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)

With hepatobiliary scintigraphy and sonography, we prospectively studied the occurrence of new hepatobiliary abnormalities in 18 patients before, and from 1 to 103 days after, bone marrow transplantation (BMT). Prior to BMT, all patients had normal hepatic uptake and visualization of the gallbladder by 60 min on scintigraphy, and no sludge, stones, or other abnormalities on sonography. After BMT, 16 patients (89%) developed new scintigraphic and/or sonographic hepatobiliary abnormalities. Fifteen patients had impaired liver uptake of mebrofenin, while 11 developed gallbladder uptake of mebrofenin, while 11 developed gallbladder sludge and/or stones, and 10 had gallbladder nonvisualization at 60 min. Nevertheless, no patient developed clinical or laboratory evidence of acute cholecystitis. New hepatobiliary abnormalities are more common during the first months post-BMT than clinically suspected, probably reflecting the combined effects of hepatotoxic chemoradiation therapy, graft-versus-host disease, and prolonged administration of parenteral alimentation. Evidence of acute cholecystitis is generally not found.
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PMID:Frequent occurrence of new hepatobiliary abnormalities after bone marrow transplantation: results of a prospective study using scintigraphy and sonography. 831 3

Multiple myeloma (MM) is the most common indication for autologous hematopoietic stem cell transplantation (HSCT) in North America. Despite occurring in up to 50% of patients undergoing allogeneic HSCT, the incidence of graft-versus-host disease (GVHD) after autologous HSCT is reportedly only 5-20%. Gastrointestinal involvement with graft-versus-host disease (GI GVHD) is a common and serious complication of allogeneic HSCT. GI GVHD after autologous transplant, which is referred to as autologous GVHD (auto-GVHD), has also been described. Auto-GVHD is usually less severe than allogeneic GVHD, and it can be one of the manifestations of engraftment syndrome with release of inflammatory cytokines and infiltration of auto-reactive T cells into affected tissue. Seventy-nine percent of patients respond well to corticosteroids without evidence of recurrence. However, cases of severe auto-GVHD lacking good response to corticosteroids have been reported, most notably in MM patients. Here we present two cases of autologous GI GVHD in recipients of autologous HSCT for treatment of MM. Our cases demonstrate two distinct clinical and endoscopic presentations of this uncommon entity. In the first case, the patient had more severe clinical symptoms accompanied by radiographic, endoscopic, and pathologic findings. The hospital course was complicated by cryptosporidium enteritis and acute cholecystitis in the setting of increased immunosuppression with a corticosteroid for presumed auto-GVHD. In contrast, the second case presented a patient with normal radiologic and endoscopic findings. Pathology revealing frequent apoptotic bodies led to auto-GVHD as a diagnosis. Both our patients received similar courses of chemotherapy prior to autologous HSCT (four cycles of a proteasome inhibitor, lenalidomide, and dexamethasone). Our work highlights the importance of maintaining a high level of clinical suspicion for auto-GVHD in patients presenting with GI symptoms after autologous HSCT, as it is a potentially treatable pathology that may be easily confused with other conditions. Health care providers should be aware of the potential complications of auto-GVHD after autologous HSCT and should be suspicious of auto-GVHD if GI symptoms occur, especially in patients receiving immunomodulatory therapy for MM, even in the absence of gross endoscopic findings.
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PMID:Autologous Graft-Versus-Host Disease of the Gastrointestinal Tract in Patients With Multiple Myeloma and Hematopoietic Stem Cell Transplantation. 2951 7