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• W2036735196 abstract "Many readers of HEPATOLOGY will recall January 1, 2000 as a New Year's day that was mildly surprisingly much like any other. The old millennium had ended with a fizzle. In addition to a tedious debate about whether 1999 was the technical end of the millennium, the months leading up to January 1, 2000 were remarkable for the variably apocalyptic predictions of the impact of the Millennium (or Y2K) Bug. The Millennium Bug arose from a spectacularly penurious quirk of early computer program design that had resulted in software that, in an attempt to save memory, identified years by two digits rather than four (presumably the same individuals who abbreviated June to JUN). The year 2000 would thus be represented by 00 and might be interpreted by software as the year 1900. It is hard to overstate the dire nature of some of the projected consequences of Y2K, which included nuclear Armageddon. The United States Deputy Secretary of Defense, John Harme, chillingly predicted that Y2K would result in “nasty surprises around the globe,” while reassuring the public that 93% of “mission critical” defense systems were Y2K compliant (“Looking at the Y2K Bug”, http://www.cnn.com/TECH/specials/y2k/). NAFLD, nonalcoholic fatty liver disease; NASH, nonalcoholic steatohepatitis; NHANES, National Health and Nutrition Education Survey; UNOS, United Network for Organ Sharing. Genetically a skeptic, I took out an extra $100 from the bank and pocketed two aspirin but otherwise made no special arrangements for January 1, 2000. We all know the outcome. A sprinkling of innocuous software failures and a global pandemic of simultaneous schadenfreude and relief was all the world had to show for the billions that had been spent on Y2K preparedness. Is the clinical impact of nonalcoholic fatty liver disease (NAFLD) the Y2K of our specialty? Have we fashioned a mountain from a molehill of end-stage liver disease? The answer merits some consideration. There is no important debate regarding the prevalence of NAFLD and nonalcoholic steatohepatitis (NASH). Ian Wanless's landmark autopsy-based cross-sectional study reported convincingly that the overall prevalence of NASH in adults in North America is 18.5% in obese and 2.7% in nonobese individuals.1 Of obese individuals found to have NASH at autopsy, about one in seven had bridging fibrosis or cirrhosis. Based on current prevalences of obesity and type 2 diabetes, NAFLD can conservatively be estimated to affect more than 30 million people in the United States.2-8 NAFLD has thus come to be regarded as a potentially important public health issue. The scale of the problem may be worsening in parallel with the relentless increases in the prevalence and severity of obesity in the United States and globally. Our communal interest in NAFLD is reflected in the number of publications that have appeared in the medical literature (Fig. 1). A simple query of PubMed using the subject search terms “NAFLD” or “NASH” reveals a logarithmic increase in the number of NAFLD-related articles in the last 10 years. State-of-the-art NAFLD presentations have become a staple at annual meetings for the American Association for the Study of Liver Diseases and the American Gastroenterology Association, each offering up a Eureka! insight into the pathophysiology of this condition, from macrophage dysfunction to lipotoxicity, that have gradually increased our understanding of the biology of this condition. Yet despite the overwhelming evidence regarding the prevalence of NAFLD and NASH and a clutch of reports describing end-stage liver disease in NAFLD,9, 10 there is an emerging sense that we may have oversold the clinical importance of NAFLD, akin to a January 1, 2000 post-Y2K feeling. Intense scientific interest and a flurry of publications do not always equate to significance (witness TT-virus and hepatitis G). The missing piece here is a well-conducted, large natural history cohort study of NAFLD. Given the need for histologic analysis to characterize NAFLD and the risk and expense associated with liver biopsies, such a study is unlikely to ever occur. Number of original publications per year, using the search terms NAFLD and NASH, is shown. Other potential sources of clues to the clinical impact of NAFLD might include the United Network for Organ Sharing (UNOS) and the National Health and Nutrition Education Survey (NHANES). Although UNOS can provide accurate nodal data concerning transplant recipients (alive or dead, retransplanted), other aspects of recipient information are plagued by unreliability and incompleteness. When entering diagnoses for liver transplant recipients at the time of listing, for example, only primary diagnosis is recorded and, until recently, NASH or NAFLD was not among the 70 available choices. Curiously, there has been room on the UNOS drop-down list for several primary diagnoses that I have never seen among patients as an indication for transplantation. There are no less than four subgroups for primary sclerosing cholangitis. The