Clinical Significances of Serum Soluble Fas and Soluble Fas Ligand in Chronic Hepatitis B / 대한간학회지

BACKGROUND/AIMS: Apoptosis via Fas/FasL system is thought to be involved in the development of hepatocyte death in viral hepatitis B. In chronic hepatitis C, sFas/sFasL system was reported to control liver injury induced by Fas/FasL mediated apoptosis. To determine the role of sFas/sFasL system in chronic hepatitis B, we analyzed serum sFas/sFasL in 58 HBV patients and 29 healthy controls. METHODS: HBV patients were categorized into two groups; normal ALT (40 IU/L). Serum sFas/sFasL levels in HBV patients were measured by ELISA and was compared with those in 29 healthy controls. Serum ALT levels, histological activity, and Fas/FasL expression of liver were compared. RESULTS: Chronic hepatitis B patients with elevated ALT had significantly higher serum sFas levels than those in healthy controls (P<0.01). Serum sFasL levels, however, were significantly lower than those in healthy controls (P<0.01). Patients with moderate to marked degree of inflammation and fibrosis had significantly higher serum sFas levels than those in healthy controls (P<0.05). Serum sFasL levels had no correlation with the hepatic histological activity. Serum sFas/sFasL levels also had no significant correlation with the Fas/FasL expression of liver. CONCLUSIONS: Serum sFas/sFasL levels play a possible role in the pathogenesis of chronic hepatitis B. These results suggest that serum sFas levels might serve as a marker for estimating the degree of hepatic histological activity.

Serum Soluble Fas Levels of Patients with Aplastic Anemia / 대한혈액학회지

BACKGROUND: Fas is a member of the tumor necrosis factor (TNF)/nerve growth factor (NGF) receptor family. Triggering of the Fas receptor pathway by its ligand results in apoptosis. Soluble Fas consists of the extracellular region of Fas receptor and it binds to Fas ligand to inhibit the Fas and Fas ligand induced apoptosis. Recently some evidence indicates that the Fas/Fas ligand system represents an important pathway responsible for the induction of apoptosis in bone marrow CD34+ cells of patients with aplastic anemia. METHODS: We measured serum soluble Fas levels in 27 patients with aplastic anemia at diagnosis using ELISA to define the status of soluble Fas in this disorder. RESULTS: Levels of serum soluble Fas in patients with aplastic anemia were lower com-pared with that of normal healthy controls. No difference was noted in the serum soluble Fas levels according to severity of disease. No correlation was found between serum soluble Fas levels and hematologic parameters at diagnosis such as neutrophil count, lymphocyte count, platelet count and corrected reticulocyte count. CONCLUSION: These results indicate that serum soluble Fas levels are decreased in patients with aplastic anemia. Further studies recruiting more patients and measuring Fas receptor on peripheral blood lymphocyte subsets and bone marrow CD34+ cells concomitantly may be helpful to determine pathophysiology of bone marrow failure.