Search

Hepatic steatosis is a frequent pathological finding in patients with chronic viral C infection (HCV) and can be independently associated with increased alcohol consumption, type 2 diabetes, obesity and hyperlipidemia. All these factors can lead to the development of hepatic steatosis in patients with HCV. There are several noninvasive techniques and scores used for diagnosing and quantifying liver steatosis. Successful eradication of HCV with interferon-free treatment regimens has been suggested to improve the level of hepatic steatosis. The precise mechanisms responsible for these beneficial effects are currently under investigation, but it is thought that the decrease in hepatic inflammation and viral replication contribute to the resolution of hepatic steatosis. Moreover, the overall enhancement in liver health and metabolic factors may also have a significant impact. [ABSTRACT FROM AUTHOR]

Hepatic diseases pose a significant public health concern. Regardless of the severity of hepatic fibrosis, treatment is recommended for all chronic hepatitis C virus (HCV) subjects. However, fibrosis and steatosis assessment remains crucial for evaluating the prognosis, progression, and hepatic disease monitoring, particularly following the treatment with direct-acting antivirals (DAAs). The aim of our study was to evaluate the impact of metabolic factors and the extent of hepatic fibrosis and fat accumulation in chronic HCV infection subjects. Additionally, another objective was to investigate modifications regarding fibrosis and steatosis three months after a successful sustained viral response (SVR). A total of 100 patients with compensated cirrhosis and chronic hepatitis C (CHC) were included in our study. These patients received treatment with DAA and underwent Fibromax assessment before and three months post SVR. After DAA treatment, a significant decrease was observed in the degree of hepatic fibrosis and hepatic steatosis. This regression was evident three months following the achievement of SVR. Chronic viral hepatitis C may trigger risk factors for metabolic syndromes, such as obesity and type 2 diabetes mellitus. Conclusions: It is crucial to monitor metabolic factors and take timely measures to prevent or treat metabolic syndrome in patients with chronic viral hepatitis C. [ABSTRACT FROM AUTHOR]

Introduction. Hepatic steatosis represents a common pathological feature in patients with chronic viral C infection and can be independently associated with obesity, increased alcohol consumption, type 2 diabetes, and hyperlipidemia. These factors can contribute to the development of hepatic steatosis in patients with chronic HCV (Hepatitis C virus) infection. Materials and methods. 64 patients who underwent treatment with oral antivirals were included and evaluated through non-invasive methods for the degree of hepatic steatosis. Results. After at least 3 months of sustained viral response, all patients with advanced hepatic steatosis were categorized into lower classes in the Steatotest evaluation. Conclusion. This study highlights the importance of direct acting antiviral (DAA) treatment in the medical care of patients with chronic viral C infection and hepatic steatosis. Thirty years after the discovery of the hepatitis C virus, treatment with oral antivirals revolutionizes the medical care of patients with this chronic infection. [ABSTRACT FROM AUTHOR]

Background and Objectives: Non-alcoholic fatty liver disease is a worldwide significant public health problem, particularly in patients with type 2 diabetes mellitus. Identifying possible risk factors for the disease is mandatory for a better understanding and management of this condition. Patatin-like phospholipase domain-containing protein 3 (PNPLA3) has been linked to the development and evolution of fatty liver but not to insulin resistance. The aim of this study is to evaluate the relationships between PNPLA3 and fatty liver, metabolic syndrome and subclinical atherosclerosis. Materials and Methods: The study group consisted of patients with type 2 diabetes mellitus without insulin treatment. The degree of liver fat loading was assessed by ultrasonography, and subclinical atherosclerosis was assessed using carotid intima-media thickness (CIMT). PNPLA3 rs738409 genotype determination was performed by high-resolution melting analysis that allowed three standard genotypes: CC, CG, and GG. Results: Among the 92 patients, more than 90% showed various degrees of hepatic steatosis, almost 62% presented values over the normal limit for the CIMT. The majority of the included subjects met the criteria for metabolic syndrome. Genotyping of PNPLA3 in 68 patients showed that the difference between subjects without steatosis and subjects with hepatic steatosis was due to the higher frequency of genotype GG. The CC genotype was the most common in the group we studied and was significantly more frequent in the group of subjects with severe steatosis; the GG genotype was significantly more frequent in subjects with moderate steatosis; the frequency of the CG genotype was not significantly different among the groups. When we divided the group of subjects into two groups: those with no or mild steatosis and those with moderate or severe steatosis it was shown that the frequency of the GG genotype was significantly higher in the group of subjects with moderate or severe steatosis. PNPLA3 genotypes were not associated with metabolic syndrome, subclinical atherosclerosis, or insulin resistance. Conclusions: Our results suggest that PNPLA3 does not independently influence cardiovascular risk in patients with type 2 diabetes mellitus. The hypothesis that PNPLA3 may have a cardioprotective effect requires future confirmation. [ABSTRACT FROM AUTHOR]