Abstract
Summary. In a previous study it was found that liver ALA synthetase activity in patients with unequivocal clinical and biochemical evidence of symptomatic porphyria was increased in less than half the patients as compared with a control group which had various forms of hepatocellular disease, but not porphyria. In the present study evidence is presented which shows that hospitalization, and the associated abstinence from alcohol, of patients with symptomatic porphyria results in liver ALA synthetase activity which is no greater than in control groups together with varying degrees of clinical and biochemical remission. When challenged with ethanol, liver ALA synthetase activity increased and uroporphyrin excretion showed a transient rise. It is suggested that ALA synthetase activity and uroporphyrin excretion are related as cause and effect and the role of ethanol is defined as an aggravating factor in this disease.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call