Morphometric analysis of hepatic steatosis in chronic hepatitis C infection

Zubair, Alia; Jamal, Shahid; Mubarik, Azhar

doi:10.4103/1319-3767.45047

Cited by 11 publications

(5 citation statements)

References 13 publications

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“…Accordingly, liver steatosis localization in HCV non-3 genotypes infected patients is similar to that observed in NAFLD/NASH ( i.e. , mostly in the centrolobular zone (acinar 3)) [ 9 ], whereas in genotype 3 infection steatosis is localized mainly in the periportal zone (acinar 1) [ 10 ]. With respect to the sustained virologic response rate to interferon-based treatment, a substantial difference in the behavior of the two types of HCV-associated NAFLD has been reported.…”

Section: Introductionmentioning

confidence: 87%

NAFLD and NASH in HCV Infection: Prevalence and Significance in Hepatic and Extrahepatic Manifestations

Adinolfi

Rinaldi

Guerrera

et al. 2016

IJMS

114

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The aim of this paper is to review and up to date the prevalence of hepatitis C virus (HCV)-associated non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) and their significance in both accelerating progression of HCV-related liver disease and development of HCV-associated extrahepatic diseases. The reported mean prevalence of HCV-related NAFLD was 55%, whereas NASH was reported in 4%–10% of cases. HCV genotype 3 directly induces fatty liver deposition, namely “viral steatosis” and it is associated with the highest prevalence and degree of severity, whereas, HCV non-3 genotype infection showed lower prevalence of steatosis, which is associated with metabolic factors and insulin resistance. The host’s genetic background predisposes him or her to the development of steatosis. HCV’s impairment of lipid and glucose metabolism causes fatty liver accumulation; this seems to be a viral strategy to optimize its life cycle. Irrespective of insulin resistance, HCV-associated NAFLD, in a degree-dependent manner, contributes towards accelerating the liver fibrosis progression and development of hepatocellular carcinoma by inducing liver inflammation and oxidative stress. Furthermore, NAFLD is associated with the presence of metabolic syndrome, type 2 diabetes, and atherosclerosis. In addition, HCV-related “metabolic steatosis” impairs the response rate to interferon-based treatment, whereas it seems that “viral steatosis” may harm the response rate to new oral direct antiviral agents. In conclusion, a high prevalence of NAFLD occurs in HCV infections, which is, at least in part, induced by the virus, and that NAFLD significantly impacts progression of the liver disease, therapeutic response, and some extrahepatic diseases.

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Section: Introductionmentioning

confidence: 87%

NAFLD and NASH in HCV Infection: Prevalence and Significance in Hepatic and Extrahepatic Manifestations

Adinolfi

Rinaldi

Guerrera

et al. 2016

IJMS

114

View full text Add to dashboard Cite

show abstract

“…So far, studies on LD accumulation in the human liver in situ focused mainly on NAFLD/ASH and ALD. In chronic hepatitis C, previous studies were able to demonstrate the importance of lipid droplet accumulation, especially for genotype 3 and of perilipin 2 for lipid droplets in HCV replication [ 59 , 60 , 61 , 62 ]; however, knowledge on steatosis pattern in chronic viral hepatitis is restricted, presumably due to a lack of representative patient material. The aim of the present study was to analyse LD-associated proteins of the perilipin family in a large collection of formalin-fixed, paraffin-embedded (FFPE) liver biopsies of viral hepatitis C of different grades and stages.…”

Section: Introductionmentioning

confidence: 99%

Lipid Droplet-Associated Proteins Perilipin 1 and 2: Molecular Markers of Steatosis and Microvesicular Steatotic Foci in Chronic Hepatitis C

