metabolic syndrome, and discusses the epidemiological evidence for alcohol's putative vascular protective effects and plausible underlying biological mechanisms.

© 2011 The Japan Society of Hepatology.