Abstract

Lidocaine, an aminoethylamide, undergoes deethylation in the liver after intravenous injection, resulting in the formation of monoethylglycinexylidide. Serum monoethylglycinexylidide concentration can be measured by a simple, rapid fluorescent polarization immunoassay. We sought to determine whether lidocaine metabolism, as indicated by monoethylglycinexylidide formation, could be used as a quantitative index of hepatic function. Therefore we measured monoethylglycinexylidide formation in 10 healthy children and in 28 children with chronic liver disease. Patients with chronic liver disease were divided by disease severity as being at low, moderate or high risk for deterioration based on a clinical scoring system for liver transplant candidates. In healthy controls, the peak monoethylglycinexylidide concentration 15 min after injection of lidocaine (1 mg/kg) was 97 +/- 12 micrograms/L (mean +/- S.E.). However, monoethylglycinexylidide concentration was decreased in 28 children with chronic liver disease (32 +/- 5 micrograms/L, p less than 0.001). Furthermore, this value was inversely proportional to the severity of liver disease. The mean difference in monoethylglycinexylidide concentration between the low-risk and high-risk groups was statistically significant (42 +/- 6 vs. 11 +/- 4 micrograms/L, respectively, p less than 0.01). We conclude that the rate of formation of the lidocaine metabolite monoethylglycinexylidide is decreased in patients with chronic liver disease and is inversely related to disease severity. Therefore measurement of monoethylglycinexylidide concentration after lidocaine injection may be used as a quantitative assessment of liver function in children. We speculate that monoethylglycinexylidide formation may be a useful prognostic index in children with liver disease.

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