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To the Editor:

In patients with chronic hepatitis C (CHC), Bedossa et al.,1 show interesting differences among nonalcoholic steatosis and nonalcoholic steatohepatitis (NASH). In fact, the authors demonstrate that subjects with CHC and NASH had advanced histological lesions. However, in our opinion one of the most interesting findings from this study was not completely discussed. The nomenclature of NASH includes several conditions that are associated with steatohepatitis but not with alcohol consumption.2 This concept is not new, but it is clear that the definition of NASH, as proposed by Ludwig et al.,3 was based on subjects who had elements of obesity and metabolic syndrome (MS). Moreover, the most significant advances in epidemiology and pathophysiology were founded on this paradigm. Considering the different etiological features, natural history, and therapeutic issues, it is clear that a differentiation between alcoholic steatohepatitis and NASH must be made. Characteristics of NASH in subjects with obesity and MS have been described and are well known, but less is known about patients without these diagnoses and specifically with CHC. Results from the current study provided criteria to classify the steatosis (and steatohepatitis) that is associated to CHC in 3 different groups (Fig. 1).

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Figure 1. Classification for steatohepatitis in chronic hepatitis C.

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Each group could be combined for clinical purposes, but the distinction could be useful to develop strategies for preventing NASH and to differentiate the natural history of each group. Those subjects with CHC and steatohepatitis related to alcohol consumption had a reduced response to treatment, had advanced histological lesions, and it was found that alcohol abstinence had important beneficial effects for them.4

Similarly, subjects with CHC and metabolic NASH (or genotype 1), had similar deleterious effects, and weight loss would be a useful treatment.5 However, those patients with CHC and nonmetabolic steatohepatitis (genotype 3), are a group with advanced histological lesions, but at present there are no clear preventive or therapeutic measures and their clinical course is unknown. Therefore we can say that, at least in CHC, not all NASH should be called NASH!

Finally, an interesting point is evident in the analyses of Bedossa et al. This is made by searching for differences between all genotypes (n = 278), genotype 1 (n = 144), and genotype 3 (n = 50). We still wonder about the genotype 4 (n = 57) group; do they have NASH? And if they do, is it CHC with metabolic NASH or nonmetabolic NASH? Perhaps Bedossa and colleagues have the answer.

References

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  • 1
    Bedossa P, Moucari R, Chelbi E, Asselah T, Paradis V, Vidaud M, et al. Evidence for a role of nonalcoholic steatohepatitis in hepatitis C: A prospective study. HEPATOLOGY 2007; 46: 380387.
  • 2
    Sanyal AJ. AGA technical review on nonalcoholic fatty liver disease. Gastroenterology 2002; 123: 17051725.
  • 3
    Ludwig J, Viggiano TR, McGill DB, Oh BJ. Nonalcoholic steatohepatitis: Mayo Clinic experiences with a hitherto unnamed disease. Mayo Clin Proc 1980; 55: 434438.
  • 4
    Chen CM, Yoon YH, Yi HY, Lucas DL. Alcohol and hepatitis C mortality among males and females in the United States: a life table analysis. Alcohol Clin Exp Res 2007; 31: 285292.
  • 5
    Bjornsson E, Angulo P. Hepatitis C and steatosis. Arch Med Res 2007; 38: 621627.

Norberto C. Chávez-Tapia M.D.*, Felix I. Tellez-Avila M.D.*, Misael Uribe M.D.*, * Department of Gastroenterology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico.