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Chronic hepatitis C infection is a systemic disease that affects over 71 million patients all over the world and it is to be considered nowadays as a new cardiometabolic risk factor. This study aimed to evaluate the weight and metabolic changes after viral eradication in patients with hepatitis C virus (HCV) infection. We conducted a prospective study between October 2017 to December 2021, in a tertiary care center, in which we included 132 patients with HCV or cirrhosis. All patients received treatment with direct antivirals (DAAs) and achieved sustained viral response at 12 weeks (SVR12). During the study, clinical laboratory data and Fibroscan examinations were recorded in all patients. The study group was evaluated at the initiation of antiviral treatment, at SVR12, and within an average follow-up period of 6 months to 12 months after the previous evaluation. Evaluation at SVR12 and the data recorded in the post-SVR surveillance period show a further increase in BMI compared with baseline measurements with a statistically significant difference (27.11 ± 3.22 vs. 27.415 ± 3.03 vs. 28.04 ± 1.11 kg/m2, p = 0.012). The same observation was noticed for waist circumference (WC) at post-SVR evaluation (87.6 ± 13.1 vs. 88.4 ± 13.6 cm, p = 0.031). Moreover, the study population registered an increase in the average total cholesterol (TC) values at post-SVR evaluation (177.01 ± 42.2 mg/dL, p = 0.014) compared to baseline. In addition, the serum level of triglycerides had been modified after viral clearance, with a minimal decrease in the mean values of triglycerides (TGD) at SVR-12 assessment (133.48 ± 41.8 mg/dL, p = 0.78), followed by a significant increase to the mean value of 145.4 ± 47.2 mg/dL (p = 0.026) in the third evaluation. Our study highlights that HCV eradication does not improve the lipid profile in the short term, and these patients still have an additional cardiovascular risk factor due to high levels of TC, TGD, and weight gain. [ABSTRACT FROM AUTHOR]

Chronic hepatitis C virus (HCV) infection induces hepatic steatosis due to viral and host factors. However, information regarding the effects of direct-acting antivirals (DAAs) therapy on liver steatosis and fibrosis is limited. Vibration-controlled transient elastography (VCTE) with a controlled attenuation parameter (CAP) represents a non-invasive method, which has been used in the last few years for the detection of hepatic steatosis and fibrosis before and at a sustained virological response at 12 weeks (SVR12). The aim of this study was to assess the modifications of liver steatosis and fibrosis in HCV-infected patients who achieved SVR12. Consecutive patients with chronic HCV infection that were treated with DAAs in a tertiary gastroenterology center from Romania were included. Demographics, laboratory data, and VCTE evaluation were recorded in all patients. Patients with previous hepatic decompensation and those who did not achieve SVR were excluded. Two hundred and eighty patients (67.1% females) who achieved SVR12 were included. Regarding the changes in biological parameters, including liver enzymes such as alanine aminotransferase (ALT) and aspartate aminotransferase (AST), reduced to normal levels at SVR12 compared to the baseline (28.72 ± 24.71 U/L vs. 40.72 ± 27.34 U/L for ALT, p < 0.013 and 27.21 ± 11.15 U/L vs. 33.35 ± 23.37 U/L for AST, p = 0.029). On the contrary, the levels of triglycerides increased significantly from the baseline to SVR12 (124.03 ± 113.49 mg/dL to 153.78 ± 94.53, p = 0.004). Regarding hepatic steatosis by CAP evaluation, at SVR12, 186 (66.4%) of the individuals had a CAP score of ≥248 dB/m, an increase of 4.6% from the baseline. After viral eradication with DAAs, we observed an increase in hepatic steatosis. Hence, a long-term follow-up is mandatory to identify HCV-infected patients with hepatic steatosis post-SVR and the risk factors for more severe outcomes. [ABSTRACT FROM AUTHOR]

Hepatocellular carcinoma (HCC) is currently the most severe form of liver disease consisting of malignant processes following fibrotic and cirrhotic damage. Despite there are several validated scores for assessing the overall risk to develop HCC in patients diagnosed with chronic liver diseases, most of these are designed for patients with viral hepatitis B and C and subsequently rely on specific measurements, such as viral load or viral profiling. PAGE-B is commonly used to predict HCC risk in patients with viral hepatitis B. In this context, this study aimed to evaluate the applicability of PAGE-B in different liver diseases predisposing to HCC. On a series of 104 consecutive patients, PAGE-B was calculated according to standard guidelines. Based on the collected data, the applicability of PAGE-B was evaluated in several liver pathologies predisposing to HCC, such as alcoholic liver disease, chronic viral hepatitis C, and non-alcoholic fatty liver disease. The mean age of the patients was 67,65 ± 1,15 years, while the sex distribution was 57,28 % males to 42,72 % females. The selected cohort consisted of 11 patients with alcoholic liver disease (10,57 %), 54 patients with chronic viral hepatitis C (51,92 %), and 39 patients with non-alcoholic fatty liver disease (37,5 %). We found that the patients with alcoholic liver disease patients scored highest for PAGE-B (20,09 ± 0,45), while non-alcoholic fatty liver disease patients score lowest (17,89 ± 0,47), significantly different from one another (p = 0,021). In conclusion, our results suggested that PAGE-B could be useful in evaluating HCC risk in chronic liver diseases, but further studies are needed to find a suitable scoring system to predict the overall risk to develop HCC in patients that are diagnosed with nonalcoholic fatty liver disease. [ABSTRACT FROM AUTHOR]