AIMTo investigate shear wave (SW) propagation velocity in patients with untreated hepatitis C and patients with sustained virological response (SVR).METHODSA total of 136 hepatitis C patients [85 patients who had not received antiviral therapy (naïve group) and 51 patients who had received antiviral therapy and subsequently achieved SVR of at least 24 wk (SVR group)] and 58 healthy volunteers and outpatients without liver disease (control group) underwent evaluation of liver stiffness by SW elastography (SWE). Various parameters were evaluated in the chronic hepatitis C patients at the time of SWE.RESULTSSW propagation velocity (Vs) was 1.23 ± 0.14 m/s in the control group, 1.56 ± 0.32 m/s in the SVR group, and 1.69 ± 0.31 m/s in the naïve group. Significant differences were seen between the control group and the SVR group (P = 0.0000) and between the SVR group and the naïve group (P = 0.01417). All four fibrosis markers were higher in the naïve group than in the SVR group. In the naïve group, Vs was positively correlated with alanine aminotransferase (ALT) (r = 0.5372), α feto protein (AFP) (r = 0.4389), type IV collagen (r = 0.5883), procollagen III peptide (P-III-P) (r = 0.4140), hyaluronic acid (r = 0.4551), and Mac-2 binding protein glycosylation isomer (M2BPGi) (r = 0.6092) and negatively correlated with albumin (r = -0.4289), platelets (r = -0.5372), and prothrombin activity (r = -0.5235). On multiple regression analysis, Vs was the most strongly correlated with ALT (standard partial regression std β = 0.4039, P = 0.00000). In the SVR group, Vs was positively correlated with AFP (r = 0.6977), type IV collagen (r = 0.5228), P-III-P (r = 0.5812), hyaluronic acid (r = 0.5189), and M2BPGi (r = 0.6251) and negatively correlated with albumin (r = -0.4283), platelets (r = -0.4842), and prothrombin activity (r = -0.4771). On multiple regression analysis, Vs was strongly correlated with AFP (standard partial regression std β = 0.5953, P = 0.00000) and M2BPGi (standard partial regression std β= 0.2969, P = 0.03363).CONCLUSIONIn hepatitis C patients, liver stiffness is higher in treatment-naïve patients than in those showing SVR. SWE may be a predictor of hepatocarcinogenesis in SVR patients.

Background and AimBased on past diagnostic classifications of gastritis, the Kyoto classification of gastritis adopts simpler, more objective gastritis findings according to Helicobacter pylori infection status and evaluates the risk of gastric cancer. To clarify whether this score can predict future gastric cancer, we retrospectively examined risk scores obtained using the Kyoto classification of gastritis a few years prior to the diagnosis of early gastric cancer.MethodsWe reviewed data from 50 individuals who had undergone upper gastrointestinal endoscopy 2–3 years prior to the diagnosis of early gastric cancer in our hospital. Two expert endoscopists evaluated and compared risk scores obtained using the Kyoto classification of gastritis between cancer and control groups.ResultsWith regard to the risk score obtained using the Kyoto classification of gastritis in all cases, atrophy, intestinal metaplasia, diffuse redness, and total score were significantly higher among gastric cancer cases. Among H. pylori‐eradicated cases, atrophy score was higher in the gastric cancer group. Among patients for whom H. pylori had been eradicated for >3 years at first endoscopy, atrophy score was still higher in the gastric cancer group.ConclusionThis retrospective study suggested that the risk score obtained using the Kyoto classification of gastritis was useful for predicting the onset of gastric cancer. In particular, patients with a high atrophy score even after H. pylori eradication may be at high risk of developing gastric cancer.

Purpose To measure changes in liver stiffness over time due to direct-acting antiviral (DAA) therapy in hepatitis C patients using shear wave elastography (SWE). Methods Patients with hepatitis C treated with DAA therapy in a university medical center between July 2015 and April 2020 were evaluated. Shear wave velocity (Vs) of the liver was measured using SWE. Alanine aminotransferase (ALT), platelet count, and α-fetoprotein (AFP) were measured at the same time, and the FIB-4 index was estimated. Absence of hepatocellular carcinoma was confirmed at baseline and end of therapy. Imaging was then performed every 6 months. Patient characteristics were compared between patients who did and did not develop carcinoma. Results The mean age of the 229 patients (93 men) was 65.6 years. Eight patients developed carcinoma during follow-up (mean 32.6 ± 19.5 months). Significant differences were found between the groups in terms of AFP, platelet count, and Fib-4 index at baseline; the pre-treatment data had the best relationship with hepatocarcinogenesis. Mean Vs decreased significantly during DAA therapy, and then decreased further. Liver stiffness 6 months after treatment ended had the best relationship with hepatocarcinogenesis. Conclusion In patients with a sustained virological response, risk of developing cancer can be predicted by measuring Vs approximately 6 months after treatment.