The sudden increase in alcoholic liver disease among women in the past 10 years has caused much speculation that they may be more susceptible to the hepatotoxic effects of alcohol than men. Women tend to present with more severe liver disease, particularly alcoholic hepatitis, and do so after a shorter period of excessive drinking and at a lower daily alcohol intake. Differences in body size and composition are partly responsible for the greater susceptibility of women, but differences in immune reactivity between the sexes may also play a part. Greater emphasis must be placed on designing abstinence programmes specifically for female patients, on earlier detection of liver disease, and on educating women about hazardous drinking levels.
IntroductionIn the past decade the number of women in Britain, particularly young women, succumbing from alcoholic liver disease has risen dramatically.' This fact and the impression that many have been social drinkers only has caused much speculation as to whether women are more susceptible to the hepatotoxic
13 June 1983 to cirrhosis. The nature of these determinants remains unknown.The involvement of host factors in determining the response to the effect of alcohol on the hepatocyte is suggested by the association between the histocompatibility antigens HLA B8 and DR3, genetic markers of several immune mediated disorders, and the more rapid development of cirrhosis,9 and an increased incidence of autoantibodies in patients with alcoholic cirrhosis.'0In the present study we have isolated hepatocytes from rabbits pretreated with ethanol, thus allowing the relevant antigen to be generated in vivo, and by means of induced cytotoxicity and immunofluorescence we have examined sera from patients with alcoholic liver damage for the presence of circulating antibodies reacting with the specific alcohol altered liver cell determinants.
Methods
PATIENTSThe 82 patients (56 men, 26 women; mean age 49 years, range 25-69 years) had had a minimum daily alcohol intake of 80 g in the men and 40 g in the 300 on 29 April 2019 by guest. Protected by copyright.
SUMMARY Detailed drinking histories were taken in 38 patients in whom dilated cardiomyopathy was diagnosed by cardiac catheterisation and left ventricular biopsy. On the basis of the drinking history twenty patients were classified as being in an abstinent or light drinking group and eighteen patients as being in a heavy drinking group (daily alcohol intake in excess of 80 g or cumulative lifetime intake exceeding 250 kg). Activities of myocardial creatine kinase, lactate dehydrogenase, a hydroxybutyric dehydrogenase, malic dehydrogenase, and aspartate aminotransferase were all higher in the heavy drinkers and myocardial enzyme activity correlated with cumulative lifetime alcohol intake, maximum daily intake, and recent daily intake. Activities of creatine kinase, a hydroxybutyric dehydrogenase, and malic dehydrogenase correlated with ejection fraction, irrespective of the alcohol intake of the patient. These findings were not altered by exclusion of patients with hypertension.The results indicate that among patients with dilated cardiomyopathy there is a group characterised by a high alcohol intake and raised myocardial tissue enzymes which supports the concept of alcoholic heart muscle disease as a distinct entity.Although the association between excessive alcohol consumption and congestive (dilated) cardio-i myopathy has long been known,1 2 a causal relation remains controversial.3 There are no studies that relate quantitative alcohol intake to myocardial damage, as there are for alcoholic liver disease.4" Indeed the clinical diagnosis of alcoholic heart muscle disease merely reflects the coexistence of global myocardial dysfunction in a heavy drinker in whom no other cause for myocardial disease has been found.Requests for reprints to Dr P J Richardson, Cardiac Department,
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