| Summary: | 碩士 === 高雄醫學大學 === 醫學研究所碩士班 === 94 === BACKGROUND AND AIM : Nonalcoholic fatty liver disease (NAFLD) is referred to the phenomenon that fat depositing into hepatocyte., and NAFLD include stages from simple fatty liver (hepatic steatosis)，nonalcoholic steatohepatitis (NASH)，and cirrhosis, all of the stages can find fat in hepatocyte. Many causes can induce NAFLD, and hepatitis C infection is one of the causes. Powell E.E. et al and other studies showed that 30-70% pathologic biopsy from chronic hepatitis C patients can find the hepatic steatosis. Besides, recent studies showed that HCV core protein can inhibit the function of microsomal triglyceride transfer protein, and secrete VLDL. So that this condition can influence the hepatocyte assemble and secrete VLDL, and then induce damage to mitochondria and oxidative stress. Oxidative stress can interfer peroxidation of fat, and then develope into hepatic steatosis. Under this ciucumstance, this resukt can add damage to hepatocytes of chronic heaptitis C patients. Because interferon used for chronic hepatitis C show the well develop in recent years, the relationship between hepatic steatosis and treatment for chronic hepatitis C is paid much attention gradually. But until now, this issue is still controversial. The aim of this study is discussing the influence of hepatic steatosis to chronic hepatitis C, such as possible causes resulting in hepatic steatosis in chronic hepatitis c patients, the influence of hepatic steatosis for the therapeutic response of therapy regimen for chronic hepatitis C, and the relationship between changing of pathologic hepatic steatosis before and after treatment and sustained virologic response (SVR).
MATERIAL ANDMETHOD: The objects in our study are patients with chronic hepatitis C patients. All of the patients received the pathologic hepatic biopsy before treatment, total 239 patients were enrolled. Among them, 150 patients received the interferon combined with ribavirin therapy for 24 weeks, and then followed up for 24 weeks. The related data, past history, including hypertension, diabetes mellitus, hyperlipidemia, and other data, such as age, sex, BMI (≧23kg/mP2P is overweight), AST(normal range is 0-33 IU/L), ALT (normal range is 0-34 IU/L), AST/ALT ratio, genotype and viral load of hepatitis C virus, pathologic presentation and change, therapeutic regimen, and rhetaprutic response, etc. After then we analyzed these data to fine the possible relationship between them.
RESULT: In our study, we enrolled 239 chronic hepatitis c patients, including 72 patients with pathologic hepatis steatosis before treatment, and 167 patients without pathologic hepatis steatosis before treatment; the rate of hepatic steatosis in chronic hepatits C patients is 31.0%. Hepatic steatosis is not associated the age, sex, AST，ALT，AST/ALT ratio, genotype and viral load of hepatitis C virus, and pathologic inflammation grade and fibrosis stage. But there are differences in hypertension (p=0.006, OR=2.63, 95% C.I=1.31-5.32), diabetes mellitus (p=0.015, OR=2.84, 95% C.I=1.19-6.77), hyperlipidemia (p=0.003, OR=4.12, 95% C.I=1.53-11.12) , and BMI value (p=0.002, OR=2.88, 95% C.I=1.44-5.77) between steatosis and non-steatosis groups.And multivariates analysis showed that hyperlipidemia and BMI≧23kg/mP2P are the important factors related to resulting in hepatic steatosis for chronic hepatitis C patients. As mention to theraueutic response, hepatic steatosis is not related to the rate of reaching SVR. Besdies, there is no relationship between heepatic steatosis and therapeutic response of genotype and viral load of hepatitis C virus to the interferon combined ribavirin therapy
On the other hand, patients with lower BMI value have higher rate of reaching SVR, and multivariate logistic regression analysis also showed that BMI was related to therapeutic response, so we think that BMI is related to chronic hepatitsi C therapy.Finally, there is no dominant relationship between rate of reaching SVR and hepatic steatosis change after treatment in patients with hepatic steatosis before treatment, and also no difference in hepatic steatosis change in patients without hepatic steatosis before treatment and the rate of reaching SVR.
CONCLUSION: In our study, hyperlipidemia and BMI≧23kg/mP2P are important factors related hepatic steatosis in chronic hepatitis C patients. Hepatic steatosis has no influence on the genotype and viral load of chronic hepatitis C virus to therapeutic response of interferon combined ribavirin therapy. In addition, the change of pathologic hepatic steatosis before and after treatment is not associated SVR.
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