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Acute upper gastrointestinal graft-versus-host disease: clinical
significance and response to immunosuppressive therapy
DJ Weisdorf, DC Snover, R Haake, WJ Miller, PB McGlave, B Blazar, NK Ramsay, JH Kersey and A Filipovich
University of Minnesota Bone Marrow Transplantation Program, Minneapolis.
Recognized manifestations of acute graft-versus-host disease (GVHD) of the
gastrointestinal (GI) tract include secretory diarrhea, abdominal pain,
and, at times, hemorrhage. In a review of 469 patients undergoing
allogeneic bone marrow transplantation (BMT) from matched sibling donors at
our institution, we have recognized a syndrome of upper GI GVHD. This
syndrome, presenting clinically as anorexia, dyspepsia, food intolerance,
nausea, and vomiting, was recognized and confirmed histologically in 62
patients (13% by Kaplan-Meier projection) at the initiation of systemic
GVHD therapy, a subset of the 197 patients developing grade II through IV
GVHD. These 62 patients with upper GI GVHD were significantly older than
the overall BMT population and older than the cohort with grade II through
IV GVHD, as well. Of the 62 patients, 25 had upper GI GVHD accompanied only
by limited (stage 1 and 2) skin GVHD; 13 others with upper GI GVHD plus
limited skin involvement at initial presentation later progressed to more
extensive multiorgan involvement; 24 others presented with upper GI along
with other organ GVHD. This upper GI GVHD syndrome, first recognized at our
center in 1983, has been diagnosed with increasing frequency (22% +/- 5%)
in the most recent 5-year interval. The upper GI GVHD syndrome is more
responsive to immunosuppressive therapy than grade II GVHD defined by
Seattle criteria, with complete and continuing responses to treatment
observed in 71% +/- 17% (95% confidence interval) of those with the upper
GI GVHD syndrome compared with only 37% +/- 10% complete responses in other
patients with grade II GVHD (P = .002). Patients failing immunosuppressive
therapy for upper GI GVHD often progress to symptomatic lower GI
involvement, suggesting that this syndrome may be an earlier and perhaps
more treatable manifestation of this unique intestinal immunopathology,
which is followed by chronic GVHD in 74% of patients. While upper GI GVHD
symptoms are nonspecific and require invasive histologic and microbiologic
studies to confirm the diagnosis, we believe this syndrome has been
underreported after allogeneic BMT and propose its recognition within the
clinical GVHD scoring system.
Volume 76,
Issue 3,
pp. 624-629,
08/01/1990
Copyright © 1990 by The American Society of Hematology
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