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)

For characterization of histopathological changes during pancreas graft rejection, pancreaticoduodenal transplants were performed in three groups: (1) Brown Norway into diabetic Lewis rats without immunosuppression, (2) Brown Norway into diabetic Lewis rats with cyclosporin A, and (3) Lewis into Lewis rats. Diffuse inflammatory infiltration of the acini by mononuclear cells indicated the onset of rejection (stage I). Shortly after acinar infiltration, damage to small and large interlobular excretion ducts occurred. This took the form of florid circumferential inflammation and vacuolar degeneration of epithelium similar to the bile duct damage seen in primary biliary cirrhosis, graft-versus-host disease, and liver allograft rejection (stage II). Thereafter, endothelialitis and destruction of islets were evident, consistent with a more advanced and irreversible stage of rejection (stage III). Acinar inflammation and moderate duct lesions were not prevented by immunosuppression but were delayed. Nonetheless, severe vascular changes and loss of islets were avoided. We conclude that duct lesions are a reliable criterion for pancreas allograft rejection. They are more sensitive than vascular changes and more specific than cellular infiltration of acinar tissue, which may also occur in infection.
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PMID:Histological features of acute pancreatic allograft rejection after pancreaticoduodenal transplantation in the rat. 178 60

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

In primary biliary cirrhosis, chronic graft-versus-host disease, and chronic liver transplant rejection, immunologic mechanisms appear to cause destruction of intrahepatic bile ducts and consequently may lead to liver failure. Understanding those mechanisms may lead to improved therapy. Recent findings and clinically relevant concepts are discussed.
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PMID:Disappearing bile ducts: immunologic mechanisms. 211 31

This paper reviews cholestatic liver diseases which are characterized by disappearance of the intrahepatic bile ducts ("vanishing bile duct" diseases). In neonates and children, the most important entities are extrahepatic bile duct atresia and paucity of intrahepatic bile ducts, including syndromatic and nonsyndromatic varieties. Immunological mechanisms play a role in the bile duct obstruction observed in primary biliary cirrhosis, graft-versus-host disease and chronic liver transplant rejection, and possibly also in primary sclerosing cholangitis and sarcoidosis with chronic intrahepatic cholestasis. Idiopathic adulthood ductopenia represents a newly defined entity, the nature of which remains unclear. Mention is made of recently reported forms of intrahepatic bile duct destruction due to toxins and drugs (iatrogenic cholangiopathies). New insight into the pathogenesis of these diseases has been brought about by progress in immunology, imaging techniques of the liver and hepatobiliary surgery.
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PMID:Destructive intrahepatic bile duct diseases. 225 46

We report a case of lichen planus associated with an active chronic hepatitis. The relationship between lichen planus and chronic hepatic disorders (chronic hepatitis, primary biliary cirrhosis) is discussed. Physiopathologic similarities with chronic graft-versus-host disease are emphasized.
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PMID:[Oral erosive lichen planus: think of chronic liver disease]. 238 3

Diseases with disappearing intrahepatic bile ducts may be developmental, immunological, infective, vascular, or chemical in origin. The immunological group includes primary biliary cirrhosis, graft-versus-host disease, and sarcoidosis. HLA class 2 antigens are displayed on the bileducts and recognition of biliary antigens by cytotoxic T-cells leads to destruction of interlobular ducts. Primary sclerosing cholangitis is associated with immunological features, but the hepatic histology is not that of immunological duct disease. The association with immunodeficiency syndromes, and the finding that secondary sclerosing cholangitis may occur in patients with the acquired immunodeficiency syndrome who are infected with cytomegalovirus, suggest that primary sclerosing cholangitis might be infective in origin. In bacterial cholangitis there is contiguity between the biliary system and the intestinal tract and usually, but not necessarily, partial biliary obstruction. Interference with the hepatic arterial supply to the bileducts leads to vascular cholangitis. Chemical cholangitis follows injection of scolicidal agents into the biliary tree. Diseases with disappearing bileducts have a long natural history and hepatocellular failure occurs late. In the late stages hepatic transplantation gives good results.
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PMID:The syndrome of disappearing intrahepatic bile ducts. 288 86

