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.

Analysis of Factors Responsible for Continuing Mortality after Paracetamol Overdose

1986 ◽  
Vol 5 (3) ◽  
pp. 201-206 ◽  
Author(s):  
R. B. Read ◽  
J. M. Tredger ◽  
R. Williams
Keyword(s):  
Liver Failure ◽  
Liver Damage ◽  
Paracetamol Overdose ◽  
Severe Liver ◽  
College Hospital ◽  
King's College ◽  
Accident And Emergency ◽  
Drinking History ◽  
Severe Liver Damage ◽  
Complete Series

1 To determine reasons for the continuing mortality in patients taking a paracetamol overdose, the presentation, drug ingestion history, patient background, use of antidote ( N-acetylcysteine and methionine), clinical course and outcome were determined in 247 patients treated at King's College Hospital in 1982 and 1983. Patients (147) were referred from other centres because of severe liver damage and 100 were local patients seen in the accident and emergency department. 2 Survival in the local patients was 100% and, for those with severe liver damage, 49 and 63% (1982 and 1983 values). Delay in initial presentation to hospital was a major factor in determination of an adverse outcome, with a median delay of 30 h in the referred patients and 8 h in the local cases. Such a delay precluded administration of antidote to the majority of patients in the referred group, but in 11 cases where antidote could have been given a full course was not provided and all 11 patients died. Included among these were four patients in whom the serum paracetamol concentration was in the ‘non-toxic’ range. 3 One patient with a chronic alcohol-drinking history (> 200 g/day) received N-acetylcysteine at 12 h but died from liver failure. However, in the complete series prior alcohol consumption was not associated with a significantly worse prognosis and simultaneous ingestion of alcohol with paracetamol had no effect on outcome. 4 The concomitant ingestion of dextropropoxyphene caused an early and marked impairment of consciousness unrelated to any hepatotoxicity but, in three cases where dextropropoxyphene combinations were used, death occurred subsequently from liver failure.

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.

LIVER DAMAGE AFTER PARACETAMOL OVERDOSE COMPARISON OF LIVER-FUNCTION TESTS, FASTING SERUM BILE ACIDS, AND LIVER HISTOLOGY

The Lancet ◽  
1975 ◽  
Vol 306 (7935) ◽  
pp. 579-581 ◽  
Author(s):  
Oliver James ◽  
S.H. Roberts ◽  
AdrianP. Douglas ◽  
M. Lesna ◽  
L. Pulman ◽  
...  
Keyword(s):  
Liver Function ◽  
Bile Acids ◽  
Liver Damage ◽  
Liver Function Tests ◽  
Liver Histology ◽  
Paracetamol Overdose ◽  
Fasting Serum ◽  
Serum Bile Acids ◽  
Function Tests

Management of serious paracetamol poisoning

1988 ◽  
Vol 26 (25) ◽  
pp. 97-99
Keyword(s):  
Renal Failure ◽  
Single Dose ◽  
Alcohol Abuse ◽  
Liver Damage ◽  
Severe Pain ◽  
Paracetamol Overdose ◽  
Chronic Alcohol ◽  
Paracetamol Poisoning ◽  
Chronic Alcohol Abuse ◽  
Acute Overdose

Several hundreds of people die from paracetamol overdose each year, many perhaps unnecessarily.1 Serious poisoning usually follows acute overdose but can also occur in patients with severe pain taking large doses (over 10g/day) on consecutive days. A single dose of as little as 10g can cause hepatic or renal failure. The outcome is determined by the amount taken and, more importantly, by whether the patient comes to hospital in time for treatment to be effective.2 Chronic alcohol abuse,3 malnutrition, or taking enzyme-inducing drugs increases the risk of liver damage.4,5

scholarly journals Disordered Hemostasis in Liver Damage from Paracetamol Overdose

1973 ◽  
Vol 65 (5) ◽  
pp. 788-795 ◽  
Author(s):  
Russell Clark ◽  
V. Borirakchanyavat ◽  
B.G. Gazzard ◽  
M.O. Rake ◽  
Κ.B. Shilkin ◽  
...  
Keyword(s):  
Liver Damage ◽  
Paracetamol Overdose

Apoptosis participates to liver damage in HSV-induced fulminant hepatitis

APOPTOSIS ◽  
2003 ◽  
Vol 8 (6) ◽  
pp. 655-663 ◽  
Author(s):  
J.-L. Prétet ◽  
L. Pelletier ◽  
B. Bernard ◽  
S. Coumes-Marquet ◽  
B. Kantelip ◽  
...  
Keyword(s):  
Liver Damage ◽  
Fulminant Hepatitis
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