Abstract

INTRODUCTION: Gastrointestinal autologous graft-versus-host disease (GVHD) has been reported in 13% of autologous stem cell transplant (auto-HCT) recipients in comparison to 40% of those who underwent allogenic-HCT. Involvement of both upper and lower GI tracts is a unique phenomenon in auto-GVHD. Herein, we present a case of biopsy-proven GVHD of the duodenum and colon after auto-HCT. CASE DESCRIPTION/METHODS: A 59-year-old male with newly diagnosed multiple myeloma of the lumbar spine received palliative radiation, followed by four cycles of chemotherapy with lenalidomide, bortezomib, and dexamethasone. He subsequently underwent auto-HCT. One month after auto-HCT, he was admitted with fever, nausea, vomiting, early satiety, diarrhea and generalized abdominal pain. Initial laboratory findings included a normal leukocyte count and mild acute kidney injury. Stool testing for infectious etiologies were negative. Additional studies were negative for Epstein–Barr virus, cytomegalovirus (CMV), parvovirus, and his thyroid function was normal. Computed tomography was remarkable for diffuse wall thickening with mucosal hyperenhancement of the entire large and small intestine. Subsequent upper endoscopy revealed atrophic, erythematous, flattened mucosa with petechia in the stomach and diffuse mucosal erythema of the duodenal bulb. Flexible sigmoidoscopy was notable for friable mucosa with altered vasculature, erythema and erosions. Histologic examination of the duodenal mucosa showed villous atrophy with increased number of crypt apoptosis and cryptitis, and active inflammation with the presence of crypt architecture distortion and numerous apoptotic bodies in the crypts of the colon. Immuno-stains for adenovirus and CMV were negative. The constellation of histomorphological features was consistent with GVHD and the patient was subsequently treated with a methylprednisolone taper, which resulted in almost complete resolution of his symptoms. DISCUSSION: GVHD represents an immunocompromised state as it reduces bowel integrity and may lead to severe infections with or without immune suppressive therapy treatment. Certain chemotherapy agents including lenalidomide, inhibit the proliferation and function of regulatory T cells, predisposing patients to GI auto-GVHD. As patients with GI auto-GVHD present with a variety of both upper and lower GI symptoms, we recommend performing endoscopic evaluation of both upper and lower GI tracts to ensure a timely diagnosis.Figure 1.: (A-B) Duodenum. A: Histologic sections of the duodenum shows abnormal villous architecture (arrows) consisting of shortening and widening. Lamina propria (star) cellularity is increased (hematoxylin and eosin stain; original magnification ×40). B: Higher magnification shows the crypts with increased number of apoptosis (arrows) (original magnification ×200). (C-D) Colon. C: Section of the colon shows marked crypt architectural distortion with the presence of acrypt abscesses (arrow). These features are those of chronic colitis with moderate activity (original magnification ×20). D: Colonic crypts show increased number of apoptosis (arrows) (origincal magnification ×200).

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