PEDIATRICS Vol. 115 No. 5 May 2005, pp. 1445-1446 (doi:10.1542/peds.2005-0193)
Misinterpretation of Liver-Function Tests and West Nile Virus Infection in Children: In Reply
Robert Yim, MDEllen R. Wald, MD
Division of Allergy, Immunology, and Infectious Disease
Children's Hospital of Pittsburgh
Pittsburgh, PA 15213-2583
We thank Dr Hochman for his thoughtful comments on our recent case report.1 Dr Hochman asserts that patient 1 had neither a fulminant hepatitis nor hepatic failure causally related to infection with West Nile virus (WNV). He correctly points out, and we agree, that transaminases may become markedly elevated with hepatotropic viruses, perfusion injuries, or hepatotoxins. As Dr Hochman states, temporal elevations of liver enzymes can be seen in many infections. However, as we have described previously, patient 1 tested negative for several of the infectious agents that can lead to fulminant hepatic failure, including cytomegalovirus, adenovirus, hepatitis A, hepatitis B, hepatitis C, and Epstein-Barr virus.1 Dr Hochman's conclusion that the abnormal transaminases are secondary to ischemia is a possibility that we also considered. However, there was lack of evidence that patient 1 had ischemic injury to other vulnerable organ systems such as the kidney or bowel. She had normal renal function and had a benign abdominal examination without any evidence of vomiting or diarrhea. We also strongly considered anticonvulsants and hepatotoxins as a source of her hepatic injury; however, anticonvulsant drug levels were normal, and urine toxicology was negative. Given these factors and the temporal relation to her diagnosis of WNV, we still conclude that the hepatitis is likely associated with WNV infection.
Dr Hochman raises a difficult question regarding the definition of fulminant hepatic failure and the application of this term to describe the condition of patient 1. Fulminant hepatic failure is well described in adults; however, it is much rarer in children. The generally accepted characteristics of fulminant hepatic failure include hepatic encephalopathy within 8 weeks of onset of disease, coagulopathy, and absence of previous hepatic disease.2 Patient 1 did present with persistent mental status changes, prolonged prothrombin time, and no previous history of liver disease. The etiology of her mental-status changes is less clear. They are either directly a manifestation of WNV infection or secondary to hepatic injury. Serious neurologic changes in WNV are rare and as yet neither well documented nor described. We agree that the characteristics described do not necessarily prove hepatic failure, given that the etiology of her mental-status changes is yet unclear. There is still a paucity of information regarding the clinical manifestations of WNV infection in children.
Dr Hochman's note underscores the need for additional investigation of WNV infection in children, particularly regarding hepatic manifestations.
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- Yim R, Posfay-Barbe KM, Nolt D, Fatula G, Wald ER. Spectrum of clinical manifestations of West Nile virus infection in children.
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PEDIATRICS (ISSN 1098-4275). ©2005 by the American Academy of Pediatrics
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Related articles in Pediatrics:
- Misinterpretation of Liver-Function Tests and West Nile Virus Infection in Children
- Jay A. Hochman
Pediatrics 2005 115: 1445.[Extract] [Full Text]
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