Schelbert

Schindeldecker

Drebber³

et al. 2022

IJMS

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Chronic infection with hepatitis C (HCV) is a major risk factor in the development of cirrhosis and hepatocellular carcinoma. Lipid metabolism plays a major role in the replication and deposition of HCV at lipid droplets (LDs). We have demonstrated the importance of LD-associated proteins of the perilipin family in steatotic liver diseases. Using a large collection of 231 human liver biopsies with HCV, perilipins 1 and 2 have been localized to LDs of hepatocytes that correlate with the degree of steatosis and specific HCV genotypes, but not significantly with the HCV viral load. Perilipin 1- and 2-positive microvesicular steatotic foci were observed in 36% of HCV liver biopsies, and also in chronic hepatitis B, autoimmune hepatitis and mildly steatotic or normal livers, but less or none were observed in normal livers of younger patients. Microvesicular steatotic foci did not frequently overlap with glycogenotic/clear cell foci as determined by PAS stain in serial sections. Steatotic foci were detected in all liver zones with slight architectural disarrays, as demonstrated by immunohistochemical glutamine synthetase staining of zone three, but without elevated Ki67-proliferation rates. In conclusion, microvesicular steatotic foci are frequently found in chronic viral hepatitis, but the clinical significance of these foci is so far not clear.

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“…The formation of a fatty liver as a later development in arsenic induced toxicity, rather than reduced levels of glutathione present at an earlier period is interesting [50]. Mixed patterns of steatosis (microvesicular and macrovesicular) in the liver biopsies of hepatitis C virus patients with the fat globules initially formed in zone 3 and then coalesced to form large droplets (macrosteatosis) with associated fibrosis [20]. Microvesicular steatosis implies the presence of mitochondrial dysfunction and oxidative stress [63].…”

Section: Discussionmentioning

confidence: 99%

“…The mean intensity of staining was proportional to the amount of lipid localized in each grid zone. Twenty five such fields were observed for each lobe (left and right lateral) per sample [20] and the gray values were pooled to obtain a mean gray value. For each group, the mean gray value from six animals was taken as the final gray value for the group.…”

Section: Methodsmentioning

confidence: 99%

Preliminary morphological and biochemical changes in rat liver following postnatal exposure to sodium arsenite

2012

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The effects of sodium arsenite exposure on the hepatic maturation period of cellular and functional reorganization in developing rat livers were evaluated. Animals received intraperitoneal injections of sodium arsenite (1.5 mg/kg body weight) or distilled water on days 9 to 28 after birth. On day 29, the animals were sacrificed either by cervical dislocation or by perfusion fixation. The perfusion fixed liver tissue was processed for paraffin embedding, sectioning and hematoxylin and eosin staining. The fresh liver tissue was processed for cryo-sectioning followed by Sudan Black B staining and for biochemical estimation of reduced glutathione. Microscopic observation revealed comparable preserved hepatic lobular patterns and distributions of uninucleate and binucleate hepatocytes in the control and the experimental groups. The mean nuclear area and diameter of the hepatocytes was increased in the experimental group. Lipid droplet distribution pattern in Sudan Black B stained sections revealed higher staining intensity towards the centrilobular area in both groups. Semiquantitative estimation of staining intensity showed lower mean gray values in zone 3 than in zones 2 and 1 (suggestive of the setting in of the adult pattern) in both groups. The reduced glutathione levels in the liver tissue and the altered nuclear size of the hepatocytes in the experimental group suggested the impairment of morphological and biochemical processes induced by arsenic exposure during the postnatal period.

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Morphometric analysis of hepatic steatosis in chronic hepatitis C infection

Cited by 11 publications

References 13 publications

NAFLD and NASH in HCV Infection: Prevalence and Significance in Hepatic and Extrahepatic Manifestations

NAFLD and NASH in HCV Infection: Prevalence and Significance in Hepatic and Extrahepatic Manifestations

Lipid Droplet-Associated Proteins Perilipin 1 and 2: Molecular Markers of Steatosis and Microvesicular Steatotic Foci in Chronic Hepatitis C

Preliminary morphological and biochemical changes in rat liver following postnatal exposure to sodium arsenite

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