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)

We report the case of a 6.5-year-old male who received an unrelated orthotopic liver transplant for hepatic failure and encephalopathy following non-A-non-B hepatitis and subsequently developed severe aplastic anemia. For treatment of his aplastic anemia, he received a successful marrow transplant from his 9-year-old genotypically HLA-identical sister following conditioning with cyclophosphamide 200 mg/kg and anti-thymocyte globulin 90 mg/kg. Significant veno-occlusive disease of the liver and graft-versus-host disease did not occur. The patient remains alive without clinical chronic active hepatitis or need for blood product therapy. His hematocrit is 36%, white blood cell count 9.7 x 10(3)/mm3, and platelet count 1.7 x 10(5)/mm3 almost 2 years after marrow transplantation.
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PMID:Successful allogeneic bone marrow transplantation in a 6.5-year-old male for severe aplastic anemia complicating orthotopic liver transplantation for fulminant non-A-non-B hepatitis. 190 74

An attachment of lymphocytes to the vascular wall, a feature called "endothelialitis" (ETL) or "endotheliitis", was investigated in various liver biopsies, including acute hepatitis (AH), hepatic infectious mononucleosis (IM), drug-induced hepatitis, alcoholic hepatitis and fibrosis, chronic persistent hepatitis (CPH), chronic active hepatitis (CAH), liver cirrhosis (LC), primary biliary cirrhosis (PBC), nonspecific reactive hepatitis (NSRH), and cases with a variety of diseases having almost normal liver histology as control material. Although ETL has been considered to be nearly pathognomic of graft-versus-host disease (GVHD) and acute transplant rejection, ETL was found in both portal and central veins with a variable incidence, not only in all categories of liver diseases, but also in the control group. The incidence of central vein ETL was significantly higher in AH, CAH, PBC, IM, alcoholic fibrosis, and NSRH than that of the control group, and that of portal vein ETL was significantly higher in AH, CPH, CAH, LC, PBC, IM, and alcoholic fibrosis. Even under the light microscope, lymphocytes attached to the endothelial cells had irregular cytoplasmic processes making contact with endothelial cells. Also lymphocytes located beneath the endothelial lining were frequently found. When ETL-positive and -negative cases in the same category were compared, the levels of serum glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) were usually higher in the ETL-positive group, and statistically significant differences were observed in CPH, CAH, LC, PBC and NSRH. In chronic hepatitis, the occurrence of portal vein ETL paralleled the histologic activity of portal inflammation, whereas central vein endothelialitis was associated with active parenchymal inflammation such as sinusoidal lymphocyte infiltration and spotty hepatocyte necrosis, indicating that ETL may be a phenomenon more frequently associated with active hepatic inflammation. Immunohistochemical observations revealed that about 70% of lymphocytes attached to the endothelial cells were T cells, while about 10% were B cells. These data indicate that ETL in the liver is not specifically pathognomonic for GVHD and rejection of liver transplants, and is universally found in a variety of liver diseases with a varying incidence and activity, related to the activity of hepatic inflammation, portal vein ETL occurring in relation to active portal inflammation and central vein ETL to parenchymal inflammation. Thus ETL is considered to be an intimate T lymphocyte-endothelial cell interaction universally associated with active hepatic inflammation; it may be an important phenomenon leading to accumulation of cellular exudates and their reaction at the site of antigen in the tissue.
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PMID:Clinicopathological study of lymphocyte attachment to endothelial cells (endothelialitis) in various liver diseases. 205 5

We have studied five long-term survivors of allogeneic bone marrow transplantation. All exhibited prolonged serum biochemical evidence of hepatic dysfunction during 2- to 5-year periods of follow-up. Two patients developed chronic cholestasis without pruritus. The serum of a third patient became chronically positive for HBsAg. A fourth patient developed an acute hepatic syndrome and high titers of antibody to cytomegalovirus. Nuclear, mitochondrial, and smooth muscle antibodies were not detected. Seven liver biopsies, obtained from three of the patients, all revealed a hepatocellular necroinflammatory lesion suggestive of chronic active hepatitis, a paucity of interlobular bile ducts, and intrahepatic cholestasis. Possible etiologies for these hepatic changes include reactivation of chronic non-A, non-B hepatitis and chronic graft-versus-host disease per se. Our study emphasizes the diagnostic problems posed by hepatic dysfunction occurring in an immunosuppressed multiply-transfused patient after bone marrow transplantation.
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PMID:The liver in long-term survivors of marrow transplant--chronic graft-versus-host disease. 674 58

We report the case of a 44-year-old male who relapsed in accelerated phase chronic myeloid leukemia 10 years after a successful bone marrow transplantation from his HLA-identical brother, and 3 years after 12 months treatment with interferon-alpha (IFN-alpha) for chronic active hepatitis C (CAH). The patient was infused with G-CSF-primed peripheral blood cells (PBSC) from the original bone marrow donor and a full donor reconstitution, with no detectable molecular disease, was obtained within 4 months without clinical aplasia or GVHD, nor help from other forms of chemotherapy or use of biological response modifiers. We speculate that IFN-alpha for CAH delayed the onset of a clinical recurrence of chronic myeloid leukemia and that in advanced disease PBSCs can provide an advantageous alternative to donor lymphocyte infusion (DLI).
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PMID:Relapsed chronic myeloid leukemia in accelerated phase 10 years after allogeneic bone marrow transplantation: full chimera reconversion with donor peripheral blood stem cells infusion. 975 51

Our two patients undergoing allogeneic bone marrow transplantation (AlloBMT) had both Hepatitis B virus (HBV) and graft-versus-host disease (GVHD). In the first patient, liver enzymes elevated three months after AlloBMT, and GVHD was diagnosed. Two weeks after the diagnosis of GVHD, HBsAg appeared in his serum. At that time, liver biopsy was not able to discriminate two disorders, but his sequential liver biopsies disclosed GVHD. Despite the patient was treated with cyclosporin A (CsA), he died for chronic GVHD. In contrast to the first patient, the second patient had HBsAg prior to GVHD. His liver enzymes deterioration was detected in the first month after AlloBMT, and reached the highest level in the third month while withdrawing CsA. In the fifth month he developed scleradermatous skin changes, and skin biopsy revealed chronic GVHD, whereas concurrent liver biopsy revealed chronic active hepatitis. This observation showed that immunosuppressive conditions such as GVHD or its prophylaxis may affect the appearance of liver pathology caused by HBV, which depends on the time of GVHD development, and the duration and depth of GVHD prophylaxis.
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PMID:Differences in liver pathology and clinical outcome between two patients with hepatitis B virus and graft versus host disease. 1049 Oct 23