Impact of alcohol-associated and metabolic dysfunction-associated steatotic liver diseases upon hepatic disorder and carcinogenesis in the current era
In this editorial, author specifically focuses upon metabolic dysfunction-associated steatotic liver disease (MASLD) and alcohol-associated liver diseases (ALD) in the current era. This editorial article is inspired by the observational study by Harris et al in the recent issue. Alcohol and metabolic dysfunction cause steatotic changes in the hepatic parenchyma. The ALD and MASLD are major cause of chronic liver disease. Liver cirrhosis (LC) is a result of chronic liver inflammation with many causes (e.g., viral hepatitis, drug, alcohol and metabolic disorder). Metabolic dysfunction-associated steatohepatitis and alcohol-associated hepatitis can lead to liver fibrosis and LC. LC leads to hepatic dysfunction and can progress to eventual liver failure and death. Though chronic viral hepatitis is considered a main cause of LC for a long time, other etiologies (i.e., ALD, MASLD) has significantly increased in the current era. From the viewpoint of carcinogenesis, LC frequently causes hepatocellular carcinoma (HCC), and HCC is the most common type of primary liver cancer worldwide. As regards major causes of HCC, chronic viral hepatitis is gradually outweighed by ALD and MASLD. Note that patients coexisting with ALD and metabolic dysfunction-associated steatohepatitis show higher occurrence of HCC. Impact of ALD and MASLD upon the development of chronic liver disease, liver fibrosis, LC, and HCC is drastically increased in the current era. Establishments of diagnostic and therapeutic strategies to overcome these hepatic disorders are still required.
- Research Article
26
- 10.1097/qad.0000000000000300
- Jun 19, 2014
- AIDS
Reducing the incidence of hepatocellular carcinoma (HCC) in HIV-infected patients has become a serious problem when managing these patients. There are many explanations for this disease evolution, which notably include their longer survival under effective antiviral therapy and also the more rapid evolution of chronic liver disease. Despite recent advances in the management of hepatitis B (HBV) and hepatitis C (HCV) viral diseases, which will probably increase the number of patients achieving a virological response, HIV-infected patients with cirrhosis are still at risk of the onset of HCC. This evolution to HCC is also correlated to other comorbidities such as excessive alcohol consumption and nonalcoholic steatohepatitis (NASH). HCC thus remains a public health issue in this population. The poor prognosis and aggressiveness of HCC have been fully demonstrated, but the mechanisms underlying this aggressiveness are not yet well defined. As well as underlying mechanisms that contribute to accelerating hepatocarcinogenesis in HIV-infected patients, there are other reasons why HIV-infected patients should be considered a higher risk population. This review discusses the principal epidemiological determinants; the mechanisms of pathogenesis; and the treatment of HCC in HIV/HBV and HIV/HCV coinfected patients. It also discusses the probable need to develop a specific screening policy for HCC in this population in order to prevent the rapid development and to make them more amenable to a curative treatment.
- Research Article
11
- 10.1097/00005176-200207001-00013
- Jul 1, 2002
- Journal of Pediatric Gastroenterology and Nutrition
The Impact of Liver Disease on Growth and Nutrition
- Research Article
67
- 10.1016/j.jceh.2014.04.003
- May 22, 2014
- Journal of Clinical and Experimental Hepatology
Hepatocellular carcinoma (HCC) is one of the major causes of morbidity, mortality and healthcare expenditure in patients with chronic liver disease. There are no consensus guidelines on diagnosis and management of HCC in India. The Indian National Association for Study of the Liver (INASL) set up a Task-Force on HCC in 2011, with a mandate to develop consensus guidelines for diagnosis and management of HCC, relevant to disease patterns and clinical practices in India. The Task-Force first identified various contentious issues on various aspects of HCC and these issues were allotted to individual members of the Task-Force who reviewed them in detail. The Task-Force used the Oxford Center for Evidence Based Medicine-Levels of Evidence of 2009 for developing an evidence-based approach. A 2-day round table discussion was held on 9th and 10th February, 2013 at Puri, Odisha, to discuss, debate, and finalize the consensus statements. The members of the Task-Force reviewed and discussed the existing literature at this meeting and formulated the INASL consensus statements for each of the issues. We present here the INASL consensus guidelines (The Puri Recommendations) on prevention, diagnosis and management of HCC in India.
