Elsevier

Human Pathology

Volume 41, Issue 8, August 2010, Pages 1178-1185
Human Pathology

Original contribution
A comparison of the fibrotic potential of nonalcoholic fatty liver disease and chronic hepatitis C

https://doi.org/10.1016/j.humpath.2009.10.025Get rights and content

Summary

In nonalcoholic fatty liver disease the amount of fibrosis for individual histologic stages is unknown. To better understand the fibrotic potential of nonalcoholic fatty liver disease, we compared the amount of fibrosis in nonalcoholic fatty liver disease versus chronic hepatitis C virus patients. The area of fibrosis for equivalent fibrosis stages was measured by micromorphometry in 70 nonalcoholic fatty liver disease and 70 matched, untreated, chronic hepatitis C virus controls. The area of fibrosis correlated with Brunt stage (r = 0.71; P < .001) in nonalcoholic fatty liver disease and METAVIR stage (r = 0.58; P < .001) in chronic hepatitis C virus. Mean area of fibrosis was similar in nonalcoholic fatty liver disease and chronic hepatitis C virus patients (7.77% versus 7.70%). Although chronic hepatitis C virus patients displayed higher area of fibrosis in early disease (no or mild fibrosis), nonalcoholic fatty liver disease and chronic hepatitis C virus patients had similar area of fibrosis in more advanced disease (7.83% versus 8.06%, respectively; P = .86 for bridging fibrosis; and 16.62% versus 12.98%, respectively; P = .29 for cirrhosis). The area of fibrosis was similar in Brunt stage 3 nonalcoholic fatty liver disease and METAVIR stage 2 chronic hepatitis C virus, the usual threshold for initiating therapy. The area of steatosis declined with increasing fibrosis stages confirming the early loss of liver fat with progressive fibrosis in nonalcoholic fatty liver disease. Fibrosis is as abundant in nonalcoholic fatty liver disease as in chronic hepatitis C virus, especially in the advanced stages of the disease. The fibrotic potential of nonalcoholic fatty liver disease is as severe as that of chronic hepatitis C virus.

Section snippets

Study population

Patients with histologically proven NAFLD who underwent liver biopsy for abnormal liver function tests between the years 2000 and 2007 were included. NAFLD was defined as the presence of steatosis greater than 20% in the absence of alcohol consumption (no more than 20 g/d for females and 30 g/d for males) and of any other cause of chronic liver disease including drug-induced liver disease [18]. Chronic hepatitis C was defined as the presence of HCV RNA in serum by polymerase chain reaction in

Correlations between the area of fibrosis and the different staging systems

The characteristics of the study population are described in Table 1. Because of the matching procedure, the mean age and the sex ratio were similar between groups. In the HCV group, 10 patients had 5% or less steatosis, whereas 60 patients had no steatosis. In the NAFLD group, 3 patients had a NAS score of 2 or less, 36 patients of 3 or 4, and 31 patients of 5 or more. In the entire population, there was a significant (P < .001) stepwise increase in the area of fibrosis according to the

Discussion

This study provides further insight into insulin resistance-related liver injury by demonstrating that NAFLD carries the potential for fibrotic scar deposition to the same extent as other established causes of severe liver disease, such as chronic hepatitis C. Despite the description of advanced histologic fibrosis stages in cohorts of NAFLD patients [3], [18], the general perception is that NAFLD is a disease of milder fibrotic severity. This could hold true as histologic staging systems are

Acknowledgments

The authors wish to thank Professor Pierre Bedossa for helpful comments.

We thank Janet Ratziu for English language assistance.

Cited by (0)

The authors declare having no conflict of interest related to the conduct of this study.

1

See Appendix A.

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