More often than not, Western physicians assume that what simply reflect the almost complete absence of etiologies is true about a disease in the Western hemisphere must be other than viral, or a difference in the severity of illness universal; that is, if a certain disease is described in Europe, observed in this series. Not only were there very few drugs the United Kingdom, or North America, that description implicated, but there were apparently no cases of Wilson's must apply to the rest of the world. We know a priori that disease, mushroom toxicity, fatty liver of pregnancy, canthis may not be true, and yet we make this assumption recer, or circulatory collapse. This seems surprising, but may peatedly in texts and review articles in regard to any number simply reflect a more advanced stage of disease at presenof topics. The article by Acharya et al. 1 in the June 1996 issue tation. The mean survival following admission was less of HEPATOLOGY describing acute liver failure (ALF) on the than 2 days, and virtually all patients were dead within Indian subcontinent challenges that assumption and, in dothe first hospital week. Referral patterns may be different ing so, sheds new insight into the impact geography makes as well, thus limiting, for example, the transfer of pregon disease characteristics.
nant patients to a tertiary care facility. However, overall The authors review an extensive experience in 423 cases survival did not differ significantly from what we would of ALF seen over a 6.5-year period in New Delhi. The reexpect. A 34% survival is excellent and somewhat better sulting survey identifies some striking differences between than pretransplant American series, 3 possibly reflecting East and West (or perhaps between tropical countries and the dominance of viral etiologies that may carry a betnorthern ''climes,'' as the authors put it). In Northern Inter survival when compared with idiosyncratic drug reacdia, hepatitis A, B, and D viruses made up 33% of cases of tions. ALF, which was not surprising; however, 62% were consid-A striking difference that emerged from the Indian exered to be non-A, non-B disease (viral markers negative, perience is that, although 25% of the women admitted for no other etiology apparent). A sample of the non-A, non-B acute liver failure were pregnant, their survival was not group tested for hepatitis E virus (HEV) RNA revealed 40% different from that observed for the nonpregnant women. with HEV RNA alone, 14% with hepatitis C virus (HCV) This seems surprising because we have always understood RNA alone, and 22% with both HEV and HCV RNA in their that hepatitis E, and perhaps A as well, is more severe serum samples. In all, nearly 90% of all cases were thought during pregnancy and that the fatality rate for hepatitis to be caused by viral hepatitis, based on the numbers and E during pregnancy approaches 70% based on previous assumptions mentioned above. Only 5% of the entire series reports principally from India. It is unfortunate that the were thought to be drug-induced, and all these were ingestauthors did not do a more detailed analysis of the preging isoniazid and rifampicin at the time of onset of illness. nant patient group, because it remains unclear based on Thus, no acetaminophen cases were seen, nor were there their experience whether the established maxim that hepthe large number of drug-induced cases commonly seen in atitis in pregnancy is associated with decreased survival Western series, such as non-steroidal anti-inflammatory is still viable. The authors examined the overall mortality drugs, antibiotics, and anticonvulsants. Can these striking rates, which were essentially similar for all etiologies. If differences in etiology of ALF be ascribed to differences in 25% of the women were pregnant, and there was no prediculture or drug availability, or are these cases, for some lection to increased fatalities in the third trimester as the reason, not referred to an urban center such as the All India authors state, then viral hepatitis itself and not preg-Institute where the study was conducted? The authors do nancy per se is the culprit. However, the authors' own data not address this question. demonstrated a marked increase in the acquisition rate of A second difference apparent between East and West is hepatitis in the pregnant versus the nonpregnant woman. the very short interval between the onset of symptoms and These data would logically lead to the conclusion that the onset of encephalopathy observed in the present study. pregnancy is associated with an increased chance of death Although a criterion for inclusion of an interval of less from hepatitis when compared with not being pregnant than 8 weeks between onset of symptoms and onset of en-(with its reduced risk of acquiring viral hepatitis). cephalopathy was used, all patients demonstrated inter-Their point is valid, but their reasoning is somewhat tauvals shorter than 3 weeks, and thus no intermediate cases tologic. between acute and subacute hepatic failure were included.
Finally, the authors apply their own unique set of crite-The authors make the point that no difference was obria for predicting survival based on regression analysis. served between survivors and nonsurvivors in terms of the
The index derived from their data set is different than interval between onset of symptoms and encephalopathy those employed in the West 4 and more likely reflects its or onset of icterus and encephalopathy. Thus, there was no bias toward Third-World countries, where the etiologies of more favorable outcome observed in those with hyperacute ALF are overwhelmingly viral. Age, bilirubin, and pro-(less than 7 days) disease than in the slower-onset cases, thrombin time are used, but in addition, a high value is as has been suggested by O'Grady et al. 2 This finding may placed on cerebral edema as a criterion for distinguishing survivors. More than 70% of patients succumbed to cerebral edema rather than to conditions such as sepsis or gastrointestinal bleeding. Nearly all patients died within Abbreviations: ALF, acute liver failure; HEV, hepatitis E virus; HCV, hepatitis C virus.
48 hours, including most of those who had cerebral edema