Expression of beta 2-microglobulin, a reliable marker of HLA Class I, on the interlobular bile ducts (bile ducts) was surveyed using an immunoperoxidase method in paraffin sections of specimens from patients with a variety of hepatobiliary diseases. Normal bile ducts showed negativity or weak cytoplasmic positivity in normal as well as diseased livers. On the other hand, abnormal bile ducts showing degenerative or proliferative changes in primary biliary cirrhosis and graft-versus-host disease revealed enhanced expression of this protein, suggesting that these damaged bile ducts might be more susceptible to T cell-mediated immune attack in these immunologic diseases. However, enhanced expression of this protein was also similarly found on abnormal bile ducts in several nonimmunologic biliary diseases including extrahepatic biliary obstruction. Enhanced expression of this protein on the interlobular bile ducts may therefore be an epiphenomenon secondary to different primary pathologic events in the biliary tree, such as immunologic and nonimmunologic processes.
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PMID:Expression of beta 2-microglobulin on interlobular bile ducts in primary biliary cirrhosis and other hepatobiliary diseases. 305 7

We studied the expression of major histocompatibility complex (MHC) class II antigens in liver biopsies taken from ten patients with clinical and biochemical evidence of liver damage after bone marrow transplantation. In all six patients who had histologically confirmed graft-versus-host disease, MHC class II antigens were detected on intrahepatic bile ducts. In four patients with no histological features of graft-versus-host disease, MHC class II antigens were not detected. In controls, a positive reaction for bile duct MHC class II antigens was only detected in the patients with primary biliary cirrhosis. Characterisation of the lymphocytes surrounding the bile ducts showed a prevalence of Leu 3+ cells in graft-versus-host disease and primary biliary cirrhosis. We propose that the aberrant expression of class II antigens on bile duct epithelium cells may play a role in the pathogenesis of graft-versus-host disease. A similar pattern in primary biliary cirrhosis may suggest a common pathogenetic mechanism.
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PMID:Expression of major histocompatibility complex class II antigens on bile duct epithelium in patients with hepatic graft-versus-host disease after bone marrow transplantation. 332 Jan 79

A 50-year-old female with primary biliary cirrhosis associated with generalized morphea is reported. She had suffered from multiple painful indurated plaques on the trunk which was diagnosed as generalized morphea; subsequently, primary biliary cirrhosis was diagnosed on the basis of her hepatic dysfunction. Although progressive systemic sclerosis has been reported to occur in patients with primary biliary cirrhosis, this localized form of cutaneous sclerosis has not previously been reported. Since generalized morphea is one of the most common manifestations of chronic graft-versus-host disease, and primary biliary cirrhosis is known to have a hepatic histology resembling chronic graft-versus-host disease, this case report may represent evidence in support of a common pathogenesis for the two entities.
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PMID:A case of primary biliary cirrhosis associated with generalized morphea. 380 74

Recognition by biopsy of liver allograft rejection has been less successful than diagnosis of rejection of cardiac and kidney allografts. In a study of 138 failed liver allografts, we recognized damage to small interlobular bile ducts by lymphocytes as the most useful indicator of the presence of rejection. This is a report of the electron microscopic features of three patients with unequivocal allograft rejection. Lymphocytes and occasional granulocytes penetrated the epithelia of interlobular bile ducts. Ducts with diameters of 30 to 60 microM were preferentially affected but ducts up to 120 microM were also occasionally involved. Point contacts between infiltrating inflammatory cells and bile duct epithelial cells were observed occasionally. Degenerative changes of bile duct epithelial cells were conspicuous and involved nuclei and cellular organelles. Degeneration was often accompanied by aggregation of dense bundles of filaments in the cytoplasm. In severely affected ducts, epithelial cell disintegration was noted. In all involved bile ducts, the basement membrane was markedly thickened. Hepatocytes were well-preserved but contained lipid vacuoles, pigment granules, and blunted canalicular microvilli. The similarity between these observations and those seen in primary biliary cirrhosis and chronic graft-versus-host disease is striking.
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PMID:Electron microscopy of rejected human liver allografts. 390 59


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