ATG for MDS – pro
Myelodysplastic syndromes (MDS) are clonal hematologic stem cell disorders characterized by ineffective and dysplastic hematopoiesis leading to progressive anemia, leukopenia, and thrombocytopenia. Low risk disease can usually be treated with supportive measures and a variety of drugs, some of which have been found ineffective for this patient. Antithymocyte globulin (ATG) has been successfully used to treat pancytopenia resulting from severe aplastic anemia. There may be some overlap between low risk MDS and aplastic anemia, in which ATG is a mainstay of treatment, and there has been interest in the use of ATG for MDS. Some studies especially in in hypoplastic refractory anemias with diploid cytogenetics have been reported. However, such conclusions about being able to select subgroups based on genetics are not securely based, having been made on the basis of case reports, series and small prospective studies; no comparative prospective studies have been conducted. I found one guideline that in the presence of a hypocellular maarow, PNH clone adn HLA-DR 15 recommends, “consider a short course of immunosupression with ATG + or minus cyclosporin” (Alberta Cancer Board guideline at http://www.cancerboard.ab.ca/NR/rdonlyres/AFC31B7D-C008-4884-883D-A466F158330B/0/LYHE_004_myelodysplastic_summary.pdf). NCCN, which a more prestigious guidelines, recommends ATG for patients with low risk MDS and high erytropoietin level with transfusion dependence. It does not include cytogenetic criteria.
http://www.nccn.org/professionals/physician_gls/PDF/mds.pdf, p.8
S Yazji et al, Antithymocyte globulin (ATG)-based therapy in patients with myelodysplastic syndromes Leukemia (2003) 17, 2101–2106.
Molldrem JJ, Jiang YZ, Stetler-Stevenson M, Mavroudis D, Hensel N, Barrett AJ. Haematological response of patients with myelodysplastic syndrome to antithymocyte globulin is associated with a loss of lymphocyte-mediated inhibition of CFU-GM and alterations in T-cell receptor Vbeta profiles. Br J Haematol 1998; 102: 1314–1322. |