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.

Serum Stem Cell Factor (SCF) Levels and In Vitro Response of Hematopoietic Progenitors to Recombinant Human SCF (rhSCF) in Patients with Aplastic Anemia / 대한혈액학회지

BACKGROUND: Stem cell factor (SCF), which is produced from stromal cells of bone marrow, is a growth factor acting in early stages of hematopoiesis. Bone marrow failure in aplastic anemia seems to be mainly due to hematopoietic stem cell defect. However, there has been some evidence that microenvironmental defects contribute to the pathophysiology of this disorder. METHODS: We measured serum SCF levels in 29 patients with aplastic anemia at diagnosis using ELISA to define the status of soluble SCF in this disorder. We also examined the effect of serum from 15 patients with aplastic anemia on the colony growth (CFU-GM and BFU-E) of normal bone marrow cells and the ability of recombinant human SCF to stimulate in vitro colony growth of bone marrow cells from 10 patients with aplastic anemia. RESULTS: Levels of serum SCF in patients with aplastic anemia were not different from those in 25 healthy controls (1,493+/-392pg/mL vs. 1,563+/-322pg/mL) or those in patients with idiopathic thrombocytopenic purpura, acute myeloid leukemia, and myelodysplastic syndrome. No correlation was found between serum SCF levels and hematologic parameters at diagnosis such as neutrophil count, hemoglobin, and platelet count. No difference was noted in the serum SCF levels according to severity of the disease. The effect of serum from patients with aplastic anemia on the colony growth of normal bone marrow cells were variable and were not correlated with serum SCF levels. rhSCF increased the colony numbers of bone marrow cells from patients with aplastic anemia. CONCLUSION: These results indicate that soluble SCF is not deficient in aplastic anemia, but SCF can stimulate the proliferation of bone marrow cells from aplastic anemia.