Liver damage in chronic alcoholism. Results of a clinical, clinical-chemical and bioptic-histologic study of 526 alcoholic patients during withdrawal treatment in a public hospital for alcoholics. 3. Bioptic-histologic findings
Lelbach, W.K.
Acta Hepato-Splenologica 14(1): 9-39
1967
ISSN/ISBN: 0001-5822 PMID: 5212259 Document Number: 5470
1. Liver tissue cylinders, sufficiently large for examination were obtained by needle biopsy from 320 alcoholic addicts on withdrawal for an average of 10 to 12 weeks. In only 22 % of the total number of cases morphological examination revealed no pathologic change. In approximately 38 % there was evidence of uncomplicated, more or less marked fatty liver. In 40 % of the cases, however, more pronounced degrees of hepatic damage were observed, i. e. inflammatory mesenchymal reactions not influenced by abstinence. Cirrhosis of the liver was present in 12 % of the cases. 2. The severity of histologic liver damage which generally increased with the mean age of the cases showed unequivocally positive correlations to the intensity of alcohol abuse as defined by duration of abuse and amount of daily intake. 3. Breakdown of the material into two equally large groups, with equal mean duration of abuse, on the basis of daily ethanol intake (ranging below or above 160 g) indicated that the incidence and severity of histological changes was significantly higher (p<0,001) in the group with an average intake of more than 160 g/die as compared to the group with a lower daily intake. As a rule, cases with normal histology and the moiety of cases with uncomplicated fatty infiltration had had a mean daily ethanol intake of less than 160 g. More pronounced liver damage, however, could only be found in alcoholics with an admitted mean intake ranging from 200 to 240 g daily. Cirrhosis was not found among alcoholics who had taken daily quantities of less than 160 g. An average intake exceeding 160 g daily was generally reached only in cases with continuous abuse but was rare in intermittent drinking. 4. The incidence of more severe histological changes showed a statistically highly significant correlation (P<0,001) to the duration of abuse. After an average duration of abuse approximating 12 to 13 years, cirrhosis of the liver was found in every fourth alcoholic and after roughly 22 years in every second alcoholic. Correspondingly, the number of cases with normal histology or uncomplicated fatty change decreased with increasing duration of abuse. 5. The incidence of potentially precirrhotic liver lesions, such as parenchymatous fatty change complicated by inflammatory mesenchymal reactions or chronic hepatitis, increased steadily up to a mean duration of alcohol abuse of 13 years. From then on, however, the incidence tended to decrease somewhat, contrary to the tendency seen in cases with uncomplicated fatty liver. This suggests that, on continuation of misuse, some of these cases will eventually develop chronic hepatitis or cirrhosis respectively and that probably simple parenchymatous fatty change is not a precursor of cirrhosis of the liver but merely an early indication of potentially reversible metabolic changes in the liver cell. 6. With regard to average age, mean duration of abuse, mean level of daily ethanol intake and with regard to the biochemical profiles, a striking similarity was found to exist between cases with normal histology and uncomplicated fatty liver. These data were in contrast to those found in cases with fatty change complicated by mesenchymal inflammatory reactions and in cases with chronic hepatitis, both of which also presented many features in common. 7. It was calculated that the development of cirrhosis of the liver (predominantly compensated forms) followed a continuous abuse of roughly 17 years duration, that of chronic hepatitis and fatty infiltration with inflammatory mesenchymal reactions an abuse of 12 or 10 years respectively. (With regard to the duration of alcohol consumption, it was found that in this material a period of prodromal, symptomatic drinking of approximately 7 years duration had to be added to these figures.) 8. In spite of the fact that in the material observed cirrhosis was found mainly in the compensated form, a sufficiently wide pattern of laboratory tests showed fairly normal profiles in only 4 Vo of the cases. 9. In contrast to the pathogenic influence of alcohol abuse, there was no evidence that antecedent hepatotropic diseases, particularly infectious hepatitis, had in any way determined the severity of histological changes in this material. Neither was there conclusive evidence that quantitative dietary deficiencies present in a number of cases, as indicated by a slight or pronou' nced reduction in body weight on admission, had had any significant influence.
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