A US study from 2011 showed that both intentional and accidental paracetamol poisoning continues to be a major public health problem [5]. Paracetamol-induced hepatotoxicity is the most common cause of liver failure in the US [6]. In adults it was demonstrated that self-treatment with paracetamol containing pharmaceuticals can lead to unintentional poisoning [7]. According to the pharmacologist K. Brune paracetamol belongs to the most hazardous substances throughout the whole world [8]. The hepatotoxic effect of paracetamol was first described in 1966 by D.G. Davidson and W.N. Eastham. They reported on two patients who had died of fulminate liver necrosis in the centrilobular areas after paracetamol overdose. Since then numerous studies have emphasized the hepatic toxicity of this substance [1]. Paracetamol is metabolized via three different pathways: conjugation with sulfate, conjugation with glucuronide and transformation with the cytochrome P450 enzyme system to the highly active metabolite N-acetyl-p-benzoquinone imine (NAPQI) [9]. The metabolite NAPQI is responsible for the severe toxic effects. When used in therapeutic dosage paracetamol is mainly metabolized via the first two pathways; only 5 % of the substance is transformed to NAPQI [9]. NAPQI is immediately conjugated with reduced glutathione to form a hazard-free metabolite [10]. However, in case of overdose the first two pathways become saturated and the majority of paracetamol is metabolized to NAPQI. The conjugation between NAPQI and glutathione leads to a decrease of glutathione stores. Subsequently, reduced glutathione cannot be reestablished as efficiently as it is needed to transform NAPQI into a harmless metabolite. High amounts of NAPQI remain unbound which results in covalent binding between free NAPQI and hepatic proteins. This covalent connection leads to hepatocellular damage [11].

Four stages of paracetamol intoxication are described (Table 2) [11, 12]. At stage one, symptoms occur shortly after poisoning and are unspecific. They often include nausea, vomiting and malaise. After one to two days the initial clinical findings diminish, but abdominal pain may occur. In this stage abnormal laboratory values are often observed, including elevated liver enzymes, increased bilirubin and prolonged prothrombin time. Stage three consists of the reappearance of initial unspecific symptoms. In addition, liver function parameters reach high abnormalities. Stage four occurs within the following four to fourteen days; during this time the outcome of the intoxication will appear. The patient will either recover or develop complete liver failure [11]. Even though it is uncommon, cases of acute renal failure without the development of liver failure have been reported [13, 14].