AIM: To identify factors associated with the age at onset of hepatitis C virus (HCV)-related hepatocellular carcinoma (HCC). METHODS: Five hundred and fifty-six consecutive patients positive for HCV antibody and treat...AIM: To identify factors associated with the age at onset of hepatitis C virus (HCV)-related hepatocellular carcinoma (HCC). METHODS: Five hundred and fifty-six consecutive patients positive for HCV antibody and treatment-nafive HCC diagnosed between 1995 and 2004 were analyzed. Patients were classified into three groups according to age at HCC onset: < 60 years (n = 79), 60-79 years (n = 439), or ≥ 80 years (n = 38). Differences among groups in terms of sex, body mass index (BMI), lifestyle characteristics, and liver function were assessed. Factors associated with HCC onset in patients < 60 or ≥ 80 years were analyzed by logistic regression analysis. RESULTS: Significant differences emerged for sex, BMI, degree of smoking and alcohol consumption, mean bilirubin, alanine aminotransferase (ALT), and γ-glutamyl transpeptidase (GGT) levels, prothrombin activity, and platelet counts. The mean BMI values of male patients > 60 years old were lower and mean BMI values of female patients < 60 years old were higher than those of the general Japanese population. BMI > 25 kg/m2 [hazard ratio (HR), 1.8, P = 0.045], excessive alcohol consumption (HR, 2.5, P = 0.024), male sex (HR, 3.6, P = 0.002), and GGT levels > 50 IU/L (HR, 2.4, P = 0.014) were independently associated with HCC onset in patients < 60 years. Low ALT level was the only factor associated with HCC onset in patients aged ≥ 80 years. CONCLUSION: Increased BMI is associated with increased risk for early HCC development in HCV-infected patients. Achieving recommended BMI and reducing alcohol intake could help prevent hepatic carcinogenesis.展开更多
Hepatitis C virus (HCV) infection disrupts the normal metabolism processes, but is also influenced by several of the host’s metabolic factors. An obvious and significantly detrimental pathophysiological fe...Hepatitis C virus (HCV) infection disrupts the normal metabolism processes, but is also influenced by several of the host’s metabolic factors. An obvious and significantly detrimental pathophysiological feature of HCV infection is insulin resistance in hepatic and peripheral tissues. Substantial research efforts have been put forth recently to elucidate the molecular mechanism of HCV-induced insulin resistance, and several cytokines, such as tumor necrosis factor-α, have been identified as important contributors to the development of insulin resistance in the distant peripheral tissues of HCV-infected patients and animal models. The demonstrated etiologies of HCV-induced whole-body insulin resistance include oxidative stress, lipid metabolism abnormalities, hepatic steatosis and iron overload. In addition, myriad effects of this condition have been characterized, including glucose intolerance, resistance to antiviral therapy, progression of hepatic fibrosis, development of hepatocellular carcinoma, and general decrease in quality of life. Metabolic-related conditions and disorders, such as visceral obesity and diabetes mellitus, have been shown to synergistically enhance HCV-induced metabolic disturbance, and are associated with worse prognosis. Yet, the molecular interactions between HCV-induced metabolic disturbance and host-associated metabolic factors remain largely unknown. The diet and lifestyle recommendations for chronic hepatitis C are basically the same as those for obesity, diabetes, and metabolic syndrome. Specifically, patients are suggested to restrict their dietary iron intake, abstain from alcohol and tobacco, and increase their intake of green tea and coffee (to attain the beneficial effects of caffeine and polyphenols). While successful clinical management of HCV-infected patients with metabolic disorders has also been achieved with some anti-diabetic (i.e., metformin) and anti-lipid (i.e., statins) medications, it is recommended that sulfonylurea and insulin be avoided.展开更多
文摘AIM: To identify factors associated with the age at onset of hepatitis C virus (HCV)-related hepatocellular carcinoma (HCC). METHODS: Five hundred and fifty-six consecutive patients positive for HCV antibody and treatment-nafive HCC diagnosed between 1995 and 2004 were analyzed. Patients were classified into three groups according to age at HCC onset: < 60 years (n = 79), 60-79 years (n = 439), or ≥ 80 years (n = 38). Differences among groups in terms of sex, body mass index (BMI), lifestyle characteristics, and liver function were assessed. Factors associated with HCC onset in patients < 60 or ≥ 80 years were analyzed by logistic regression analysis. RESULTS: Significant differences emerged for sex, BMI, degree of smoking and alcohol consumption, mean bilirubin, alanine aminotransferase (ALT), and γ-glutamyl transpeptidase (GGT) levels, prothrombin activity, and platelet counts. The mean BMI values of male patients > 60 years old were lower and mean BMI values of female patients < 60 years old were higher than those of the general Japanese population. BMI > 25 kg/m2 [hazard ratio (HR), 1.8, P = 0.045], excessive alcohol consumption (HR, 2.5, P = 0.024), male sex (HR, 3.6, P = 0.002), and GGT levels > 50 IU/L (HR, 2.4, P = 0.014) were independently associated with HCC onset in patients < 60 years. Low ALT level was the only factor associated with HCC onset in patients aged ≥ 80 years. CONCLUSION: Increased BMI is associated with increased risk for early HCC development in HCV-infected patients. Achieving recommended BMI and reducing alcohol intake could help prevent hepatic carcinogenesis.
文摘Hepatitis C virus (HCV) infection disrupts the normal metabolism processes, but is also influenced by several of the host’s metabolic factors. An obvious and significantly detrimental pathophysiological feature of HCV infection is insulin resistance in hepatic and peripheral tissues. Substantial research efforts have been put forth recently to elucidate the molecular mechanism of HCV-induced insulin resistance, and several cytokines, such as tumor necrosis factor-α, have been identified as important contributors to the development of insulin resistance in the distant peripheral tissues of HCV-infected patients and animal models. The demonstrated etiologies of HCV-induced whole-body insulin resistance include oxidative stress, lipid metabolism abnormalities, hepatic steatosis and iron overload. In addition, myriad effects of this condition have been characterized, including glucose intolerance, resistance to antiviral therapy, progression of hepatic fibrosis, development of hepatocellular carcinoma, and general decrease in quality of life. Metabolic-related conditions and disorders, such as visceral obesity and diabetes mellitus, have been shown to synergistically enhance HCV-induced metabolic disturbance, and are associated with worse prognosis. Yet, the molecular interactions between HCV-induced metabolic disturbance and host-associated metabolic factors remain largely unknown. The diet and lifestyle recommendations for chronic hepatitis C are basically the same as those for obesity, diabetes, and metabolic syndrome. Specifically, patients are suggested to restrict their dietary iron intake, abstain from alcohol and tobacco, and increase their intake of green tea and coffee (to attain the beneficial effects of caffeine and polyphenols). While successful clinical management of HCV-infected patients with metabolic disorders has also been achieved with some anti-diabetic (i.e., metformin) and anti-lipid (i.e., statins) medications, it is recommended that sulfonylurea and insulin be avoided.
