Where necessary, the plasma paracetamol plots were extended to 24 h.
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22.214.171.124 Results of treatment The actual or extrapolated plasma paracetamol concentration 4 h after ingestion was used as a guide to the risk of liver damage.
Specific treatment with methionine is required if the plasma paracetamol concentration falls above a line which on a semilog graph joins plots of 200 mg/l (1.32 mmol/l) at 4 h and 30 mg/l (0.33 mmol/l) at 15 h after the overdose (see Fig.
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Since systemic adverse effects have not been reported following oral therapy with either N-acetylcysteine or methionine, it is not so important to identify patients requiring treatment by prior measurement of the plasma paracetamol concentration.
Intravenous and oral N-acetylcysteine and oral methionine are normally indicated in patients who are thought to have taken more than 100 mg paracetamol/kg in the preceding 24 h, or who have plasma paracetamol concentrations above a treatment line joining plots on a semilogarithmic graph of 200 mg/l at 4 h after ingestion and 30 mg/l at 15 h.
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To assess the effects of treatment within 10 h, patients were placed into four groups of increasing risk according to the 4-h plasma paracetamol concentration (<150, 150-250, 250-300, and > 300 mg/l).
Additional blood samples were taken 4-8 hourly for up to 72 h and the plasma concentrations of unchanged paracetamol in these and the admission sample were subsequently determined by gas-liquid chromatography (Prescott, 1971a).
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Graphica, Rue des Pelletiers, 16, Bruges, Imprimé en Belgique Translated from the French by the Ocean Plasma Team
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Before analysis it is necessary to deproteinise the plasma sample by mixing with sulfosalicylic acid.
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The differences in plasma methionine concentrations were not statistically significant.
Aerospace Plasma Laboratory - Missouri S&T
(1987) reported a decrease in the mean peak plasma N-acetylcysteine level of 29% and a decrease in mean plasma AUC of 39% in the activated charcoal group.
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(1977) first reported the effects of N-acetylcysteine given in a dose of 300 mg/kg body weight over 20 h to 15 patients whose plasma paracetamol concentrations (range 262-369 mg/l at 4 h) suggested the likelihood of subsequent hepatic dysfunction.
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The total plasma concentration of N-acetylcysteine, including protein-bound N-acetylcysteine, was assayed after initial reduction of disulfide bonds in plasma.
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(1988), plasma proteins were precipitated with perchloric acid and dithiothreitol and the supernatant stored at -70 °C to prevent oxidation of reduced N-acetylcysteine.
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Rapid uptake and deacetylation by tissues in the gut wall and liver, to form cysteine, glutathione, and inorganic sulfite, have been proposed to be the most probable explanation for the extensive first-pass effect (Borgstrom et al., 1986; Olsson et al., 1988).
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3.9.1 Absorption and bioavailability Human studies that attempt to quantify N-acetylcysteine absorption have shown great variations in plasma area under the curve (AUC).
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3.5.3 Methods for analysis of the antidote in biological samples Techniques for quantifying N-acetylcysteine in plasma and urine by high performance liquid chromatography have been developed and appear to be highly accurate (Kagedal et al., 1984; Lewis et al., 1984).
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