Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018133 (graft-versus-host disease)
 18,032 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A pronounced similarity exists between liver allograft rejection and graft-versus-host disease (GVHD) in the damage and eventual destruction of small intrahepatic bile ducts. Although an immunologic reaction has an important role, precisely identifying the target antigens or reason for persistence of the immune response has been difficult. An important difference between GVHD and liver rejection is the development of obliterative arteriopathy only in rejection. The three main histopathologic features of acute rejection are a predominantly mononuclear but mixed portal inflammation, subendothelial inflammation of portal or terminal hepatic veins (or both), and bile duct inflammation and damage. In acute rejection, a controversial issue is determining when therapeutic intervention is needed. The recommended approach is to base treatment on a combination of histopathologic changes and liver injury or dysfunction. Chronic rejection, which usually does not occur before 2 months after transplantation, is characterized by two main histopathologic features: (1) damage and loss of small bile ducts and (2) obliterative arteriopathy. Acute GVHD begins within the first month after transplantation and most commonly involves the skin, gastrointestinal tract, and liver, whereas chronic GVHD usually develops more than 80 to 100 days after liver transplantation and affects 30 to 50% of long-term survivors. Recognition of the early, cellular stages of chronic GVHD is important in preventing irreversible damage.
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PMID:Immune cholangitis: liver allograft rejection and graft-versus-host disease. 955 43

Bone Marrow Transplant (BMT) is a critical therapeutic intervention for a variety of diseases occurring in the pediatric patient. Complications of allogeneic BMT include graft-versus-host disease (GVHD), infection, drug toxicity, thrombotic microangiopathy, and veno-occlusive disease. With solid organ transplantation, chronic vascular rejection has emerged as a major factor limiting long-term survival of the graft. We present a vasculopathy of small muscular arteries in 6 patients after allogeneic BMT. Cases include 4 boys and 2 girls ranging in age from 4 months to 13 years with full or partial human leukocyte antigen matching. Five of the 6 transplants were from related donors. The vasculopathy occurred 13 to 418 days after transplant and was noted in surgical specimens (2) and at autopsy (4). It was seen in the gastrointestinal tract and lung in 3 cases each. Vascular changes in small muscular arteries include concentric intimal or medial hyperplasia with luminal narrowing, prominent myxoid change, extravasated red blood cells, and presence of some foamy histiocytes with no evidence of thrombotic microangiopathy. Vasculopathy contributed to intestinal compromise requiring surgical intervention 3 times in 1 patient, and diffuse alveolar damage with hemorrhage in another. All 6 patients are dead. The cause of this unusual vasculopathy present in patients after BMT is likely to be multifactorial, involving effects of irradiation, chemotherapy, cyclosporine, and GVHD. Together these may create a negative synergy which produces an obliterative arteriopathy that should be recognized as a pathological entity and may be a harbinger of a poor prognosis.
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PMID:Vasculopathy of small muscular arteries in pediatric patients after bone marrow transplantation. 1041 90