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The analysis of the combined effects of nutritional factors with other putative disease determinants in log-linear or logistic models is methodologically complicated by the strong multicollinearity between nutritional factors, resulting in poor precision in estimating the parameters. Furthermore, the generally used multiplicative structure is not always the most appropriate for describing the resulting joint effect of two or more factors on the disease risk. The authors addressed such problems in a case-control study assessing the interactions between alcohol intake, chronic hepatitis C virus (HCV) infection, and nutrient intake on the risk of liver cirrhosis. During the period from November 1989 to May 1990, 282 patients admitted to the medical departments of the hospitals of the Province of L'Aquila (central Italy) were enrolled: 115 cirrhotic patients aged 24-82 years (78 of whom were males) hospitalized because of liver decompensation, and 167 control patients aged 25-84 years (100 of whom were males) admitted to the same hospitals for acute diseases unrelated to alcohol intake, infection with hepatotropic viruses, and nutrition. No dose-effect relation was found between the intake of any nutrient and the risk of cirrhosis using classical methods. The analysis of principal components showed, however, that a pattern of higher lipid but lower protein and carbohydrate intakes was significantly associated with the risk of cirrhosis. The Breslow and Storer parametric family of relative risk functions showed that a multiplicative structure was the most adequate to describe the joint effect of nutritional pattern with alcohol intake and/or chronic HCV infection, whereas an additive structure best described the joint effect of chronic HCV infection and alcohol intake. In conclusion, the analysis of principal components and the Breslow and Storer family are useful tools to explore the role of diet on disease risk when precise pathogenic knowledge is not available. As an original finding, the authors suggest that a higher lipid intake, combined with lower protein and carbohydrate intakes, modifies multiplicatively the risk of cirrhosis associated with alcohol intake and/or chronic HCV infection.

A total of 198 alcoholic subjects was recruited into a treatment programme according to Hudolin's method. The programme included three steps: (1) presentation of the programme to the alcoholic family (four meetings); (2) a therapeutic community that met weekly over 4 months; and (3) attendance at an on-Treatment Alcoholic Club located close to the family's home residence (weekly self-conducted meetings). Data on the families' compliance to the treatment programme were obtained in January 1993 and the prognostic significance of 11 variables collected during the first step was determined by the proportional hazards regression model. The cumulative proportion of family compliance after 40 months was 36.4%, with similar drop-out rates at each of the three steps of the programme. The prognostic factor which was the major determinant of family compliance to treatment was the active presence of the whole family in the first step, while a good job performance was independently associated with family compliance, being a significant prognostic factor in the second step of the programme. Alcohol abstinence was obtained in 35.9% of the whole study group. This programme provided results for alcohol abstinence which are comparable with methods that require more expensive resources.

Liver cirrhosis is one of the main causes of death in Mediterranean countries. A trend towards a global reduction in the mortality rate has been recently reported. In order to clarify better this trend and in an attempt to hypothesize the future pattern of mortality, we analysed data from 254,834 Italian subjects aged 30-79 who died from liver cirrhosis during the period 1972-1986. We used a log-linear Poisson model to examine the effects of age, calendar period of death and birth cohort. Our data confirm that both in the population as a whole and after stratification for three geographical areas (Northern, Central and Southern Italy) the mortality rate is decreasing. The age-effect analysis showed an exponentially rising effect in the Southern population, in accordance with the viral aetiology of cirrhosis, whereas an increased effect followed by a decreased effect was observed in the Northern and Central population, suggesting the alcoholic aetiology for the disease. The results from the birth-cohort effect suggested that in the Northern and Central populations mortality should continue to decrease over the next decade, possibly due to the implementation of better prevention programmes for cirrhotics and to decreased alcohol consumption in Italy. In the Southern population, however, mortality is still rising and this will probably continue for the next decade, as the generations born between 1940 and 1950 who are at high risk of carrying chronic hepatitis B virus infection, reach the age of higher risk of death from liver cirrhosis.(ABSTRACT TRUNCATED AT 250 WORDS)

We carried out a hospital-based case-control study to assess the association of both the daily amount and the duration of alcohol intake with the risk of developing non-cirrhotic chronic liver disease (chronic hepatitis) in 121 chronic hepatitis patients diagnosed by laparoscopy and liver biopsy, and in 242 matched 'controls' randomly selected from inpatients of the same hospital. Alcohol intake was quantified in all subjects using a standardized questionnaire administered by two doctors unaware of the aim of the study. The odds ratio (OR) for chronic hepatitis was estimated by conditional logistic regression and increased exponentially from 1.0 for non-drinkers to 11.4 for daily alcohol intake of 325 g or more. Considering duration of alcohol consumption from up to 10 to up to 30 years, the ORs for chronic hepatitis consistently decreased for the daily alcohol intake categories of 25-50 g (from 74.1 to 0.7 respectively), 75-100 g (from 149.7 to 0.7 respectively) and 125 g or more (from 212.0 to 1.8 respectively). Our results suggest the existence of a dose-dependent individual susceptibility to the damaging effect of alcohol on the liver.