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)

This work presents some investigation results of lymphoid subpopulation functional activity: Tg+1, Tg-1, Theophylline-resistant and Theophylline-sensitive lymphocytes and O-1 isolated from the peripheral blood of patients with bacterial dysentery (BD) in local xenogenic GVHD. It has been established that Tg+1 and Tg-1 have stimulating effect on local xenogenic GVHD, but O-1 are inert though the quantity of Fcg+--receptor carrying lymphocytes among O-1 in BD and nonspecific ulcerative colitis is increased compared with donors. Theophylline-resistant and Theophylline-sensitive lymphocytes demonstrated inhibiting effect on GVHD formation which was evident in the latter case.
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PMID:[Characteristics of lymphoid subpopulations of peripheral blood of patients with shigellosis]. 142 Dec 34

Gastrointestinal inflammation after allogeneic bone marrow transplantation may be due to acute graft-versus-host disease (GVHD) and/or superinfection with opportunistic organisms. Twenty-eight patients with barium studies suggesting gastrointestinal inflammation after bone marrow transplantation and either acute GVHD, viral infection, or both were studied to characterize the radiographic appearances of each disease and to determine whether acute GVHD could be distinguished from viral superinfection on the basis of radiographic findings. Thirteen patients had minimal or no acute GVHD, with viral infection proved in eight and strongly suspected in four others; the remaining patient was thought to have nonspecific inflammatory bowel disease. Five patients had pure acute GVHD, and 10 patients had viral enteritis superimposed on acute GVHD. Radiographic abnormalities were found in the gastrointestinal tract in both acute GVHD and viral infection and were more extensive than previously reported. Findings were similar in both entities, although gastric abnormalities were not seen in pure acute GVHD but only in viral infection, either alone or together with acute GVHD. Prolonged small bowel barium coating occurred in both viral infection and acute GVHD. Fold thickening evolved into fold effacement with a shaggy contour in two patients with viral infection. Colonic findings in all groups mimicked ulcerative colitis. Our data indicate that differentiation between acute GVHD and viral enteritis is not possible on the basis of radiographic findings alone. Both entities should be considered when gastrointestinal inflammation occurs after bone marrow transplantation.
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PMID:Gastrointestinal inflammation after bone marrow transplantation: graft-versus-host disease or opportunistic infection? 327 85

Colon transplantation has been proposed as a method to improve the function of an intestinal allograft. The present study examined the risk of colon rejection and the effect of FK506 on colon rejection in BN-->LEW rats with orthotopic bowel transplants. The first 4 groups included rats with untreated allografts (group 1), rats with isografts treated with 0.6 mg/kg FK506 (group 2), rats with allografts treated with 0.6 mg/kg FK506 (group 3), and rats with allografts treated with 0.4 mg/kg FK506 (group 4). In each of these groups (10-12 rats), half of the animals received a small bowel graft only (SB), while the other half received a small bowel, ascending colon, and cecum graft (SBC). The animals were followed daily until they died or were killed at 4 weeks. In group 5, an additional 18 untreated rats with SBC allografts were randomly killed on the third, fifth, seventh, and tenth postoperative days to study the sequential histopathologic and immunopathologic changes of colon rejection. There was no difference in survival, body weight, nutritional parameters, or bacterial contamination after SB and SBC transplantation. Intestinal transit was slower after SBC than SB transplantation (P < 0.05). Sequential histopathologic studies revealed that (1) the severity and time course of colon rejection was similar to small intestine rejection, and (2) the features of colon rejection were similar to ulcerative colitis. There was no evidence of graft-versus-host disease after SBC transplantation. In summary, adding a segment of large bowel to a small bowel allograft does not increase the risk of rejection or surgical complications. The transplanted colon slows intestinal transit. Treatment with FK506 effectively prevents colon rejection. These data suggest that adding a colon graft may improve the outcome of clinical small bowel transplantation.
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PMID:Treatment with FK506 prevents rejection of rat colon allografts. 751 86

