Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-two patients with previous hepatic compromise who underwent allogeneic bone marrow transplant (BMT) for treatment of hematologic malignancy or other hematologic disease between 1984 and 1990 were chosen for the present study. After transplant, 19 (86.4%) of the patients developed hepatitis, including six cases (27.3%) of acute hepatitis, 12 (54.6%) of chronic hepatitis and one uncharacterized hepatitis. Nine chronic hepatitis patients were followed-up for 7-56.5 months (medium 35.5 months) with biochemistry studies and ultrasonography. Throughout the observation period, liver cirrhosis or hepatoma were not detected and no patients developed veno-occlusive disease. Furthermore patients who developed hepatitis after transplant had worse prognoses. Based on serial serological survey of the various hepatitis B virus (HBV) antigens and antibodies, we have found that most of the recurrent viral hepatitis in transplant patients could be attributed to the reactivation of the virus. In addition, the use of immunosuppressive drugs, persisting infection by HCV and the development of graft-versus-host disease may also play a role in modulating the course of viral hepatitis in BMT patients.
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PMID:Liver disease in patients with liver dysfunction prior to bone marrow transplantation. 162 24

The now common practice of joint kidney and pancreas or heart or lung transplantation is being completed by other combinations. This is shown by our case of en bloc liver-pancreas-stomach-duodenum-small bowel transplantation in an 18-month-old infant with small bowen atresia complicated by biliary cirrhosis secondary to total parenteral feeding, after the failure of an intraperitoneal visceral transplant at 1 year of age. The graft was taken from an 8-year-old donor and was not pretreated. Being made of the whole intraperitoneal visceral mass, it had to be adapted to the recipient's size by ex vivo exeresis of the right liver, of the spleen, of the terminal ileon and of the colon. Following intraperitoneal visceral exenteration in the recipient, the graft was inserted in an orthoptic position with a digestive reconstruction by esogastric anastomosis and terminal ileostomy. Immunosuppression combined steroids, azathioprine, ciclosporine, and the biological and immunological follow-up regarded the hepatic and pancreatic functions. The intestinal graft was controlled by repeated biopsies through the stomy. Rectal biopsies and lymphocyte typing in the peripheral blood allowed watching for the occurrence of a possible graft-versus-host disease. The outcome was marked by the persistence of massive lymphorrhea during three months and severe central neurological disorders caused by the difficulties to adapt the level of ciclosporine. The hepatic and pancreatic functions became normal within a few days, and the intestinal function allowed progressively suppressing parenteral feeding.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[En bloc transplantation of liver, stomach, pancreas and small intestine in an infant. Apropos of a case]. 184 19

Intralobular changes of the liver in experimental graft-versus-host disease (GVHD) across minor histocompatibility barriers were investigated for up to 14 months after bone marrow transplantation. Sinusoidal lymphocyte infiltration, and necrosis and degeneration of hepatocytes were evident by day 4 and reached a maximum level at 2 weeks after transplantation, then gradually decreased, but they persisted during the entire period of observation, indicating that more or less hepatocyte injury may persist continuously in hepatic GVHD. Piecemeal necrosis was transiently observed around 2 weeks after transplantation, in parallel with the peak of lymphocyte infiltration into the portal area. Similarly, central vein endothelialitis (attachment of lymphocytes to endothelial cells) was transiently observed with a peak activity at 2 weeks after transplantation. Mild centrilobular and portal fibroplasia were evident by 2 weeks after transplantation, but they hardly progressed and no cases developed liver cirrhosis. Frequently lymphocytes were found located beneath endothelial cells and attached to hepatocytes. Ultrastructural observation revealed that sinusoidal lymphocytes were occasionally in contact with endothelial cells by means of cytoplasmic pseudopods. Also lymphocytes were frequently in close contact with hepatocyte plasma membranes over short distances. Lymphocytes occasionally accompanied other inflammatory cells, such as eosinophilic leukocytes and mononuclear phagocytic cells. Hepatocytes in close contact with lymphocyte and other inflammatory cells showed a varying degree of degenerative changes, including condensation of cytoplasm and nucleus with irregular nuclear contours, dilatation of endoplasmic reticulum and mitochondria, formation of cytoplasmic vacuoles, and loss of microvilli.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Histological changes of the liver in experimental graft-versus-host disease across minor histocompatibility barriers. V. A light and electron microscopic study of the intralobular changes. 188 59

