GRAFT-VERSUS-HOST DISEASE INDUCED BY SMALL BOWEL ALLOGRAFTS

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Abstract
The histopathological changes and the course of graftversus-host (GVH) disease were studied in the rat model of small-bowel transplantation using the Lewis→LBNF1 strain combination. Allograft-induced GVH disease led to the recipients' death from enteritis, dermatitis and emaciation after 14.4±2.9 days (heterotopic grafts) and 14.0±0.7 days (orthotopic grafts). Histologic evidence of dermatitis (epidermal hyperkeratosis and cutaneous infiltration by mononuclear and polymorphonuclear cells) and enteritis (villous blunting and sloughing, inflammatory infiltrate of the recipient's own intestine) appeared on the 9th to 13th postoperative days, and these changes became fulminant within 2–3 days. The lymphatic tissues of the Lewis grafts and the LBNF1 host underwent a course of progressive lymphoid depletion and loss of follicular architecture beginning on the 5th postoperative day. Throughout the postoperative course, the small-bowel graft remained intact. The relative spleen weight progressively increased until shortly before death, when a marked reduction was observed. The clinical triad of diarrhea, diffuse dermatitis, and hypertrophy of the lymphoid organs followed by their atrophy suggests a diagnosis of GVH disease rather than rejection of the small-bowel allograft. The diagnosis can be confirmed by biopsy of a recipient lymph node or the intestinal allograft (cave perforation) if it is accessible.