Histopathological Diagnosis of Non-Alcoholic and Alcoholic Fatty Liver Disease

Tannapfel, Andrea; Flott-Rahmel, B.

doi:10.5772/19403

Cited by 29 publications

(42 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…47,49 Because the majority of these patients were infected with HCV genotype 1, it is likely that the histopathologic evidence of NASH was more likely the result of metabolic factors associated with NASH in non-HCV patients, as opposed to the steatotic effects of HCV which are more often observed with genotype 3. 49,50 Despite categorizing patients with coexistent definitive histopathologic NASH and active HCV infection in the NASH group, measures of synthetic liver function, MELD scores, and histopatholgic fibrosis were all less severe and OS after curative therapy was prolonged among NASH patients relative to HCV/ALD counterparts. Interestingly, none of the NASH patients with metabolic syndrome had coexistent HCV infection.…”

Section: Discussionmentioning

confidence: 99%

“…7,51 Sampling variability and adequacy and tumor viability (particularly in cases of previous TACE or Y-90 treatment) may have influenced histologic interpretations. 6,7,43,50 Because only cases of definitive or borderline NASH were included in the NASH group, we may have underestimated the incidence of HCC arising from NASH. It is increasingly recognized that a large percentage of patients with HCC arising from cryptogenic cirrhosis in fact may have ''burnt-out NASH'' because characteristic steatosis, lobular inflammation, and ballooning degeneration may disappear with fibrosis progression.…”

Section: Discussionmentioning

confidence: 99%

“…It is increasingly recognized that a large percentage of patients with HCC arising from cryptogenic cirrhosis in fact may have ''burnt-out NASH'' because characteristic steatosis, lobular inflammation, and ballooning degeneration may disappear with fibrosis progression. 1,2,6,8,12,20,30,38,40,43,50,52 Occult alcohol use may have clouded the differentiation between alcoholic and nonalcoholic steatohepatitis. 50 Because preoperative serum triglyceride, high-density lipoprotein, and/ or fasting glucose levels, waist circumference, and blood-pressure measurements were not available for most patients, we used surrogates for each parameter, including medication treatment and BMI.…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Outcomes of curative treatment for hepatocellular cancer in nonalcoholic steatohepatitis versus hepatitis C and alcoholic liver disease

et al. 2012

View full text Add to dashboard Cite

Concomitant increasing incidences of hepatocellular carcinoma (HCC) and nonalcoholic steatohepatitis (NASH) suggest that a substantial proportion of HCC arises as a result of hepatocellular injury from NASH. The aim of this study was to determine differences in severity of liver dysfunction at HCC diagnosis and long-term survival outcomes between patients undergoing curative therapy for HCC in the background of NASH compared to hepatitis C virus (HCV) and/or alcoholic liver disease (ALD). Patient demographics and comorbidities, clinicopathologic data, and long-term outcomes among patients who underwent liver transplantation, hepatic resection, or radiofrequency ablation for HCC were reviewed. From 2000 to 2010, 303 patients underwent curative treatment of HCC; 52 (17.2%) and 162 (53.5%) patients had NASH and HCV and/or alcoholic liver disease. At HCC diagnosis, NASH patients were older (median age 65 versus 58 years), were more often female (48.1% versus 16.7%), more often had the metabolic syndrome (45.1% versus 14.8%), and had lower model for end-stage liver disease scores (median 9 versus 10) (all P < 0.05). NASH patients were less likely to have hepatic bridging fibrosis or cirrhosis (73.1% versus 93.8%; P < 0.001). After a median follow-up of 50 months after curative treatment, the most frequent cause of death was liver failure. Though there were no differences in recurrence-free survival after curative therapy (median, 60 versus 56 months; P 5 0.303), NASH patients had longer overall survival (OS) (median not reached versus 52 months; P 5 0.009) independent of other clinicopathologic factors and type of curative treatment. Conclusion: Patients with HCC in the setting of NASH have less severe liver dysfunction at HCC diagnosis and better OS after curative treatment compared to counterparts with HCV and/or alcoholic liver disease. (HEPATOLOGY 2012;55:1809-1819 C oncomitant increases in the incidence of hepatocellular carcinoma (HCC) and prevalence of nonalcoholic fatty liver disease (NAFLD) suggest that a substantial proportion of HCC arises as a result of hepatocellular injury from nonalcoholic steatohepatitis (NASH). As a result, HCC is the most rapidly increasing cause of cancer death in the United States.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Outcomes of curative treatment for hepatocellular cancer in nonalcoholic steatohepatitis versus hepatitis C and alcoholic liver disease

