Moreover, fibrosis remained an independent

predictor of liver-related mortality in a series of 257 NAFLD patients after a median follow-up of 146 months. Knowing that fibrosis obviously dictates survival for patients with NAFLD2 and that inflammation is the precursor lesion of fibrosis,5 we thought that it would be interesting to assess whether the findings published in the aforementioned studies1, 2 could be reproduced in a cohort of European patients with NAFLD who were evaluated at a single tertiary liver center. To this end, we compared the diagnostic AG-014699 order yields of the two most widely followed histological classifications for our cohort of 96 NAFLD patients without cirrhosis. Histological liver samples were evaluated by a single experienced liver pathologist (L.L.); only biopsy samples at least 15 mm long with at least six portal tracts were considered eligible for analysis. According to Brunt’s criteria, 31 patients did not have SH, and 65 patients did have SH; according to Kleiner’s criteria, 61 patients did not have SH (i.e., NAS ≤ 4), and 35 did have SH (i.e., NAS

≥ 5). NAS was ≥5 in 53.8% and ≤4 in 46.2% of the patients with SH according to Brunt’s criteria, this website whereas NAS was ≤4 in 100% of those without SH. All biopsy samples with NAS ≥ 5 fulfilled Brunt’s diagnostic criteria for SH. NAS ≤ 4 did not indicate benign histological findings; this agreed with Brunt’s most recent study1 Fludarabine chemical structure because 49.8% of the patients with NAS ≤ 4 had SH according to Brunt’s original criteria.3 Table 1 shows the independent predictors of SH according to a stepwise multivariate logistic regression analysis. On the basis of our experience and the findings of recent studies,1, 2 we can conclude

that both classifications faithfully mirror metabolic derangements typical of SH. Moreover, the correlation between Brunt’s and Kleiner’s original classifications3, 4 is fair to moderate [κ statistic = 0.43, 95% CI = 0.27-0.59 (this study)]. This agreement, however, might be increased up to 0.74 (0.55-0.93) if the SH cutoff were lowered to NAS = 4 or up to 0.66 (0.47-0.85) if patients with a Brunt grade of 1 were no longer considered to have SH. Finally, we maintain that, by reflecting both inflammation and fibrosis more analytically, Brunt’s original classification1 provides more substantial information to the practicing clinical hepatologist. Stefano Ballestri M.D.*, Amedeo Lonardo M.D.*, Paola Loria M.D.*, * Unit of Internal Medicine, Department of Internal Medicine, Endocrinology, Metabolism, and Geriatrics, University of Modena and Reggio Emilia, Modena, Italy. “
“Innes et al.1 must be congratulated for providing important data on liver-related morbidity and mortality in patients treated for hepatitis C virus (HCV) infection. The authors underlined the importance of comorbidity, particularly in alcohol consumption. Recently, Backus et al.