Different from the study by Mederacke et al., where the authors did not observe any increase in LS values in patients with baseline values over 10 kPa, a cutoff value that allows predicting significant or advanced fibrosis but not cirrhosis,3 the results of the present investigation clearly indicate that LS values increase after a standardized meal in patients with chronic HCV infection at any stage of fibrotic evolution and in patients with compensated cirrhosis. The increase in LS, with return to baseline values within 120 minutes, is not just RG 7204 related to the rapid assumption
of the liquid volume but rather associated with the overall caloric intake of the meal. The meal test with postmeal portal blood flow (PBF) measurements has been suggested as a reproducible
noninvasive test to evaluate the severity of portal hypertension in cirrhosis patients. The effect of postprandial hyperemia on portal pressure has been reported 30 minutes after the onset of the meal both by direct measurement18 and by Doppler sonography19 in cirrhosis patients. Data in normal subjects and in noncirrhosis patients with CLD are scarce and obtained only by Doppler sonography,20-22 but indicate that an increase in PBF is detectable by Doppler sonography also 30 minutes after the onset of the meal. Changes in LS values following a test meal are likely a consequence of the adaptation of the hepatic microcirculation to an increased PBF8, 9 and are in overall agreement with the
observation that postprandial hyperemia is associated with a greater increase in portal pressure in cirrhosis patients. In this context, the progressive increase in postmeal delta LS values along with the fibrotic evolution of chronic HCV hepatitis could represent an indirect index of the progressive impairment of the mechanisms responsible for this adaptation, particularly sinusoidal Sulfite dehydrogenase circulation autoregulation, as a consequence of tissue fibrosis, inflammatory infiltration, and neoangiogenesis.23-25 Overall, these findings highlight an interesting potential of TE in detecting dynamic changes in LS related to both the anatomical modifications and hemodynamic alterations occurring in the progression of chronic HCV hepatitis. Accordingly, we tested whether or not the delta stiffness increase in postmeal LS values had advantages, when compared with premeal baseline LS values, in assessing the probability of liver fibrosis according to the Metavir staging system. While premeal baseline LS values were rather accurate in defining the probability of fibrosis stage and in agreement with previous observations by our group in a completely different cohort of patients with HCV-induced CLD,3 an analysis of the performance of the postmeal delta stiffness increase revealed that changes in LS values occurring after the meal test do not offer any advantage in the detection of different stages of fibrosis, whose definition becomes actually less accurate.