- Research Article
562
- 10.1053/j.gastro.2004.09.020
- Nov 1, 2004
- Gastroenterology
More than 18 million adults in the United States abuse alcohol, a prevalence 5 times higher than that of hepatitis C. Chronic alcohol use of greater than 80 g/day for more than 10 years increases the risk for hepatocellular carcinoma (HCC) approximately 5-fold; alcohol use of less than 80 g/day is associated with a nonsignificant increased risk for HCC. The risk for HCC in decompensated alcohol induced cirrhosis approaches 1% per year. The risk does not decrease with abstinence, and HCC can occur in a noncirrhotic liver. Alcohol use in chronic hepatitis C doubles the risk for HCC as compared with the risk in hepatitis C alone. Furthermore, there may be synergism between alcohol and hepatitis C in the development of HCC, and in these patients HCC may occur at an earlier age and the HCC may be histologically more advanced. Studies in the United States and Italy suggest that alcohol is the most common cause of HCC (accounting for 32%-45% of HCC). The mechanisms by which alcohol causes HCC are incompletely understood, but may include chromosomal loss, oxidative stress, a decreased retinoic acid level in the liver, altered DNA methylation, and genetic susceptibility. Alcohol use is increasing in many countries, suggesting that alcohol will continue to be a common cause of HCC throughout the world.
- Front Matter
30
- 10.1053/j.gastro.2011.11.004
- Nov 19, 2011
- Gastroenterology
Lipids in Liver Disease: Looking Beyond Steatosis
- Discussion
18
- 10.1016/j.jhep.2013.10.003
- Oct 8, 2013
- Journal of Hepatology
Focus
- Research Article
19
- 10.1016/j.isci.2020.101690
- Oct 15, 2020
- iScience
SummaryHepatocellular carcinoma (HCC) initiation is characterized by stepwise accumulation of molecular alterations, during which the early events are largely unknown. Here, we presented a comprehensive genomic and transcriptomic landscape at stages of hepatitis, cirrhosis, and HCC by using a diethylnitrosamine-induced rat HCC model. We observed the early occurrence of gene instability and aberrant cancer associated signaling pathways in liver hepatitis. We further characterized the progressive molecular changes during hepatocarcinogenesis, wherein the intense rivalry between tumor-suppressive and oncogenic strengths occurred in cirrhosis stage. Despite the significant pathological difference, mutation signatures and expression landscape are highly similar between hepatitis and cirrhosis stages. Furthermore, we identified PI3K-Akt signaling pathway as a key pathway in the process of hepatocarcinogenesis through integrative analysis, and PIK3CD is a potential biomarker indicating HCC recurrence. The dynamic immune response during hepatocarcinogenesis, such as continuous decline of monocytes, suggests an immunological intervention strategy beyond chemoprevention for liver cancer.
- Research Article
4
- 10.1053/j.gastro.2006.10.067
- Dec 1, 2006
- Gastroenterology
Shall We Bury the Sword? Imaging of Hepatic Fibrosis
- Discussion
49
- 10.1016/j.jhep.2012.10.010
- Oct 17, 2012
- Journal of Hepatology
miR-122 acts as a tumor suppressor in hepatocarcinogenesis in vivo
- Front Matter
24
- 10.1016/j.jhep.2005.01.003
- Jan 22, 2005
- Journal of Hepatology
Time-dependent events in natural history of occult hepatitis B virus infection: the importance of population-based long-term follow-up study with repeated measurements
- Research Article
6
- 10.1111/j.1872-034x.2010.00655.x
- May 19, 2010
- Hepatology Research
Is the measurement of tumor marker levels effective for monitoring patients after the treatment of hepatocellular carcinoma? RECOMMENDATIONFor patients in whom tumor marker levels were elevated before treatment, tumor markers measured after treatment may serve as useful indices of the effects of treatment.(grade C1) 30
- Research Article
358
- 10.1053/j.gastro.2019.02.049
- Apr 12, 2019
- Gastroenterology
Surveillance for Hepatocellular Carcinoma: Current Best Practice and Future Direction.
- Research Article
599
- 10.1002/hep.27222
- Aug 25, 2014
- Hepatology
Epidemiology of hepatocellular carcinoma in the United States: where are we? Where do we go?
- Research Article
1057
- 10.1053/j.gastro.2004.08.052
- Dec 1, 2004
- Gastroenterology
Serum markers detect the presence of liver fibrosis: A cohort study
- Discussion
- 10.1053/j.gastro.2005.05.068
- Aug 1, 2005
- Gastroenterology
What are helicobacter doing in the hepatobiliary system?
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