Letter to the Editor: Response to “Liver Transplantation for Acute Liver Failure Due to Dengue Fever”

Potential conflict of interest: Nothing to report. To The Editor: I read with great interest the excellent report by Galante and colleagues regarding liver transplantation carried out in a patient with dengue virus–induced acute liver failure (ALF).1 Their report highlights the catastrophic suddenness with which dengue ALF commonly presents compared with ALF from conventional hepatitis virus. Dengue ALF is considered, albeit incorrectly, a consequence of secondary liver failure, and because of this, liver transplantation is not an accepted indication and is therefore not normally considered.2 However, as reported,1 the patient recovered swiftly from ALF and the associated profound circulatory disturbance after a timely liver transplantation, indicating the pivotal role played by the liver microcirculatory disturbance in causing ALF. This information receives scarce attention, and the report by Galante and coworkers will likely broaden the knowledge on the mechanism of dengue ALF. However, a few points need to be addressed by the authors: The authors ascribed the ~40% steatosis in the liver explant to a preexisting disease; steatosis is one of the hallmark features in liver biopsy specimens from patients with dengue hepatitis,3 although the exact reasons are not clear. The massive rise in transaminases (aspartate aminotransferase > 20,000 IU/L and alanine aminotransferase > 4,000 IU/L) reported by Galante et al.1 and other series in dengue ALF4 often occurs when patients are hemodynamically stable. In the absence of shock, these biochemical features may be ascribed to liver‐specific sinusoidal microcirculatory dysfunction leading to ischemia. These features may lead to reversal of portal blood flow and portal hypertension and have been described in dengue ALF but not in other viral liver infections.5 So, it would be interesting to know whether this feature was present in the authors' report. One of the classic teachings in hepatology is to investigate extrahepatic sources for a massive rise in transaminases, particularly when total bilirubin is mildly or modestly elevated, such as in the authors' report. Further, dengue‐induced rhabdomyolysis has been described. Was the creatinine phosphokinase level measured or was rhabdomyolysis ruled out? Dengue virus is not a classic hepatotropic virus.2 Therefore, liver immunohistochemistry for dengue viral antigen and its location in hepatocytes or its microcirculation will throw more light on the pathogenesis of dengue hepatitis in general and in ALF in particular. Because the entire explant is available for analysis, this information is very important to understand the pathogenesis of the disease.