et al. 2012

View full text Add to dashboard Cite

show abstract

“…It is characterized by hepatocellular lipid accumulation, on the ground of which inflammation and fibrosis may develop. The histological picture closely resembles alcoholic liver disease [10]. In nonalcoholic steatohepatitis (NASH) and alcoholic steatohepatitis (ASH) as well as in other chronic liver diseases like viral hepatitis, hepatic fibrosis is the peril that determines morbidity and mortality.…”

Section: Introductionmentioning

confidence: 97%

Protective effect of xanthohumol on toxin-induced liver inflammation and fibrosis

Dorn¹,

Heilmann²,

Hellerbrand³

2012

Z Gastroenterol

View full text Add to dashboard Cite

“…The prevalence of NAFLD has increased rapidly in parallel with dramatic increases in obesity and diabetes and is becoming the most common liver disease worldwide (Sugihara et al, 2013). Although NAFLD is one of the most common chronic hepatic diseases, its fundamental molecular pathways remain unclear (Tannapfel et al, 2011). Hepatic lipid and lipoprotein abnormalities accompanied by chronic inflammation play a vital role in NAFLD pathogenesis and progression (Fon Tacer and Rozman, 2011).…”

Section: Discussionmentioning

confidence: 99%

Correlation between MTP -493G>T polymorphism and non-alcoholic fatty liver disease risk: a meta-analysis

L¹,

Sj²,

Shi³

et al. 2014

Genet. Mol. Res.

View full text Add to dashboard Cite

ABSTRACT. Several studies have found that microsomal transfer protein (MTP) may be important in the development and progression of non-alcoholic fatty liver disease (NAFLD). In this meta-analysis, we evaluated the relationships between a common polymorphism (-493G>T, rs1800591 G>T) in the MTP gene and NAFLD risk. The PubMed, CISCOM, CINAHL, Web of Science, Google Scholar, EBSCO, Cochrane Library, and CBM databases were searched for relevant articles published before October 1, 2013 without any language restrictions. Meta-analysis was conducted using the STATA 12.0 software. Crude odds ratios (ORs) with 95% confidence intervals (95%CIs) were calculated. Eleven case-control studies were included in this meta-analysis. A total of 636 NAFLD patients and 918 healthy control subjects were examined in this meta-analysis. Our results indicate that the MTP -493G/T polymorphism increases the risk of NAFLD (G allele vs T allele: OR = 1.39, 95%CI = 1.17-1.65, P < 0.001; GG + GT vs TT: OR = 1.46, 95%CI = 1.02-2.09, P = 0.038, respectively). Subgroup analyses indicated that the MTP -493G/T polymorphism was associated with an increased risk of NAFLD in population-based, MTP -493G>T polymorphism and NAFLD risk hospital-based, polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP), and large sample-size subgroups under the allele and dominant models (all P < 0.05). However, we found no association between non-PCR-RFLP polymorphism and small samplesize subgroups (all P > 0.05). Our findings indicate that the MTP -493G/ T polymorphism may contribute to the development of NAFLD. Thus, the MTP -493G/T polymorphism may be a biomarker for the early detection of NAFLD.

show abstract

Histopathological Diagnosis of Non-Alcoholic and Alcoholic Fatty Liver Disease

Cited by 29 publications

References 36 publications

Outcomes of curative treatment for hepatocellular cancer in nonalcoholic steatohepatitis versus hepatitis C and alcoholic liver disease

Outcomes of curative treatment for hepatocellular cancer in nonalcoholic steatohepatitis versus hepatitis C and alcoholic liver disease

Protective effect of xanthohumol on toxin-induced liver inflammation and fibrosis

Correlation between MTP -493G>T polymorphism and non-alcoholic fatty liver disease risk: a meta-analysis

Contact Info

Product

Resources

About