Saudi Journal of Gastroenterology
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Year : 2009  |  Volume : 15  |  Issue : 1  |  Page : 1
Steatosis is a lot more than holes in hepatocytes

Department of Pathology, Schulich School of Medicine, The University of Western Ontario, and London Health Sciences Centre, London, Ontario, Canada

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How to cite this article:
Chakrabarti S. Steatosis is a lot more than holes in hepatocytes. Saudi J Gastroenterol 2009;15:1

How to cite this URL:
Chakrabarti S. Steatosis is a lot more than holes in hepatocytes. Saudi J Gastroenterol [serial online] 2009 [cited 2022 Nov 29];15:1. Available from:

Chronic hepatitis C infection remains a common and significant cause of liver disease leading to end-stage cirrhosis and liver failure. It is also a common indication for the necessity of a liver transplant. Histologically, chronic inflammation and fibrosis are characteristic features of this disease. The stage and grade of the disease process is measured by the amount of fibrosis and severity of the inflammation. Focal fatty change is a known histological finding of hepatitis C infection. However, the exact significance of such a finding is not clear.

In this issue, Zubair et al. [1] demonstrated that the presence of fat, especially macrovesicular steatosis, is associated with a higher stage of fibrosis. They used a routine histological analysis as well as a morphometric evaluation to demonstrate an association. The authors suggested that such fat may result from mitochondrial oxidative stress. Hence, along with viral infection and inflammation, the presence of fat may also modulate the progression of this disease.

Fat accumulation is known to cause fibrosis in alcoholic and non alcoholic fatty liver disease. Such changes may occur due to the release of adipocytokines causing tissue damage. [2],[3],[4] In addition, mitochondrial oxidative stress may lead to the activation of proinflammatory and fibrogenic factors. [5],[6],[7] It is, however, interesting to note that only macrovesicular steatosis has a pronounced effect on an advanced hepatitis C induced lesion. This point is of significant interest from a pathogenetic point of view. However, although this study was not designed to answer the reasons behind such findings, it suggested a possible relationship. In previous studies, it has been shown that serum HCV RNA levels correlate with histological liver damage and concur with steatosis and a high viral load acts together with steatosis in accelerating the progression of liver injury. [8] In an earlier study, this group had also demonstrated that patients with genotype 3a showed a significantly higher prevalence of steatosis compared with those infected with other genotypes. [9] In another study, although hepatic steatosis was not associated with HCV RNA levels, it was associated with being overweight, hepatic fibrosis, and triglyceride levels in chronic hepatitis C infection. [10]

Nevertheless, an inevitable question that may arise is whether an assessment of a change in fat is to be included in a routine pathology report to determine a prognosis. This is not easy to answer. However, larger multi-center studies may be required to address such questions. A large-scale study with a detailed clinico-pathological correlation may provide valuable insight. Furthermore, investigations as to the specific mechanisms by which only macrovesicular fat causes tissue damage are very important. Such analysis may have far reaching implications and may also be of importance in other liver diseases associated with fat accumulation in the hepatocytes.

Understanding pathogenetic mechanisms is fascinating but a difficult undertaking. Extensive basic science research is needed to address these questions. We need to have concerted efforts involving hepatologists, pathologists, translational researchers, and basic scientists to identify such pathogenetic mechanisms since only a better understanding of such pathogentic mechanisms will lead to the development of specific treatment for advanced tissue damage in hepatitis.

   References Top

1.Zubair A, Jamal S, Mubarik A. Morphometric analysis of hepatic steatosis in chronic hepatitis C infection. Saudi J Gastroenterol 2008;15: 11-4.  Back to cited text no. 1    
2.Watanabe S, Yaginuma R, Ikejima K, Miyazaki A. Liver diseases and metabolic syndrome. J Gastroenterol 2008;43:509-18.  Back to cited text no. 2  [PUBMED]  [FULLTEXT]
3.Bertolani C, Marra F. The role of adipokines in liver fibrosis. Pathophysiology 2008;15:91-101.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]
4.van der Poorten D, George J. Disease-specific mechanisms of fibrosis: Hepatitis C virus and nonalcoholic steatohepatitis. Clin Liver Dis 2008;12:805-24.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Tirosh O, Ilan E, Anavi S, Ramadori G, Madar Z. Nutritional lipid-induced oxidative stress leads to mitochondrial dysfunction followed by necrotic death in FaO hepatocytes Nutrition. 2008 Oct 21 [Epub ahead of print].  Back to cited text no. 5    
6.Urtasun R, de la Rosa LC, Nieto N. Oxidative and nitrosative stress and fibrogenic response. Clin Liver Dis 2008;12:769-90.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]
7.Tsukada S, Parsons CJ, Rippe RA. Mechanisms of liver fibrosis. Clin Chim Acta 2006;364:33-60.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]
8.Adinolfi LE, Utili R, Andreana A, Tripodi MF, Marracino M, Gambardella M, et al . Serum HCV RNA levels correlate with histological liver damage and concur with steatosis in progression of chronic hepatitis C. Dig Dis Sci 2001;46:1677-83.  Back to cited text no. 8  [PUBMED]  [FULLTEXT]
9.Adinolfi LE, Utili R, Andreana A, Tripodi MF, Rosario P, Mormone G, et al . Relationship between genotypes of hepatitis C virus and histopathological manifestations in chronic hepatitis C patients. Eur J Gastroenterol Hepatol 2000;12:299-304.  Back to cited text no. 9  [PUBMED]  
10.Hsieh MH, Lee LP, Hsieh MY, Tsai KB, Huang JF, Hou NJ, et al . Hepatic steatosis and fibrosis in chronic hepatitis C in Taiwan. Jpn J Infect Dis 2007;60:377-81.  Back to cited text no. 10  [PUBMED]  [FULLTEXT]

Correspondence Address:
Subrata Chakrabarti
Department of Pathology, The University of Western Ontario Pathologist, London Health Sc. Ctr. 339 Winderemere Rd, London, Ontario, N6A 5A5
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1319-3767.45045

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