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

A 9-yr-old white girl with acute monoblastic leukemia received an HLA-identical, mixed lymphocyte culture-nonreactive bone marrow transplant from her sister. Twelve days after the transplant, a diffuse, pruritic, maculopapular rash involving the entire body surface (including the palms and soles) developed. Subsequent skin biopsy was consistent with cutaneous graft-versus-host disease, and biopsy-proven hepatic involvement manifested by severe, unremitting cholestatic jaundice soon followed. The patient's biliary status as monitored by serial liver biopsies demonstrated progression from chronic graft-versus-host disease to cirrhosis, culminating in death secondary to liver failure 25 mo after transplant.
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PMID:Secondary biliary cirrhosis as a consequence of graft-versus-host disease. 229 82

Neopterin is a pyrazino-pyrimidine compound which is biosynthesized by macrophages. Increased concentrations of neopterin have been reported in conditions causing stimulation of cellular immunity, such as viral and other infections, graft versus host disease, autoimmune diseases and different malignancies. Recently, increased urinary neopterin levels have been found in patients with acute viral hepatitis and NANB chronic hepatitis. In the present study, neopterin serum levels were measured in 23 cirrhotic patients (6 HBV related, 7 alcoholic and 10 cryptogenetic cirrhosis) and in 24 normal subjects. Mean values of serum neopterin were statistically increased in cirrhotics (3.92 +/- 3.28 ng/mL versus 1.24 +/- 0.51 ng/mL in controls, p less than 0.01). Serum neopterin values were not statistically different either in cirrhotics assessed in three different classes according to Child's classification or in cirrhotics with or without serological findings of active disease. In fact, in cirrhotic patients, serum neopterin levels did not correlate with serum aspartate and alanine aminotransferases, alkaline phosphatase, gamma-glutamyltransferase and gammaglobulins values. These data show that increased levels of serum neopterin occur in cirrhotic patients, but there is no relation between serum neopterin values and the histological activity or the clinical severity of the disease. The results are consistent with the hypothesis that activated macrophages are involved in all forms and in all stages of liver cirrhosis.
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PMID:[Blood levels of neopterin in patients with liver cirrhosis]. 248 6

Neopterin is a pyrazino-pyrimidine compound which is biosynthesized by macrophages. Increased concentrations of neopterin have been reported in conditions causing a stimulation of cellular immunity, such as viral and other infections, graft versus host disease, autoimmune disease and different malignancies. Recently, urinary neopterin levels have been found increased in patients with acute viral hepatitis and NANB chronic hepatitis. In the present study, neopterin serum levels have been measured in 23 cirrhotic patients (6 HBV related, and 17 cryptogenetic cirrhosis, 7 of them occurring in alcoholic subjects) and in 24 normal subjects. Mean values of serum neopterin were significantly increased in cirrhotics (3.92 +/- 3.28 ng/ml versus 1.24 +/- 0.51 ng/ml in controls, p less than 0.01). Serum neopterin values were not found to be significantly different in cirrhotics assessed in three different clinical classes according to Child's classification and in cirrhotics with and without serological findings of active disease. In fact, in cirrhotic patients, serum neopterin levels did not correlate with the values of serum AST, ALT, ALP, GGT and gamma-globulin. These data show that increased levels of serum neopterin occur in cirrhotic patients, but there is no relation between serum neopterin values and the activity or the clinical severity of the disease. The results are consistent with the hypothesis that activated macrophages are involved in all stages of liver cirrhosis irrespective of its aetiology.
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PMID:Serum neopterin levels in liver cirrhosis. 263 48

