Blog
About

9
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: not found
      • Article: not found

      Alcoholic liver disease

      Read this article at

      ScienceOpenPublisher
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Related collections

          Most cited references 160

          • Record: found
          • Abstract: found
          • Article: not found
          Is Open Access

          Global burden of alcoholic liver diseases.

          Liver diseases contribute markedly to the global burden of mortality and disease. This paper provides an overview from a global perspective of the contribution of alcohol to liver diseases. The Global Burden of Disease study methodology was used to estimate the burden of alcohol-attributable liver cirrhosis and alcohol-attributable liver cancer in 2010 as measured by deaths and disability adjusted life years (DALYs). This methodology estimates attributable fractions based on alcohol exposure distribution and relative risks associated with different levels of drinking. Globally, in 2010, alcohol-attributable liver cirrhosis was responsible for 493,300 deaths (156,900 female deaths and 336,400 male deaths) and 14,544,000 DALYs (4,112,000 DALYs for women and 10,432,000 DALYs for men), representing 0.9% (0.7% for women and 1.2% for men) of all global deaths and 0.6% (0.4% for women and 0.8% for men) of all global DALYs, and 47.9% of all liver cirrhosis deaths (46.5% for women and 48.5% for men) and 46.9% of all liver cirrhosis DALYs (44.5% for women and 47.9% for men). Alcohol-attributable liver cancer was responsible for 80,600 deaths (14,800 female deaths and 65,900 male deaths) and 2,142,000 DALYs (335,000 DALYs for women and 1,807,000 DALYs for men). The burden of alcohol-attributable liver cirrhosis and liver cancer is high and entirely preventable. Interventions to reduce alcohol consumption are recommended as a population health priority and may range from taxation increases for alcoholic beverages to increases in screening and treatment rates for alcohol use disorders. Copyright © 2013 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Alcohol as a risk factor for liver cirrhosis: a systematic review and meta-analysis.

            Alcohol is an established risk factor for liver cirrhosis. It remains unclear, however, whether this relationship follows a continuous dose-response pattern or has a threshold. Also, the influences of sex and end-point (i.e. mortality vs. morbidity) on the association are not known. To address these questions and to provide a quantitative assessment of the association between alcohol intake and risk of liver cirrhosis, we conducted a systematic review and meta-analysis of cohort and case-control studies. Studies were identified by a literature search of Ovid MEDLINE, EMBASE, Web of Science, CINAHL, PsychINFO, ETOH and Google Scholar from January 1980 to January 2008 and by searching the references of retrieved articles. Studies were included if quantifiable information on risk and related confidence intervals with respect to at least three different levels of average alcohol intake were reported. Both categorical and continuous meta-analytic techniques were used to model the dose-response relationship. Seventeen studies met the inclusion criteria. We found some indications for threshold effects. Alcohol consumption had a significantly larger impact on mortality of liver cirrhosis compared with morbidity. Also, the same amount of average consumption was related to a higher risk of liver cirrhosis in women than in men. Overall, end-point was an important source of heterogeneity among study results. This result has important implications not only for studies in which the burden of disease attributable to alcohol consumption is estimated, but also for prevention.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Autophagy reduces acute ethanol-induced hepatotoxicity and steatosis in mice.

              Alcohol abuse is a major cause of liver injury. The pathologic features of alcoholic liver disease develop over prolonged periods, yet the cellular defense mechanisms against the detrimental effects of alcohol are not well understood. We investigated whether macroautophagy, an evolutionarily conserved cellular mechanism that is commonly activated in response to stress, could protect liver cells from ethanol toxicity. Mice were acutely given ethanol by gavage. The effects of ethanol on primary hepatocytes and hepatic cell lines were also studied in vitro. Ethanol-induced macroautophagy in the livers of mice and cultured cells required ethanol metabolism, generation of reactive oxygen species, and inhibition of mammalian target of rapamycin signaling. Suppression of macroautophagy with pharmacologic agents or small interfering RNAs significantly increased hepatocyte apoptosis and liver injury; macroautophagy therefore protected cells from the toxic effects of ethanol. Macroautophagy induced by ethanol seemed to be selective for damaged mitochondria and accumulated lipid droplets, but not long-lived proteins, which could account for its protective effects. Increasing macroautophagy pharmacologically reduced hepatotoxicity and steatosis associated with acute ethanol exposure. Macroautophagy protects against ethanol-induced toxicity in livers of mice. Reagents that modify macroautophagy might be developed as therapeutics for patients with alcoholic liver disease. Copyright © 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.
                Bookmark

                Author and article information

                Journal
                Nature Reviews Disease Primers
                Nat Rev Dis Primers
                Springer Nature America, Inc
                2056-676X
                December 2018
                August 16 2018
                December 2018
                : 4
                : 1
                Article
                10.1038/s41572-018-0014-7
                © 2018

                http://www.springer.com/tdm

                Comments

                Comment on this article