The measure of life-time alcohol consumption in patients with cirrhosis: reproducibility and clinical relevance.

Our aims were to design a reproducible method of measuring life-time alcohol consumption in patients with cirrhosis, and to assess the risk of liver decompensation associated with alcohol intake using a case-control design and a multivariate analysis. We studied 439 patients ("cases") with decompensated cirrhosis, and 233 with compensated cirrhosis ("controls"). Mean life-time daily amount and duration of alcohol intake were measured by a standardized questionnaire, whose reproducibility, assessed by interviewing 75 relatives, was 70% for daily alcohol intake and 84% for duration of intake. Better reproducibility was found by re-interviewing patients at discharge from hospital. Daily alcohol intake was significantly higher in males, younger patients and patients with liver decompensation. After stratification according to the average life-time daily alcohol intake, we found a significant increase in the risk of liver decompensation from 125 g ethanol intake per day onwards. No association was found between duration of alcohol intake and risk of liver decompensation. We conclude that alcohol intake can be reliably and reproducibly measured: in patients with cirrhosis, increased alcohol intake is associated with increased risk of liver decompensation, with a significant dose-effect above a daily intake of 125 g ethanol.

[1]  G. Corrao,et al.  Effect of age, birth cohort and period of death on Italian liver cirrhosis mortality, 1972-1986. , 1993, International journal of epidemiology.

[2]  G. Corrao,et al.  Alcohol consumption and non-cirrhotic chronic hepatitis: a case-control study. , 1991, International Journal of Epidemiology.

[3]  P. Bedossa,et al.  A simple biological index for detection of alcoholic liver disease in drinkers. , 1991, Gastroenterology.

[4]  G. Corrao,et al.  A case-control study on alcohol consumption and the risk of chronic liver disease. , 1991, Revue d'epidemiologie et de sante publique.

[5]  C. Lieber,et al.  High blood alcohol levels in women. The role of decreased gastric alcohol dehydrogenase activity and first-pass metabolism. , 1990, The New England journal of medicine.

[6]  T. Sørensen.  Alcohol and liver injury: dose-related or permissive effect? , 2008, Liver.

[7]  K. Ishak,et al.  Alcohollike liver disease in nonalcoholics. A clinical and histologic comparison with alcohol-induced liver injury. , 1988, Gastroenterology.

[8]  R. Capocaccia,et al.  Mortality from liver cirrhosis in Italy: proportion associated with consumption of alcohol. , 1988, Journal of clinical epidemiology.

[9]  C. la Vecchia,et al.  Mortality from alcohol related disease in Italy. , 1986, Journal of epidemiology and community health.

[10]  O. Skog.  The wetness of drinking cultures: a key variable in epidemiology of alcoholic liver cirrhosis. , 2009, Acta medica Scandinavica. Supplementum.

[11]  J. Saunders,et al.  What Determines Susceptibility to Liver Damage from Alcohol?: Discussion Paper , 1984, Journal of the Royal Society of Medicine.

[12]  Y. Israel,et al.  Alcoholic liver disease: Information in search of knowledge? , 1981, Hepatology.

[13]  J. Saunders,et al.  Do women develop alcoholic liver disease more readily than men? , 1981, British medical journal.

[14]  Y. Israel,et al.  RELIABILITY OF ASSESSMENT OF ALCOHOL INTAKE BASED ON PERSONAL INTERVIEWS IN A LIVER CLINIC , 1979, The Lancet.

[15]  A. Tuyns,et al.  Ascitic cirrhosis in relation to alcohol consumption. , 1978, International journal of epidemiology.

[16]  W. K. Lelbach,et al.  CIRRHOSIS IN THE ALCOHOLIC AND ITS RELATION TO THE VOLUME OF ALCOHOL ABUSE , 1975, Annals of the New York Academy of Sciences.