Effect of Ethanol on the Activity of Microsomal Enzymes

1971 ◽  
pp. 85-92 ◽  
Author(s):  
C. S. Lieber
Keyword(s):  
Microsomal Enzymes

Role of estrogens in phenobarbital induction of liver microsomal enzymes

1975 ◽  
Vol 80 (3) ◽  
pp. 1043-1045
Author(s):  
P. V. Sergeev ◽  
N. N. Vedernikova ◽  
A. I. Maiskii ◽  
N. V. Shapoval ◽  
V. A. Volov
Keyword(s):  
Microsomal Enzymes ◽  
Phenobarbital Induction ◽  
Liver Microsomal Enzymes

Paracetamol overdose

1976 ◽  
Vol 14 (2) ◽  
pp. 5-7
Keyword(s):  
At Risk ◽  
Liver Damage ◽  
Fulminant Hepatitis ◽  
Therapeutic Dose ◽  
Renal Damage ◽  
Hepatic Necrosis ◽  
Paracetamol Overdose ◽  
Microsomal Enzymes ◽  
Concomitant Increase ◽  
Main Metabolite

Paracetamol is a main metabolite of phenacetin, and since its introduction it has become increasingly popular as a mild analgesic which is available without prescription. When taken in the recommended therapeutic dose of l g 6-hourly, paracetamol is relatively free from unwanted effects, and in particular, unlike phenacetin, there is little to associate it with renal damage. However, when taken as a single overdose, paracetamol can cause hepatic necrosis, the severity of which seems to be proportional to the dose of drug absorbed. All patients ingesting over 10 g (20 × 500 mg tablets) are at risk from liver damage, which may be potentiated by previous consumption of substances that induce microsomal enzymes, such as barbiturates or alcohol. Since the first reported cases of fulminant hepatitis due to paracetamol overdose in 1966 the number of cases of such self-poisoning has risen annually, with a concomitant increase in the number of deaths.

Prescribing for patients with liver damage

1970 ◽  
Vol 8 (24) ◽  
pp. 93-94
Keyword(s):  
Liver Disease ◽  
Liver Damage ◽  
Enzyme Induction ◽  
Liver Enzymes ◽  
Liver Microsomes ◽  
Microsomal Enzymes ◽  
Impaired Liver ◽  
Conjugated Bilirubin

Many drugs are metabolised in the liver, and the duration and intensity of action of such drugs are increased in some patients with liver disease. However, many patients react normally to drugs, for although some mechanisms, such as the secretion of conjugated bilirubin into the bile, may be impaired, liver enzymes may continue to metabolise drugs normally. The function of liver microsomes is probably preserved because many drugs stimulate the synthesis of microsomal enzymes (enzyme induction), even in the failing liver,1 and thereby increase the metabolism of a variety of drugs. About 200 compounds have so far been shown to induce these enzymes.

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