Cytomegalovirus infection is usually reported in immunocompromised patients. In this study, 19 patients with cytomegalovirus (CMV) infection of the alimentary tract were reviewed, none of whom had acquired immunodeficiency syndrome. The patients' sex distribution was similar, and their ages ranged from 22 to 84 yr (mean = 61 yr). Only four patients had underlying diseases resulting in immunocompromise. The most common presentation was gastrointestinal bleeding, which occurred in 11 of the 19 patients (58%). Two patients had an unusual presentation of obstructive jaundice due to exuberant growth of granulation tissue at the ampulla of Vater. The majority of the lesions (n = 23) occurred in the large intestine and duodenum. Sixteen of these 23 lesions (69.6%) showed ulceration. Of these 16 lesions, six were diagnosed macroscopically as malignant by the endoscopists. It was observed histologically that a predominant epithelial distribution of the CMV inclusion bodies was associated with no or only mild inflammation, whereas a predominant endothelial distribution of the inclusion bodies was associated with ulcerative, severely inflamed lesions. From these observations, we conclude that ulceration probably is due to an ischemic process resulting from narrowing of capillary lumens by swollen endothelial cells affected by CMV infection. Concomitant infection by Candida species was found in only one patient. One patient had coexistent ulcerative colitis while another also suffered from graft-versus-host disease after bone marrow transplantation. In five of the eight cases with follow-up biopsies, the CMV inclusion bodies disappeared in subsequent biopsies. To conclude, a high degree of alertness is required for the histological diagnosis of unexpected CMV infection of the alimentary tract, in order to warrant correct treatment for the patients.
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PMID:Cytomegalovirus infection of the gastrointestinal tract in non-AIDS patients. 823 36

A13D8 is a monoclonal IgM antibody that identifies an as yet unknown antigen that is expressed intensely and ubiquitously in enterocytes. Immunohistochemically, it was shown that A13D8 has a granular supranuclear staining pattern in columnar epithelial cells of normal small intestine and the colon. In ulcerative colitis, this staining pattern was retained. However, during active inflammation, staining also was evident in goblet cells. To test whether this feature of goblet cell staining was unique to ulcerative colitis, tissue sections from a variety of colitides were examined. Crohn's disease, infectious colitis, and ischemic colitis had similar staining patterns to that seen with ulcerative colitis. There was significantly more inflammation in the biopsies from patients with ulcerative colitis and Crohn's disease with positive goblet cell staining than in the biopsies from those patients with negative goblet cell staining. Almost all positive goblet cell staining in ulcerative colitis and Crohn's disease occurred in biopsies that were actively inflamed, whereas there was rare staining in biopsies that were noninflamed (regardless of whether or not there was active inflammation elsewhere in the colon). Ileal goblet cells stained positively with A13D8 only in cases of active ileitis. In cases of collagenous colitis, with comparable degrees of inflammation to that seen in ulcerative colitis and Crohn's disease, there was rarely goblet cell staining and in graft-versus-host disease goblet cell staining of A13D8 was not observed. The binding of A13D8 to tissue sections was completely inhibited by N-acetyl-D-galactosamine. These results, in conjunction with immunochemical studies, suggest that the antibody recognizes an N-acetyl-D galactosamine-containing epitope on a glycoprotein(s). In conclusion, these data suggest that A13D8 recognizes a glycoprotein expressed by intestinal columnar epithelial cells and during specific inflammatory states, particularly those associated with a neutrophilic infiltrate, becomes evident in goblet cells. Further work is required to establish the exact nature of this molecule and whether it is a pro- or anti-inflammatory factor.
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PMID:The differential expression of a novel intestinal epithelial glycoprotein in various forms of inflammatory bowel disease. 870 31

