John B. Saunders

ACCELERATED DEVELOPMENT OF ALCOHOLIC CIRRHOSIS IN PATIENTS WITH HLA-B8

To test whether the increased prevalence of HLA-B8 reported in patients with alcoholic cirrhosis is due to the antigen being a genetic marker of susceptibility to liver damage from alcohol, patients who had cirrhosis of comparable clinical and histological severity were investigated for HLA-B8 status and cumulative alcohol intake. Both male and female cirrhotics with HLA-B8 had been drinking greater than 40 g alcohol/day for a shorter period of time (16.6 +/- 1.4 men, and 9.4 +/- 2.0 years, women) than their counterparts without this antigen (23.7 +/- 1.7, p less than 0.005, and 15.8 +/- 2.0 years, p less than 0.05, respectively), but the mean daily alcohol intake was similar whether patients had HLA-B8 or not. These results suggest that genetic determinants linked to HLA-B8 enhance the rate of development of liver damage in those who drink potentially hepatotoxic amounts of alcohol.

Identification of alcohol dehydrogenase and aldehyde dehydrogenase isoenzymes in human liver biopsy specimens

A sensitive method for detecting isoenzymes of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) in human liver biopsy specimens by simultaneous starch gel electrophoresis is described. All the currently recognised hepatic isoenzymes of ADH and ALDH which are concerned with ethanol metabolism can be identified. The method is suitable for amounts of liver biopsy material weighing as little as 2.5 mg and also allows spectrophotometric assay of ADH activity (at pH 8.8 and 11.0) and of ALDH.