Complete recovery of marrow function after treatment with anti‐lymphocyte globulin is associated with high, whereas early failure and development of paroxysmal nocturnal haemoglobinuria are associated with low endogenous G‐CSA‐release

Publisher Website
Google Scholar
Abstract
24 patients who were treated with antilymphocyte globulin (ALG) for severe aplastic anaemia (SAA) were tested for endogenous release of granulocyte colony stimulating activity (G-CSA) prior to, and at various intervals after treatment. CSA-production in vitro was induced with autologous serum as a source of ''releaser'' activity, avoiding the use of plant mitogens. Before treatment, G-CSA-release was highly variable. Though mean values were higher in the 17 patients who subsequently responded to ALG treatment than in the six non-responders, this difference was not statistically significant. In the 17 responders, G-CSA-release strongly increased prior to improvement of peripheral blood counts. In one responder patient tested before, and at regular intervals after ALG, CSA-release was high before, abnormally low at 7 d and increased again to high values before the onset of bone marrow reconstitution. In six patients who did not respond to ALG-treatment, G-CSA release decreased after treatment, and a second course of ALG was ineffective when given during this low CSA-phase. Five of the 24 patients developed paroxysmal nocturnal haemoglobinuria (PNH) at 9 months to 3 years after ALG-treatment. In all, the onset of PNH was associated with very low G-CSA-release, whether it had been high or low before treatment. We conclude that low-CSA-release after ALG treatment is a poor prognostic sign. it either indicates progression of marrow failure or heralds PNH. Such patients may be candidates for early bone marrow transplantation or treatment with G-CSF or GM-CSF.