Medicine:
doi: 10.1097/MD.0000000000005832
Research Article: Observational Study
Fatty liver is the most common form of chronic liver disease in children and adults worldwide and has a large spectrum of causes including many general or systemic diseases, genetic-metabolic causes, hereditary genetic disorders, and drug hepatotoxicities.[1] Chronic infections with hepatitis B and C viruses (HBV and HCV, respectively) are among the many possible causes of liver steatosis.
The relationship between chronic hepatitis C (CHC) and liver steatosis is well documented.[2–6]
Steatosis is a common finding in the course of CHC and occurs in approximately 50% of adults with CHC and up to 74% of patients infected with HCV genotype 3.[7–9] Both host and viral factors may contribute in the formation of steatosis. In adults with CHC, there are 2 different possible pathomechanisms for developing hepatic steatosis, including viral and metabolic, depending on the virus genotype. HCV genotype 3 directly affects the infected hepatocytes, and this cytopathic effect leads to viral-induced steatosis, which is correlated with HCV viral load.[7–10] In this type, the degree of steatosis may improve after antiviral therapy after achieving a sustained viral response.[9] Steatosis associated with non-3 genotype HCV is a marker of metabolic abnormalities, and insulin resistance playing a key role in its pathophysiology.[7,8] Several studies have confirmed that the presence of steatosis in patients with CHC has prognostic and therapeutic implications due to its independent prediction of fibrosis progression and its association with a lower rate of response to the antiviral therapy.[4,7,11–14]
Steatosis is a common finding in the course of CHC and occurs in approximately 50% of adults with CHC and up to 74% of patients infected with HCV genotype 3.[7–9] Both host and viral factors may contribute in the formation of steatosis. In adults with CHC, there are 2 different possible pathomechanisms for developing hepatic steatosis, including viral and metabolic, depending on the virus genotype. HCV genotype 3 directly affects the infected hepatocytes, and this cytopathic effect leads to viral-induced steatosis, which is correlated with HCV viral load.[7–10] In this type, the degree of steatosis may improve after antiviral therapy after achieving a sustained viral response.[9] Steatosis associated with non-3 genotype HCV is a marker of metabolic abnormalities, and insulin resistance playing a key role in its pathophysiology.[7,8] Several studies have confirmed that the presence of steatosis in patients with CHC has prognostic and therapeutic implications due to its independent prediction of fibrosis progression and its association with a lower rate of response to the antiviral therapy.[4,7,11–14]
In contrast to CHC, liver steatosis has not been adequately analyzed in chronic hepatitis B (CHB), and available data on its prevalence and significance in patients with HBV infection are much less abundant and consistent.[11,15] The frequency of hepatic steatosis in adults with CHB was estimated to be 22% to 76%.[15–18] Available data suggest that steatosis in HBV infection is more strongly associated with metabolic factors than viral determinants.[11,19] However, the ability of HBV to indirectly facilitate the development of steatosis has also been considered.[20] The implications of liver steatosis on disease progression and response to antiviral treatments in patients with CHB remain unknown.[11]
Only scarce and inconsistent data are available about liver steatosis in children with CHB and CHC with respect to its prevalence, pathogenesis, relation to metabolic and viral determinants, and impact on disease progression or response to the treatment.[3,6,21] However, pediatric patients are considered to be an ideal model to study hepatic steatosis because they are not often affected by other potential confounding risk factors responsible for its development, such as alcohol intake, metabolic syndrome, dyslipidemia, insulin-resistance, or diabetes.[3,21] Thus, the aim of this study was to evaluate the prevalence of liver steatosis in children with CHB and CHC and analyze its relationship with clinical and laboratory factors to assess its predictors and impact on the disease progression
View full text online.....
No comments:
Post a Comment