We thank Dr Padda for his interest in our article and for the thoughtful questions he raised. Splenomegaly, not seen in any patient with viral FHF in our study but present in 48% of our patients with MHsFHF, does appear to have the same significance as hepatomegaly. However, when we used stepwise discriminant function analysis to identify variables predictive of discriminating MHsFHF vs viral FHF, prothrombin time and hepatomegaly were identified as the best predictors. During the review process, we deleted the discriminant analysis as suggested because prothrombin time alone had a concordance of 98%. In our study, none of the patients in the MHsFHF group had serologic markers of hepatitis B infection. Therefore, we did not discuss malaria and hepatitis B coinfection. As reported, 19 patients in the viral FHF group had serologic markers of acute hepatitis B infection without smears positive for malarial parasites. As Dr Padda stated, hepatitis B may affect the outcome of severe malaria, although currently there is no clear evidence that it does. In the study by Barcus et al,1Barcus MJ Hien TT White NJ et al.Short report: hepatitis B infection and severe Plasmodium falciparum malaria in Vietnamese adults.Am J Trop Med Hyg. 2002; 66: 140-142PubMed Google Scholar hepatitis B surface antigen positivity alone did not affect mortality; thus, other factors may play a role. In another study,2Brown AE Mongkolsirichaikul D Innis B Snitbhan R Webster HK Falciparum malaria modulates viremia in chronic hepatitis B virus infection [letter].J Infect Dis. 1992; 166: 1465-1466Crossref PubMed Scopus (13) Google Scholar among 4 patients with acute malaria who were also positive for hepatitis B surface antigen, levels of hepatitis B virus DNA became detectable in 2 with undetectable hepatitis B virus DNA before malaria. In the remaining 2 patients with high levels of hepatitis B virus DNA, there was a transient decrease in DNA titer during episodes of malaria. These findings suggest that altered immune responses during acute malaria may influence hepatitis B viremia. However, there is no convincing evidence of exacerbation of underlying hepatitis B-related liver disease during acute falciparum malaria infection. Further studies are needed to clarify the effect of underlying hepatitis B infection on acute falciparum malaria and vice versa. Furthermore, both of the aforementioned studies suffered from selection bias and lacked a control arm. The levels of alkaline phosphatase were high in both groups we reported, and the difference was not statistically significant (263.1 ± 29.32 vs 321.48 ± 61.57; P=.14). Malarial Hepatitis Simulating Fulminant Hepatic FailureMayo Clinic ProceedingsVol. 80Issue 6PreviewTo the Editor: I read the article on malarial hepatitis by Devarbhavi et al,1 published in the March 2005 issue of the Mayo Clinic Proceedings, with much interest because I live in southern California, where unexpectedly heavy rainfall this year is anticipated to result in increased numbers of cases of mosquito-related illnesses. Their valuable study helps differentiate cases of malarial hepatitis simulating fulminant hepatic failure (MHsFHF) from viral-associated FHF. However, I have a few concerns. Full-Text PDF