A SINGLE COURSE OF REMISSION REINDUCTION CHEMOTHERAPY FOR ACUTE MYELOGENOUS LEUKEMIA RELAPSING AFTER ALLOGENEIC BONE-MARROW TRANSPLANTATIONIS COMPLICATED BY GRAFT-VERSUS-HOST DISEASE AND FOLLOWED BY SUSTAINEDCOMPLETE REMISSION
P. Vandenberghe et al., A SINGLE COURSE OF REMISSION REINDUCTION CHEMOTHERAPY FOR ACUTE MYELOGENOUS LEUKEMIA RELAPSING AFTER ALLOGENEIC BONE-MARROW TRANSPLANTATIONIS COMPLICATED BY GRAFT-VERSUS-HOST DISEASE AND FOLLOWED BY SUSTAINEDCOMPLETE REMISSION, Leukemia, 11(10), 1997, pp. 1775-1778
Graft-versus-host disease (GVHD) remains a major immunological complic
ation after allogeneic bone marrow transplantation (allo-BMT), but als
o favors development of the beneficial graft-versus-leukemia (GVL) eff
ect. A patient with AML-M4 (inv (16)) is described, who was given non-
myeloablative remission reinduction therapy for leukemic relapse (inv
(16), trisomy 8) diagnosed on day 184 after HLA-compatible sibling BMT
. On day 236, ie about 6 weeks after completion of this course, a clin
ical syndrome suggestive of acute GVHD grade 3 had developed. Skin bio
psy confirmed the clinical diagnosis of GVHD, with a compatible liver
biopsy. Transfusion-associated GVHD was ruled out by analysis of short
tandem repeat (STR) alleles in the skin biopsy, revealing alleles fro
m donor and recipient but not from third party origin. Cyclosporin A (
CsA) therapy, which had been tapered between days 150 and 175, was res
umed, resulting in a favorable response and gradual transition to limi
ted chronic GVHD. The patient has since remained in complete remission
with an excellent performance status for more than 40 months, without
further chemotherapy. Thus this biopsy proven case of GVHD was induce
d by marrow donor lymphocytes more than 200 days after transplantation
and apparently triggered by remission reinduction chemotherapy. The c
ase indicates that intensive non-myeloablative chemotherapy can cure A
ML relapsing after allo-BMT. The therapeutic effect in this case proba
bly involved a direct pharmacological suppression of the leukemic clon
e followed by a GVL effect initiated by donor-derived alloreactive T l
ymphocytes.