The toxic dose of<unk>  is highly variable. In general the recommended maximum daily dose for healthy adults is 4 grams. Higher doses lead to increasing risk of toxicity. In adults, single doses above 10 grams or 200 mg/kg of bodyweight, whichever is lower, have a reasonable likelihood of causing toxicity. Toxicity can also occur when multiple smaller doses within 24 hours exceed these levels. Following a dose of 1 gram of<unk>  four times a day for two weeks, patients can expect an increase in alanine transaminase in their liver to typically about three times the normal value. It is unlikely that this dose would lead to liver failure. Studies have shown significant hepatotoxicity is uncommon in patients who have taken greater than normal doses over 3 to 4 days. In adults, a dose of 6 grams a day over the preceding 48 hours could potentially lead to toxicity, while in children acute doses above 200 mg/kg could potentially cause toxicity. Acute<unk>  overdose in children rarely causes illness or death, and it is very uncommon for children to have levels that require treatment, with chronic larger-than-normal doses being the major cause of toxicity in children. Intentional overdosing (self-poisoning, with suicidal intent) is frequently implicated in<unk>  toxicity. In a 2006 review,<unk>  was the most frequently ingested compound in intentional overdosing. In rare individuals,<unk>  toxicity can result from normal use. This may be due to individual ("idiosyncratic") differences in the expression and activity of certain enzymes in one of the metabolic pathways that handle<unk>  (see<unk> 's metabolism). Risk factors A number of factors can potentially increase the risk of developing<unk>  toxicity. Chronic excessive alcohol consumption can induce CYP2E1, thus increasing the potential toxicity of<unk> . In one study of patients with liver injury, 64% reported alcohol intakes of greater than 80 grams a day, while 35% took 60 grams a day or less. Whether chronic alcoholism should be considered a risk factor has been debated by some clinical toxicologists. For chronic alcohol users, acute alcohol ingestion at the time of a<unk>  overdose may have a protective effect. For non-chronic alcohol users, acute alcohol consumption had no protective effect. Fasting is a risk factor, possibly because of depletion of liver glutathione reserves. The concomitant use of the CYP2E1 inducer isoniazid increases the risk of hepatotoxicity, though whether 2E1 induction is related to the hepatotoxicity in this case is unclear. Concomitant use of other drugs that induce CYP enzymes, such as antiepileptics including carbamazepine, phenytoin, and barbiturates, have also been reported as risk factors.
Paracetamol poisoning
Alcoholism
Carbamate poisoning
Viral hepatitis
Salicylate poisoning
Gastroenteritis
Cyanide poisoning
Secondary poisoning