Massive hepatic necrosis (MHN) is defined as hepatocyte death exceeding 70% in the entire liver. Acute liver failure induced by MHN can lead to death in nearly half of patients. However, the vast majority of lost hepatocyte conditions can recover in about half of these patients. Hepatocyte function restoration and gradual differentiation into mature hepatocytes primarily rely on the rapid activation and proliferation of liver progenitor cells (LPCs) in these survived patients. This paper mainly describes the cellular and molecular mechanisms by which LPCs restore liver function and rescue patients following the occurrence of MHN.

Massive hepatic necrosis (MHN) is defined as hepatocyte death exceeding 70% in the entire liver. Acute liver failure induced by MHN can lead to death in nearly half of patients. However, the vast majority of lost hepatocyte conditions can recover in about half of these patients. Hepatocyte function restoration and gradual differentiation into mature hepatocytes primarily rely on the rapid activation and proliferation of liver progenitor cells (LPCs) in these survived patients. This paper mainly describes the cellular and molecular mechanisms by which LPCs restore liver function and rescue patients following the occurrence of MHN.

OBJECTIVESTo study the relationship between serum levels of hyaluronic acid (HA), type III procollagen (PCIII), laminin (LN), type IV collagen (IV-C) and hepatic fibrosis and to determine their value in clinical practice.

METHODS2600 serum samples from chronic hepatitis patients were assayed for fibrosis indexes including HA, PCIII, LN and IV-C with RIA. Liver biopsy was performed in 280 of those patients and the biopsy material was examined histopathologically. The inflammation grade of the liver, stage of fibrosis and degree of chronic hepatitis were recorded and were compared with fibrotic indexes.

RESULTSAmong 2600 chronic hepatitis patients, every fibrotic index had a significant correlation with the inflammation grade, fibrosis staging and the degree of chronic hepatitis (P < 0.01). The coefficient correlation of the results of histopathological examinations to HA was 0.544, 0.548 and 0.468 respectively, that to PCIII, 0.495, 0.424 and 0.335, that to LN, 0.214, 0.204 and 0.184, and that to IV-C, 0.406, 0.404 and 0.412, respectively.

CONCLUSIONSSerum fibrosis indexes are fairly well correlated with the inflammation grade of the liver, fibrosis staging and the degree of chronic hepatitis. However, as diagnostic markers, they should be considered in combination with liver function tests, ultrasonography and clinical manifestations.

Adolescent ; Adult ; Aged ; Collagen Type III ; blood ; Collagen Type IV ; blood ; Female ; Hepatitis, Chronic ; blood ; diagnosis ; Humans ; Hyaluronic Acid ; blood ; Laminin ; blood ; Liver Cirrhosis ; blood ; diagnosis ; Male ; Middle Aged ; Procollagen ; blood ; Prognosis

Objective To observe the dynamic changes in collagen type Ⅰ and collagen type Ⅲ in rabbits with schistosomiasis japonica and the treatment effect of gamma interferon on the degradation of collagens in schistosomal hepatic fibrosis.Methods Each rabbit was infected with 80?1 S japonicum cercariae. Liver operations were done at different time points after infection and the liver specimens were embedded with paraffin and stained with ? SMA, HE and picric acid Sirius red. The stained slides were observed under polarizing microscope and different collagen areas calculated by computer imagine analysis system. At the 16th week after infection, the infected rabbits received a single dose of praziquantel and gamma interferon for 8 weeks.Results The area percent of collagen type Ⅰ at the 28th week after infection (40 14?17 00) increased about seven fold compared with the 8th week group (5 73?3 40). The area percent of collagen type Ⅲ at the 28th week after infection (6 80?5 19) increased about six fold compared with the 8th week group (1 15?1 34). The ? SMA positive cells also increased significantly. After gamma interferon treatment, the area percent of collagen type Ⅰ and type Ⅲ decreased significantly, from 18 51?7 52 and 4 63?3 64 (before treatment) to 3 09?1 54 and 0 40?0 37 (0 and 4 weeks after treatment) ( P