[1-14C]Ethanol breath test in alcoholic liver disease.

The activity of ethanol metabolising enzymes was assessed in 51 patients with alcoholic and non-alcoholic liver disease using tracer doses of [1-14C]ethanol and measuring 14CO2 excretion in the breath. Alcoholic patients with only fatty infiltration of the liver showed significantly increased activity compared with controls. Comparing alcoholic patients with cirrhosis and a serum albumin greater than 28 g/l, activity in those with a recent history of continued heavy drinking was significantly greater than in patients who had abstained from alcohol. In addition, both groups of alcoholic cirrhosis showed significantly more activity than patients with non-alcoholic cirrhosis. The activities of patients with acute alcoholic or viral hepatitis were normal when their prothrombin times were less than 7 sec prolonged, but were reduced when prolongation exceeded 7 sec. These results demonstrate that in chronic alcoholic liver disease, even with cirrhosis, alcohol can still increase the activity of ethanol oxidising enzymes provided hepatic function remains adequate. However, this response is lost in acute liver damage and in chronic alcoholic disease with severe hepatic dysfunction.

Urinary D-glucaric acid excretion and plasma antipyrine kinetics during enzyme induction.

1 Changes in urinary D-glucaric acid excretion following a 14 day course of antipyrine to produce enzyme induction have been compared in normal volunteers with changes in plasma half lives and steady state levels of antipyrine. 2 Urinary D-glucaric acid excretion for the group rose significantly with induction, while there was a significant fall in the mean plasma antipyrine half life and steady state levels. The extent of the increase in urinary D-glucaric acid excretion was inversely related to the pre-induction level, and this also applied to the change in antipyrine half lives. 3 Although in individuals, urinary D-glucaric acid excretion and plasma levels of antipyrine changed in parallel, there was no numerical correlation in the group as a whole between these two tests either before or after enzyme induction. 4 These findings are consistent with other recently reported evidence that plasma drug kinetics and other microsomal enzyme functions are not necessarily affected to the same degree by agents with enzyme inducing properties.

Reduction of absorption of paracetamol by activated charcoal and cholestyramine: a possible therapeutic measure.

The absorption of an oral 2-g dose of paracetamol was markedly reduced by the simultaneous oral administration of either activated charcoal or cholestyramine but was only slightly reduced when the adsorbents were given 60 minutes after the paracetamol. Since the absorption of a larger dose of the drug will probably be slow, the administration of adsorbents may be of value even when delayed several hours.