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

Four children with acute lymphoblastic leukaemia had autologous bone marrow (BM) or peripheral stem cell (PSC) transplantation with low dose of cyclosporine (CsA, img/kg/d i.v. during the first 28 d) to induce an autologous GVHD (auto-GVHD). Two children did not have clinical auto-GVHD and they relapsed 3 and 4 months after treatment. The 2 other children had clinical signs of auto-GVHD (grade I and grade II); they both are in complete remission but after a first normal haematological recovery they had a prolonged period of aplasia until month 9 for 1 patient and still persistent at month 7 in the other case. We studied lymphocyte subsets reconstitution after transplantation in these patients. All patients had an important decrease in the CD4/CD8 ratio related both to a strong decrease in the CD4+ cells and a strong increase in the CD8+ cells. Most of the CD8+ cells were of the CD8bright+ CD28- phenotype. These CD8bright+ CD28- T-cells represented from 33% to 68% of the total lymphocytes. We discuss the role of these cells after autologous transplantation with CsA, and wonder if these cells could mediate cytotoxicity. In conclusion, among 4 children who received autologous BM or PBC transplantation with low dose of CsA, we observed a complete remission after an auto-GVHD and a prolonged period of aplasia in 2 patients and a relapse of leukaemia in 2 other patients. All these 4 patients had an increase in the CD8bright+ CD28- T lymphocytes.
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PMID:Strong increase in the percentage of the CD8bright+ CD28- T-cells and delayed engraftment associated with cyclosporine-induced autologous GVHD. 859 29

Primary biliary cirrhosis (PBC) and graft-versus-host disease (GVHD) are thought to have common immunopathologic features and previous studies have reported that 5.2 to 81% of patients with chronic GVHD after allogeneic hematopoietic cell transplant have antimitochondrial antibodies (AMA). We studied a total of 89 patients with chronic GVHD and 60 controls for AMA reactivity by ELISA and immunoblotting using recombinant PDC-E2, BCOADC-E2, and OGDC-E2, immunoblotting of beef heart mitochondrial proteins, and reactivity to nuclei, smooth muscle (ASMA), ribonucleoprotein JO-1, extractable nuclear antigen, nuclear proteins SSA/ SSB, ribonucleic P proteinase III, cardiolipin (ACA), liver kidney microsomal, thyroid microsomal, myeloperoxidase, and the reactivity of rheumatoid factor. A subset of 60 chronic GVHD sera were tested for reactivity to gp210 and LBR. Finally, liver tissue from patients with chronic GVHD and PBC was studied by immunohistochemistry to determine whether there was comparable abnormal apical staining of biliary epithelial cells using PDC-E2-specific monoclonal antibodies. Surprisingly, there were no AMA found in the sera from the 89 patients with chronic GVHD. Review of published data on AMA in GVHD suggests that previous results were primarily false positives. In contrast, sera from the patients with GVHD did have a variety of other autoantibodies and, in particular, 20/89 (22.4%) positive ANA, 23/89 (25.8%) positive ASMA, and 9/89 (10.1%) positive ACA. The other autoantibodies assayed were not statistically different from controls. Finally, abnormal biliary epithelial luminal staining of bile ducts was found, as expected, in liver tissue of patients with PBC but was absent in chronic GVHD.
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PMID:Autoantibodies in human chronic graft-versus-host disease after hematopoietic cell transplantation. 1021 61

UDCA exerts its beneficial effect in liver diseases through a diverse, probably, complementary array of mechanisms. The clinical use and efficacy of UDCA in PBC have been evident. UDCA may also have a place in the management of PSC, ICP, cystic fibrosis, PFIC and GVHD involving the liver, although, more studies are needed to further determine its therapeutic potential in these diseases and in other hepatobiliary disorders such as liver allograft rejection, drug and TPN-induced cholestasis, NASH, and alcoholic liver disease.
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PMID:Ursodeoxycholic acid 'mechanisms of action and clinical use in hepatobiliary disorders'. 1149 32

The morbidity and mortality from chronic biliary diseases (i.e., the cholangiopathies) remains substantial. End-stage liver disease from biliary causes of cirrhosis (e.g., primary biliary cirrhosis [PBC], and primary sclerosing cholangitis) account for approximately one third of patients referred for liver transplantation. A single-topic conference sponsored by the American Association for the Studies of Liver Diseases entitled "The Pathobiology of Biliary Epithelia" brought together investigators to review the status of the field of cholangiocyte pathobiology, identify new areas of interest, and propose future directions. This information was presented in 6 sessions: "Structural and Functional Characteristics of the Bile Duct System," "Biological Topics from Nonbiliary Epithelia," "Malignant Transformation of Cholangiocytes," "Cholangiocyte Proliferation and Death," "Transport Mechanisms in Bile Duct Epithelia," and "Pathobiology of Biliary Epithelia." In the 7 years since the first symposium on this topic, major advances have been made in our understanding of ductal bile formation, including, greater insight into the hormones, intracellular signaling mechanisms, and effector proteins responsible for bile secretion and absorption. More sophisticated imaging technologies have increased our understanding of the polarity of cholangiocytes, their embryology and ultrastructural anatomy, and in vivo human secretory responses to current medical therapy. Information on mediators of inflammation permeated many sessions, having potentially important roles in malignant transformation of cholangiocytes, cholangiocyte apoptosis, fluid and electrolyte transport, and have begun to be specifically characterized for certain biliary diseases, e.g., acquired immunodeficiency syndrome (AIDS) cholangiopathy and graft-versus-host disease (GVHD).
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PMID:The pathobiology of biliary epithelia. 1198 76