situation may be worse for cryptogenic cirrhosis, a likely alternative primary diagnosis for patients with cirrhosis due to NAFLD. Nurse coordinators or administrative assistants who enter this data would have to select “cirrhosis cryptogenic” rather than four other similar choices: “choles liver disease other”, “cirrhosis chronic active hepatitis etiology unknown”, “cirrhosis other specify”, and “other specify”. Good luck! NASH now appears on the drop-down list of primary diagnoses as “cirrhosis fatty liver (NASH)”. Even when this primary diagnosis is selected, there are no criteria required for doing so, making the accuracy of the diagnosis unknowable. With those caveats in mind, it would seem to be hardly worth asking UNOS for data regarding the frequency of NAFLD as a primary diagnosis. Yet a report of such a query was published in Liver Transplantation, yielding some intriguing observations.11 One of the most striking was that there had been a 35-fold(!) increase in the frequency of NAFLD as a primary diagnosis between 2001 and 2005. Most or all of that increase, however, is likely to have been attributable to the addition of NAFLD/NASH as a choice on the list of primary diagnoses in 2004, when the spike in NAFLD/NASH as a primary diagnosis occurred (from an n = 26 to n = 128). A more reliable index is probably the combined frequency of cryptogenic cirrhosis and NAFLD/NASH. This combination of primary diagnoses has increased from 3.6% to 6.9% in the 5 years between 2001 and 2005. Even this is likely to be an underestimate, because patients with a hepatocellular carcinoma occurring on a background of cryptogenic cirrhosis or NAFLD will not be included because only the primary diagnosis (hepatocellular carcinoma in these cases) is recorded by UNOS at the time of listing for liver transplantation. A reasonable estimate would be that NAFLD is currently the underlying cause of liver disease in between 5%-10% (n = ∼325-650 recipients, based on 2006 liver transplant volume [http://www.ustransplant.org/]). This is a notable number but not a catastrophic one. The rate of increase in liver transplantation is in keeping with earlier projections that may well see NAFLD overtake hepatitis C virus as the most common primary diagnosis of liver failure in liver transplant recipients by 2020. The frequency of hepatitis C virus as an indication for liver transplantation peaked in 2002 at 28% in the United States and has declined every year since, with most recent frequency of 23% (http://www.ustransplant.org/). Are there patients with NAFLD dying from liver-related causes that never make it to transplantation? Without a doubt, although we can only guess how many. In lieu of a population-based study, the best potential source of information regarding the frequency of NAFLD as a cause of end-stage liver disease may be the third National Health and Nutrition Survey (NHANES III). Three groups have studied the NHANES III regarding NAFLD.8, 12, 13 The prevalence of unexplained elevations in alanine aminotransferase was 7% in individuals with the metabolic syndrome and 3.5% in those without the metabolic syndrome. Because many patients with NAFLD have normal alanine aminotransferase levels, these frequencies almost certainly underestimate the actual frequency of NAFLD. And, more importantly, they tell us nothing about the frequency of liver-related deaths. In a community population-based study, the absolute risk of death from NAFLD appeared to be low, with a reported standardized mortality ratio of 1.34 (95% confidence interval, 1.003-1.76; P = 0.03).14 Extrapolating these numbers, of 100 patients diagnosed with NAFLD, five will develop cirrhosis, and three will develop liver-related complications (for example, hepatocellular carcinoma) within 10 years. With a current projected prevalence of NAFLD in the United States of ∼30 million, this would produce 90,000 patients/year with end-stage liver disease due to NAFLD. Many of these 90,000 patients each year will have strong relative or absolute contraindications to liver transplantation due to other complications of the metabolic syndrome and obesity. The frequency of end-stage liver disease due to NAFLD thus may be less than we expected but still substantial. Of course, I'm just guessing, using the best data I can find. A plea for better data is, ultimately, my reason for penning this article. If you have such data, HEPATOLOGY is eager to hear from you. We can assure you a fair and expeditious review. Otherwise, we will again be watching the clock for the New Year. In this case, we will be waiting for 2020 to find out if NAFLD is the real Millennium Bug, King of the Indications for Liver Transplantation, depleter of organs, and taker of life. Or not so much." @default.
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• W2036735196 date "2008-04-05" @default.
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• W2036735196 title "Cirrhosis and liver failure in nonalcoholic fatty liver disease: Molehill or mountain?" @default.
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