目的:通过对慢性肝炎患者及正常人血清组织金属蛋白酶抑制物-1(tissueinhibitors of metalloproteinases-I,TIMP-1)的检测,探讨其在病毒肝炎性肝纤维化发生、发展机制中的意义。方法:本研究测定了58例慢性病毒性肝炎患者的血清TIMP-1,...目的:通过对慢性肝炎患者及正常人血清组织金属蛋白酶抑制物-1(tissueinhibitors of metalloproteinases-I,TIMP-1)的检测,探讨其在病毒肝炎性肝纤维化发生、发展机制中的意义。方法:本研究测定了58例慢性病毒性肝炎患者的血清TIMP-1,采用双夹心ELISA法。结果对正常对照组和慢性肝炎组的测定结果进行t检验,差异有统计学意义(P〈0.01)。结论:血清TIMP-1水平反映了慢性肝病肝内炎症和纤维化的一些重要特征,在目前情况下是一种较好的肝纤维化无创诊断和随访指标。展开更多
The 148 Isoleucine to Methionine protein variant(I148M)of patatin-like phospholipase domain-containing 3(PNPLA3),a protein is expressed in the liver and is involved in lipid metabolism,has recently been identified as ...The 148 Isoleucine to Methionine protein variant(I148M)of patatin-like phospholipase domain-containing 3(PNPLA3),a protein is expressed in the liver and is involved in lipid metabolism,has recently been identified as a major determinant of liver fat content.Several studies confirmed that the I148M variant predisposes towards the full spectrum of liver damage associated with fatty liver:from simple steatosis to steatohepatitis and progressive fibrosis.Furthermore,the I148M variant represents a major determinant of progression of alcohol related steatohepatitis to cirrhosis,and to influence fibrogenesis and related clinical outcomes in chronic hepatitis C virus hepatitis,and possibly chronic hepatitis B virus hepatitis,hereditary hemochromatosis and primary sclerosing cholangitis.All in all,studies suggest that the I148M polymorphism may represent a general modifier of fibrogenesis in liver diseases.Remarkably,the effect of the I148M variant on fibrosis was independent of that on hepatic steatosis and inflammation,suggesting that it may affect both the quantity and quality of hepatic lipids and the biology of non-parenchymal liver cells besides hepatocytes,directly promoting fibrogenesis.Therefore,PNPLA3 is a key player in liver disease progression.Assessment of the I148M polymorphism will possibly inform clinical practice in the future,whereas the determination of the effect of the 148M variant will reveal mechanisms involved in hepatic fibrogenesis.展开更多
文摘目的:通过对慢性肝炎患者及正常人血清组织金属蛋白酶抑制物-1(tissueinhibitors of metalloproteinases-I,TIMP-1)的检测,探讨其在病毒肝炎性肝纤维化发生、发展机制中的意义。方法:本研究测定了58例慢性病毒性肝炎患者的血清TIMP-1,采用双夹心ELISA法。结果对正常对照组和慢性肝炎组的测定结果进行t检验,差异有统计学意义(P〈0.01)。结论:血清TIMP-1水平反映了慢性肝病肝内炎症和纤维化的一些重要特征,在目前情况下是一种较好的肝纤维化无创诊断和随访指标。
基金Supported by Associazione Malattie Metaboliche del Fegato ONLUS(Non-profit organization for the Study and Care of Metabolic Liver Diseases)Centro Studi Malattie Metaboliche del Fegato,Universitàdegli Studi di Milano
文摘The 148 Isoleucine to Methionine protein variant(I148M)of patatin-like phospholipase domain-containing 3(PNPLA3),a protein is expressed in the liver and is involved in lipid metabolism,has recently been identified as a major determinant of liver fat content.Several studies confirmed that the I148M variant predisposes towards the full spectrum of liver damage associated with fatty liver:from simple steatosis to steatohepatitis and progressive fibrosis.Furthermore,the I148M variant represents a major determinant of progression of alcohol related steatohepatitis to cirrhosis,and to influence fibrogenesis and related clinical outcomes in chronic hepatitis C virus hepatitis,and possibly chronic hepatitis B virus hepatitis,hereditary hemochromatosis and primary sclerosing cholangitis.All in all,studies suggest that the I148M polymorphism may represent a general modifier of fibrogenesis in liver diseases.Remarkably,the effect of the I148M variant on fibrosis was independent of that on hepatic steatosis and inflammation,suggesting that it may affect both the quantity and quality of hepatic lipids and the biology of non-parenchymal liver cells besides hepatocytes,directly promoting fibrogenesis.Therefore,PNPLA3 is a key player in liver disease progression.Assessment of the I148M polymorphism will possibly inform clinical practice in the future,whereas the determination of the effect of the 148M variant will reveal mechanisms involved in hepatic fibrogenesis.