Review of the medical records of 43 patients with common variable immunodeficiency (CVID) and 23 patients with X-linked agammaglobulinemia (XLAG) revealed a high incidence of chronic gastrointestinal complaints, most commonly diarrhea. Thirty-eight biopsies, four small-bowel resection specimens, and one autopsy from 10 patients with CVID and one patient with XLAG showed a wide range of abnormalities. A pattern resembling acute graft-versus-host disease, with apoptotic bodies and lymphocytes in crypts, was seen in the stomach (four patients), small bowel (three patients), and colon (three patients). Small-bowel specimens from three CVID patients with malabsorption showed mild to severe villous atrophy. Three CVID patients had Giardia in biopsies. Two cases of small bowel lymphoma associated with nodular lymphoid hyperplasia were identified in CVID patients. One patient's small bowel contained foamy histiocytes in the lamina propria, resembling Whipple's disease or chronic granulomatous disease, with numerous apoptotic bodies in crypts. Ultrastructurally, the histiocytes contained cellular debris. The patient with XLAG had recurrent fissuring necrosis of small bowel resembling Crohn's disease; a patient with CVID had colitis with features similar to ulcerative colitis. Poorly formed granulomas were seen in the stomach (one CVID patient) and the colon (two CVID patients). Lymphocyte populations were dominated by T cells; B cells were scarce except in lymphoid follicles in CVID patients with nodular lymphoid hyperplasia. Patients with CVID and XLAG manifest a spectrum of abnormalities in the gastrointestinal tract, with patterns superficially resembling graft-versus-host disease, inflammatory bowel disease, and Whipple's disease, but often lacking some of the diagnostic features of the diseases. Many of the CVID patients with chronic gastrointestinal complaints (62%) also had evidence of autoimmune phenomena, suggesting that in some patients the inflammatory process in the gastrointestinal tract has an autoimmune component.
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PMID:Gastrointestinal pathology in patients with common variable immunodeficiency and X-linked agammaglobulinemia. 882 31

The CD95 (APO-1/Fas) receptor mediates programmed cell death in apoptosis sensitive cells upon oligomerization either by CD95 antibody or by its natural ligand, CD95 ligand (CD95 L). Studies on tissue distribution have shown that CD95 is broadly expressed in normal adult tissues. Furthermore, the spectrum of CD95-expressing cells in inducibly enlarged in the context of chronic inflammation. In contrast, the number of cells capable of expressing CD95 L is strikingly limited to small subsets of lymphocytes and histiocytes and to some specialized normal epithelia. This suggests that cell death via this receptor/ligand system, although possible in almost every tissue and cell type, is limited to very special scenarios one of which is chronic lymphohistiocytic inflammation. The lpr/lpr mouse and the gld/gld mouse are well-known models for autoimmune disorders. Both mutants have abnormal B and T lymphocytes and high titers of autoantibodies. Recently, these mice have been discovered to have functional defects in the murine equivalents of human CD95 and CD95 L, respectively. This suggests that the CD95/CD95 L system might act by preventing autoimmune disease, e.g., by preventing emergence of autoreactive T and B lymphocytes. A human homologue of the lpr mutation has been described as autoimmune lymphoproliferative syndrome. We show that, in mice, CD95/ CD95 L might be operative in experimental graft versus host disease. Further, we suggest a role of this system in early steps of ulcerative colitis. Considering our observations against the background of current literature, CD95/CD95 L is likely to play a dual role in induction and maintenance of peripheral tolerance on the one hand and in tissue damage by chronic inflammation on the other.
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PMID:[CD95 (APO-1/Fas) and CD95-ligand (CD95L). Implications of these apoptosis mediating receptor/ligand systems in the pathogenesis of autoimmune diseases]. 906 94

A 37-year-old man with acute myeloblastic leukemia in first remission developed ulcerative colitis and bronchiolitis obliterans organizing pneumonia (BOOP) 7 months after bone marrow transplantation (BMT) from an HLA-matched brother who suffered from severe Crohn's disease. BOOP occurred 20 days after idiopathic interstitial pneumonia, in the context of severe ulcerative colitis. Lung and colon biopsies showed no signs of CMV infection or GVHD. The patient was treated with oral methylprednisolone 1 mg/kg/day and his clinical status and chest X-ray improved slowly. Remarkably, the symptoms of colitis also resolved with prednisone therapy and he is now symptom-free. We hypothesize that ulcerative colitis may have been transmitted from donor to recipient (adoptive autoimmunity) and that it was complicated by BOOP. However, other factors such as CMV may have contributed to the occurrence of BOOP.
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PMID:Bronchiolitis obliterans organizing pneumonia and ulcerative colitis after allogeneic bone marrow transplantation. 961 91

