Abstract
s / Digestive and Liver Disease 47S (2015) e221–e225 e225 age of these patients was 61 years (SD 12); 53% were female. Compared to HCV patients without steatosis (3347), in patients with steatosis: BMI was ≥25 in 44% vs. 36% (p<0.05) and ≥30 in 18% vs 11% (p=0.05); F4/cirrhosis was present in 28% vs. 32% (p=ns). Among HCV patients with and without steatosis, similar distribution of HCV genotypes, transaminases and gamma GT levels, lipid pattern and other comorbidities were observed. Of 1295 patients with steatosis, in 167 (1.3%) liver biopsy was available and confirmed the NAFLD diagnosis. In this last group of patients the prevalence of diabetes and of cardiovascular disease were higher compared to patients without steatosis (18% vs 11% (p<0.05) and 35% vs 31% p=ns) and to patients with diagnosis of steatosis diagnosed only by US. Conclusion: The single evaluation of US steatosis is not a helpful factor that could predict liver disease progression and/or specific comorbidities. PITER could be a useful cohort in which the role of steatosis could be prospectively evaluated through an additive diagnostic data set. Better definition of NAFLD markers and their validation in the PITER cohort compared to data derived by a dedicated NAFLD/NASH cohort is worth to be addressed. http://dx.doi.org/10.1016/j.dld.2015.07.022
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