Relationships between blood lead concentration and aminolevulinic acid dehydratase in alcoholics and workers industrially exposed to lead.

Blood lead concentration (Pb-B), aminolevulinic acid dehydratase (ALAD), and gamma-GT were measured in 265 workers industrially exposed to lead and in 184 patients with liver disease resulting from alcohol consumption. The first group was divided according to alcohol use, i.e., nondrinkers, moderate drinkers, and heavy drinkers. The second group was divided according to the following criteria: hepatopatic without cirrhosis, hepatopatic with compensated cirrhosis, and hepatopatic with decompensated cirrhosis. Heavy drinkers who were industrially exposed had the highest Pb-B (40.4 +/- 14.6 micrograms/dl) and the lowest ALAD (22.2 +/- 9.1 U/L). The correlations between Pb-B and ALAD show no significant change with the increase of Pb-B. In the alcoholic group, 76 patients with alcoholic liver disease without cirrhosis had the highest Pb-B (40.3-9.1 micrograms/dl) and ALAD the lowest (18.6 +/- 7.7 U/L). The negative correlation between Pb-B and log ALAD disappeared completely in individuals with Pb-B that exceeded 50 micrograms/dl, independent from the seriousness of illness.

Blood-lead levels in patients with chronic liver diseases.

Blood-lead concentrations (Pb-B) were measured in 318 adult inpatients with chronic liver diseases. The Pb-B was highest (387 +/- 96 micrograms/l) in 102 patients with alcoholic liver disease without cirrhosis. The Pb-B was still high, but significantly lower in 60 patients with compensated alcoholic cirrhosis (342 +/- 100 micrograms/l) and in 72 patients with decompensated alcoholic cirrhosis (312 +/- 97 micrograms/l). This difference was in part due to a significant decrease of the hematocrit which fell from 44.4 +/- 4.9% to 42.4 +/- 27.2% and to 39.2 +/- 7.4% respectively. In patients with viral or cryptogenic liver diseases the Pb-B was 211 +/- 69 micrograms/l in 11 patients with chronic persistent hepatitis, 219 +/- 72 micrograms/l in 19 with chronic active hepatitis, 206 +/- 94 micrograms/l in 28 with compensated cirrhosis, and 226 +/- 98 micrograms/l in 26 with decompensated cirrhosis, without any significant difference. The Pb-B of the male patients showed no correlation to age, with the exception of 25 male patients with chronic persistent and active hepatitis (r = 0.626, P less than 0.001).