Graft versus host disease (GVHD) occurs in up to 75% of patients who have had an allogeneic bone marrow transplant (BMT). However, the pathophysiology of this disorder, including the mechanisms responsible for enhanced apoptosis, are poorly understood. Bcl-2 is a cellular protein known to inhibit apoptosis in a variety of human tissues. Therefore, the aim of this study was to evaluate the expression of Bcl-2 in colonic GVHD and to determine its relationship to cell proliferation and apoptosis in this disease. Routinely processed colonic mucosal biopsy specimens from 47 allogeneic BMT patients with diarrhea were evaluated histologically for the grade of GVHD (0-4) and for the degree of apoptosis (apoptosis index). Immunohistochemical staining for Bcl-2 and MIB-1, a cell proliferation marker, was performed, and the results were correlated with the histological findings and with each other. Normal-appearing colonic mucosal biopsy specimens from 10 age-matched patients with noncolonic diarrhea served as controls. Also evaluated were 13 colonic biopsy specimens from 13 patients with chronic ulcerative colitis (three inactive, four mild chronic-active, six moderately severe chronic active) to test the specificity of our findings. When compared with controls, a slight trend toward increased Bcl-2 expression was noted in patients with high-grade GVHD (grade 3 or 4) (P=.09). However, Bcl-2 expression did not correlate with the degree of apoptosis in these patients. In contrast, the degree of Bcl-2 staining correlated positively with the crypt proliferative rate (P=.04). Furthermore, crypt proliferation was significantly higher in the GVHD patients in comparison with controls (MIB-1 index, 27.7+/-17.1 v 15.6+/-11.4, =.02), and increased progressively with each successively higher grade of GVHD, and with the degree of apoptosis. Similar to GVHD, Bcl-2 expression was increased in biopsy specimens of CUC patients with higher grades of active injury and epithelial regeneration. This immunohistochemical study does not provide support for Bcl-2 in the pathogenesis of GVHD-induced apoptosis in the colon, but instead, indicates that this protein may play a nonspecific role in the generalized response to cellular injury in GVHD.
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PMID:Relationship of Bcl-2 expression with apoptosis and proliferation in colonic graft versus host disease. 971 31

Therapy of acute intestinal GVHD is still one of the main challenges after allogeneic transplantation. Increasing systemic immunosuppression (IS) is the first choice and includes corticosteroids and lymphocyte antibodies, often associated with severe side-effects. In inflammatory bowel diseases such as Crohn's disease and ulcerative colitis, topical steroid therapy is used very successfully. Because of the similarity between these and acute intestinal GVHD we conducted a trial with oral budesonide (Budenofalk), a new topically active glucocorticoid, to treat patients with acute GVHD > or = grade II. After a diagnosis of aGVHD > or = grade II, 22 patients received increased IS, mainly systemic corticosteroids, and additionally budesonide 9 mg/day divided into three doses. Improvement in aGVHD, infectious side-effects, reduction of systemic IS and outcome were documented. Results were compared with the results of 19 control patients, who were treated only by increasing IS dose. In 17/22 patients (70%), treated with budesonide, the acute intestinal GVHD resolved and no relapse occurred after decreasing the systemic IS, while continuing budesonide. In only 8/19 patients in the control group did the acute intestinal GVHD resolve and 2/8 patients had a relapse of intestinal GVHD after decreasing IS, with an overall response of 33%. No severe intestinal infections occurred. We conclude that budesonide may be effective in acute intestinal GVHD as a topical corticosteroid and prospective, randomized studies should demonstrate its efficacy in allowing reduction of systemic immunosuppressive therapy, and its side-effects.
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PMID:Feasibility and response to budesonide as topical corticosteroid therapy for acute intestinal GVHD. 1064 6


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