Graft-versus-host disease (GVHD) across minor histocompatibility antigens was developed in mice and the bile duct lesions were surveyed for up to 7.5 months after spleen and bone marrow cell transplantation. Lymphoid cell infiltration was evident by day 3, reached maximum at 2 weeks, then reduced gradually and persisted during the observation period. Fibrous expansion of the portal tracts paralleled with the time after transplantation, but none of the cases progressed into liver cirrhosis. The infiltrates abutted the interlobular and septal bile ducts and distorted their appearance with a frequent infiltration of mononuclear lymphoid cells into the duct epithelial layer. The duct epithelium showed a variety of degenerative and hyperplastic changes, including nuclear enlargement with anisonucleosis, nuclear pyknosis, cytoplasmic and nuclear darkness, cytoplasmic vacuolization, focal epithelial dropout, formation of apoptotic bodies, and micropapillary infolding. Disappearance of the bile ducts and formation of granuloma around the bile ducts were not seen. Immunocytochemical study revealed the exclusive preponderance of helper/inducer T cells in the portal infiltrates and marked expression of I-A antigen on the bile duct epithelium in GVHD mice. These results suggest that immunological mechanisms by helper/inducer T cells against minor histocompatibility antigen on bile duct epithelium in association with class II molecules of MHC are important in the pathogenesis of the bile duct lesions. A putative role of such lymphocytes is discussed.
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PMID:Histological changes of bile duct in experimental graft-versus-host disease across minor histocompatibility barriers. I. Light microscopic and immunocytochemical observations. 330 87

A 28-yr-old woman with severe idiopathic aplastic anemia received an HLA-identical mixed lymphocyte culture nonreactive bone marrow transplant from her brother. In the months after successful engraftment, she developed cutaneous and hepatic graft-versus-host disease, associated with marked cholestatic jaundice. Despite a series of therapeutic maneuvers, cholestasis persisted but remained relatively stable over the ensuing 10 yr. However, serial liver biopsies revealed progressive biliary-type fibrosis culminating in cirrhosis. Subsequently, her clinical course deteriorated and she developed signs of hepatic failure, and ultimately died 10.5 yr after bone marrow transplantation. The evolution of chronic graft-versus-host disease to cirrhosis may be a limiting factor in the long-term survival of this group of bone marrow transplant recipients. The lack of correlation between the stable clinical or biochemical indices and the progressive hepatic disease underscores the need for sequential liver biopsies in patients with sustained liver function abnormalities after bone marrow transplantation.
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PMID:Cirrhosis as a consequence of graft-versus-host disease. 353 93

To investigate the causes of impaired liver function (LF)* after BMT, 88 patients were included for analysis of hepatitis B virus (HBV) and hepatitis C virus (HCV) infections, transplant methods, preconditioning regimens, and graft-versus-host disease (GVHD). Fifty of them (56.8%) developed abnormal LF after BMT and among them, 29 (32.9%) developed chronic hepatitis (CH). By univariate analysis, HCV infection, pretransplant abnormal LF, allogeneic BMT, and preconditioning regimen with total body irradiation were all significantly related to higher incidence of post-BMT impaired LF. However, only HCV infection, pretransplant abnormal LF, and acute GVHD were associated with higher incidence of CH. By multivariate logistic regression analysis, HCV infection and pretransplant abnormal LF were the two most significant interpreters for abnormal LF, especially for CH (odds ratios: 7.86 and 4.735, respectively) after BMT. Although the incidence of abnormal LF was found high in this study, there was no significant disadvantage in terms of survival for patients who developed abnormal acute and chronic liver function after BMT. However, a long-term follow-up is needed to evaluate survival pathology of CH, such as liver cirrhosis and hepatoma.
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PMID:Liver disease after bone marrow transplantation--the Taiwan experience. 773 60


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