Acquired aplastic anemia: Antibody‐mediated hematopoietic failure
Melvin H. Freedman, Erwin W. Gelfand, E. Fred Saunders
Abstract
Melvin H. Freedman, Erwin W. Gelfand, E. Fred Saunders
Abstract
Abstract The hematopoietic failure in aplastic anemia was studied in six patients by assessing marrow erythroid stem cell (CFU‐E) and granulocytic stem cell (CFU‐C) colony growth in vitro. CFU‐E and CFU‐C were absent or reduced in five patients, and their serum did not inhibit CFU‐E or CFU‐C growth from control marrows. In contrast, marrow from one patient yielded 80 CFU‐E/105 and 16 CFU‐C/105 (control CFU‐E: 197/105 cells plated, range 110–387; control CFU‐C: 48/105, range 15–106). His serum decreased CFU‐E (122 to 9/105) and CFU‐C (71 to 32/105) from control marrow, and CFU‐E from his own marrow (80 to 37/105). His peripheral blood lymphocytes cocultured with autologous or control marrow similarly decreased CFU‐C. The inhibition was more marked in cocultures using a B‐cell enriched lymphocyte fraction obtained by albumin density gradient centrifugation. IgG separated from the patient's serum demonstrated a dose‐responsive suppression of CFU‐E (102 to 8/105), and of CFU‐C (58 to 28/105) from control marrow. We conclude that of the six patients, one demonstrated an antibody‐mediated hematopoietic failure. It is recommended that all patients with acquired aplastic anemia be studied for this, since in vitro testing can detect those in whom immunosuppression and plasmapheresis may be more appropriate therapy than marrow transplantation.
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Abstract The hematopoietic failure in aplastic anemia was studied in six patients by assessing marrow erythroid stem cell (CFU‐E) and granulocytic stem cell (CFU‐C) colony growth in vitro. CFU‐E and CFU‐C were absent or reduced in five patients, and their serum did not inhibit CFU‐E or CFU‐C growth from control marrows. In contrast, marrow from one patient yielded 80 CFU‐E/105 and 16 CFU‐C/105 (control CFU‐E: 197/105 cells plated, range 110–387; control CFU‐C: 48/105, range 15–106). His serum decreased CFU‐E (122 to 9/105) and CFU‐C (71 to 32/105) from control marrow, and CFU‐E from his own marrow (80 to 37/105). His peripheral blood lymphocytes cocultured with autologous or control marrow similarly decreased CFU‐C. The inhibition was more marked in cocultures using a B‐cell enriched lymphocyte fraction obtained by albumin density gradient centrifugation. IgG separated from the patient's serum demonstrated a dose‐responsive suppression of CFU‐E (102 to 8/105), and of CFU‐C (58 to 28/105) from control marrow. We conclude that of the six patients, one demonstrated an antibody‐mediated hematopoietic failure. It is recommended that all patients with acquired aplastic anemia be studied for this, since in vitro testing can detect those in whom immunosuppression and plasmapheresis may be more appropriate therapy than marrow transplantation.
Key concepts: Aplastic anemia, Bone marrow, Haematopoiesis, Immunology, Anemia, CFU-GM, Medicine, Colony-forming unit