Paracetamol metabolism following overdosage: application of high performance liquid chromatography

Passage of paracetamol into breast milk and its subsequent metabolism by the neonate.

“…The biotransformation of paracetamol in the adult is well established and the major metabolites are PG and PS (Prescott, 1980). A small proportion of the drug (<10% ) is oxidised by the mixed function oxidase system to a reactive intermediate(s) which conjugates with hepatic glutathione and appears in the urine as paracetamol cysteine (PC) and paracetamol mercapturic acid (PM) (Mitchell et al, 1973(Mitchell et al, , 1974Davis et al, 1976;Howie et al, 1977;Slattery & Levy, 1979). Any oxidised metabolite that does not combine with glutathione is a potential cause of cell damage.…”

Comparison of the effect of cisapride and metoclopramide on morphine‐ induced delay in gastric emptying.

“…Plasma was separated immediately and stored at -20°C. Plasma paracetamol concentrations were measured subsequently by high performance liquid chromatography (Howie et al, 1977). Plasma morphine concentrations in the venous blood samples taken 20 min after the premedication were also measured by high performance liquid chromatography (Aitkenhead et al, 1984).…”

The third Lilly Prize Lecture. University of London, January, 1979. The nephrotoxicity and hepatotoxicity of antipyretic analgesics.

“…(Howie et al, 1977 (Forrest, Finlayson, Adjepon-Yamoah & Prescott, its metabolites (O glucuronide;. In addition, the overall urinary excretion of e; A mercapturate) with time in a paracetamol metabolites, including the cysteine and developed severe liver damage mercapturic acid conjugates, is the same in such vith intravenous L-methionine patients as in healthy volunteers (Forrest, Adriaenssens, Finlayson & Prescott, 1979).…”

“…Detailed studies of paracetamol metabolism in poisoned patients have failed to show any obvious change as a result of treatment with cysteamine, L-methionine or N-acetylcysteine. On the other hand, the pattern of urinary excretion of paracetamol and its metabolites is dependent on the presence and severity of liver damage, irrespective of treatment (Howie et aL, 1977). Patients with severe liver damage excrete proportionately less paracetamol sulphate and more cysteine and mercapturic acid conjugates than those without, and in all patients there is evidence of saturation of sulphate conjugation (Figure 3).…”