Multi-state models are highly relevant for studies of cirrhosis patients; both the classical perception of cirrhosis as either compensated or decompensated and the recent more complex models of cirrhosis progression are multi-state models. Therefore, researchers who conduct clinical studies of cirrhosis patients must realize that most of their research questions

assume a multi-state disease model. Failure to do so can result in severely biased results and bad clinical decisions. The analyses that can be used to study disease progression in a multi-state disease model may be called competing risks analysis, named after the competing risks disease model which is the simplest multi-state disease model. In this review article we introduce multi-state disease models and competing risks analysis and explain why the standard armamentarium of Kaplan-Meier selleck compound check details survival estimates and Cox regression sometimes gives bad answers to good questions. We also use real data to answer typical research questions about the course of cirrhosis and illustrate biases resulting from inadequate methods. Finally, we suggest statistical software packages that are helpful and accessible to the clinician-researcher. (Hepatology 2014;) “
“I read with great interest the article by Das et al.1 Although presence of nonalcoholic fatty liver (NAFL) in nonobese individuals is a fairly common observation

in India, this is the first such scientific documentation for the same. However, I would like to make a few points in this regard. First, NAFL constitutes a wide spectrum of liver disease with varied natural history extending from simple steatosis to more sinister variants, i.e., nonalcoholic steatohepatitis (NASH) and fibrosis/cirrhosis. Only a proportion of NAFL actually progresses to the more sinister end of this spectrum.

Therefore, instead of a blanket focus on NAFL, it would be more appropriate to identify the subset of patients with NAFL who are more likely to progress to NASH. In this regard, the authors have defined “potentially significant NAFL” as “subjects with definite NAFL who had persistently elevated ALT (>40 IU/L)”. However, even in this study only find more one-third of these subjects with “potentially significant NAFL” were found to have NASH on liver biopsy, which means elevated ALT alone is not a good enough marker of “potentially significant” NAFL. A full panel of noninvasive markers of liver fibrosis would be more appropriate to define this subset and save costly and/or potentially harmful procedures like liver biopsy or computed tomography scans for them. Second, although the authors have claimed to have excluded people with alcohol consumption from this study, this population in context comes largely from a tribal background who indulges in many nonconventional forms of ethanol consumption, e.g., mahua flower (Madhuca longifolia).