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To the Editor.—
I write to add several comments about the recent report in Pediatrics on 4 cases of West Nile virus (WNV) infection in children.1 With regard to the first patient, the authors comment numerous times about the unusual presentation of a "fulminant hepatitis." In addition, they use the term "hepatic failure" to describe the marked elevation of transaminases along with a mild coagulopathy. Based on my careful reading, I conclude that this patient had neither fulminant hepatitis nor hepatic failure. Furthermore, I think the assertion that this child's liver injury is causally related to WNV is misleading.
Among hepatologists, the most widely accepted definition of fulminant hepatic failure includes the onset of hepatic encephalopathy <8 weeks after the beginning of liver disease. Failure of the liver and loss of hepatocyte function results in the inability to remove neurotoxins and synthesize vital proteins that are needed to sustain life. This patient did have a prolonged seizure, but it is unlikely that it was a result of hepatic dysfunction. In fact, this patient had normal transaminases on arrival to the hospital. The presence of a coagulopathy caused by liver dysfunction is a worrisome sign but does not indicate liver failure.
The fact that the initial transaminases were normal also casts doubt on the possibility of WNV involvement of the liver. It is counterintuitive to hypothesize that liver involvement would occur rapidly 24 hours after the onset of the illness. Moreover, marked elevation of transaminases is seen most often when there is a hepatotropic virus such as hepatitis A or B or in circumstances that can cause centrilobular necrosis. This latter condition can be seen when there is a perfusion injury or with certain hepatotoxins such as acetaminophen. My interpretation of the abnormal transaminases is that they are most likely secondary to the prolonged seizure resulting in ischemic hepatitis. The rapid resolution of the transaminases over 8 days would be typical in this scenario and very atypical for most viral hepatitis cases. Supporting evidence includes the increased creatine kinase levels and transiently increased the creatinine level. In addition, a coagulopathy is seen in 25% to 50% of cases of ischemic hepatitis.2 Certainly the high fever, the coexistent use of anticonvulsants, and the administration of antipyretics may have contributed to the hepatic injury.
In summary, this case of WNV infection highlights 2 important points. First, the degree of transaminase elevation frequently does not correlate with the severity of liver disease; therefore, it is a mistake to interpret transaminases as a measure of liver function. Second, temporal elevation of liver enzymes is often seen in many infections. Many factors need to be considered before assigning causality.
REFERENCES
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