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Abstracts of Posters; Presented at the International Anesthesia Research Society; 73rd Clinical and Scientific Congress; Los Angeles, CA; March 12-16, 1999: Pediatric Anesthesia


Njoku, D.B.; Bourdi, M.; Martin, J.L.; Greenberg, R.S.; Pohl, L.R.

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doi: 10.1097/00000539-199902001-00300
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Abstract S303

INTRODUCTION: Environmental exposure to volatile anesthetics is of concern to all exposed individuals, since reports of hepatic injury in operating room personnel, laboratory workers and others chronically exposed to sub-anesthetic concentrations of anesthetic gases have been cited in the literature. [1-2] Anesthetic-induced hepatic injury is thought to have an immune mediated basis, at least in part, because many patients who develop this toxicity have serum autoantibodies that react with one or more specific liver proteins. In an earlier study it was found that some anesthesiology personnel also have autoantibodies against one of these proteins, P450 2E1. [3] In a preliminary study, we reported that the sera of 9% of general anesthesiologists and 23% of pediatric anesthesiologists reacted significantly against liver endoplasmic reticulum p58 (ERp58), while 4 and 8% respectively, reacted against cytochrome P450 2E1 (P450 2E1). This was compared to 19% and 62% of halothane hepatitis patients who reacted significantly against ERp58 and P450 2E1, respectively. In the present study, we have investigated whether pediatric anesthesiologists demonstrate higher levels of inhalational anesthetic-associated autoantibodies than general anesthesiologists in a large cohort of pediatric anesthesiologists from multiple institutions.

METHODS: Sera were collected from 107 pediatric anesthesiologists, 53 general anesthesiologists, 20 halothane hepatitis patients and 20 patients with no exposure to volatile anesthetics. P450 2E1 and ERp58 autoantibodies were measured in the sera of these subjects by established enzyme-linked immunosorbent assays. Values were considered significant if they were two standard deviations above the mean values of the control patients.

RESULTS: 40% of pediatric anesthesiologists demonstrated autoantibodies against ERp58, and 62.6%, demonstrated autoantibodies against P450 2E1. This was compared to 6% and 2% of general anesthesiologists, and, 55% and 75% of halothane hepatitis patients demonstrating autoantibodies against ERp58 and P450 2E1, respectively. Additionally, 69.2% of pediatric anesthesiologists demonstrated autoantibodies against either ERp58 or P450 2E1. (Figure 1 and Figure 2)

Figure 1
Figure 1
Figure 2
Figure 2

DISCUSSION: The findings of this study indicate that there is a higher incidence of anesthetic-hepatitis associated autoantibodies in pediatric anesthesiologists in this larger cohort. It remains to be determined why many of these individuals have not developed liver injury or whether further exposure will place them at risk. Also, this study may help determine the role of autoantibodies in the development of drug-induced liver injury. Perhaps further longitudinal studies with a larger cohort of anesthesiologists, as well as anesthesiologists who have developed anesthetic-induced liver injury will help resolve these questions.


1. NEJM, Volume 280, p.515,1969.
2. British Journal of Industrial Medicine, Volume 45, p. 716, 1988.
3. Chem. Res. Toxicol., Volume 9, p. 1159,1996.
© 1999 International Anesthesia Research Society