Cell- and humoral-mediated granulopoietic failure detected by CFU-GM assay in one case of Felty's syndrome unresponsive to prednisone treatment

In one case of Felty's syndrome the authors studied marrow and circulating CFU-GM growth under various experimental conditions in order to assess possible cell- and/or humoral-mediated mechanisms inhibiting granulopoiesis. Base line marrow CFU-GM growth was subnormal; marrow cell pretreatment with anti-lymphocyte globulin (ALG) enhanced CFU-GM growth. Peripheral blood mononuclear leukocytes from the patient, co-cultured with autologous marrow cells, inhibited cluster and colony growth. Patient's serum inhibited both autologous and heterologous marrow CFU-GM growths. Cortisol failed to enhance marrow and circulating CFU-GM growths. Colony stimulating activity of peripheral blood leukocytes from the patient, tested against autologous and heterologous marrow CFU-GM, was markedly decreased. Spleen contraction test with adrenalin infusion did not show a splenic reservoir of progenitor cells. In conclusion, their results suggest that a) neutropenia in this patient may be mediated by cell and humoral mechanisms suppressing CFU-GM growth; b) inhibiting cells were steroid unresponsive; c) there was no splenic reservoir for CFU-GM. The authors felt that since their patient did not show an expanded CFU-GM pool marginated in the spleen accompanying humoral and cellular inhibition of CFU-GM growth, she would not benefit from splenectomy.