Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From 1984 to 1991, 514 patients were treated by BMT in 1 center. 254 patients survived more than 3 months and, in 38 patients, 47 liver biopsies were performed for chronic liver dysfunction characterized by cholestasis. The aim of the present study was to evaluate the possible causes of liver disease at the time of biopsy. One clinician analyzed clinical data and was able to propose up to 3 diagnoses including GVHD, viral hepatitis, drug-related hepatitis, chronic veno-occlusive disease (VOD) or other. Two pathologists reviewed histologic sections and were also able to propose up to 3 diagnoses. Clinically, 1, 2 or 3 diagnoses were proposed in 30, 60 and 10% of cases, respectively. Pathologically, 1, 2 or 3 diagnoses were proposed in 13, 62 and 25%, respectively. Histologic changes of GVHD were present in 40 of 47 biopsies and concordance between the clinician and the pathologists on the presence of GVHD lesions was found in 77% of biopsies. Viral hepatitis was proposed 22 times by the clinician and 19 times by pathologists. Viral hepatitis, usually hepatitis C, was associated with GVHD in 16 cases. Diagnoses of chronic VOD and drug-related hepatitis were proposed less often. In summary, more than 1 diagnosis was suggested for many of the patients studied, GVHD being the most frequent. The simultaneous presence of GVHD, viral diseases, chronic VOD and drug-induced diseases could explain the high incidence of cholestasis in the long-term post-BMT.
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PMID:Chronic cholestasis in patients after allogeneic bone marrow transplantation: several diseases are often associated. 758 Nov 45

Autologous bone marrow transplantation (AuBMT) is an accepted treatment modality for patients with high-risk or relapsed hematological malignancies. Hepatotoxicity, in particular veno-occlusive disease (VOD), is a significant complication of this therapy. The purpose of this study was to determine the clinical relevance of abnormal liver function in the patients who received high-dose cytotoxic therapy and AuBMT for hematological malignancies at Memorial Sloan Kettering Cancer Center. Medical records of 180 consecutive patients between 1984 and 1991 treated with cytotoxic chemotherapy and AuBMT for acute myelogenous leukemia, non-Hodgkin's lymphoma, and Hodgkin's disease were reviewed. Forty-six patients (26%) developed jaundice with bilirubin > 4 mg/dl. These patients had a 43% toxic death rate compared to an 11% toxic death rate in patients with lower bilirubins (p < 0.001). The main etiology of hyperbilirubinemia was VOD of the liver noted in 22 of the 180 patients (12%). Other etiologies of jaundice included hepatitis, sepsis with multiorgan dysfunction, cholecystitis, and recurrent disease. Hyperbilirubinemia of various etiologies is a significant complication of AuBMT. Several new strategies are under investigation to decrease the toxicity of intensive therapy.
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PMID:Abnormal liver function in patients undergoing autologous bone marrow transplantation for hematological malignancies. 762 20

Radiation-induced liver disease (RILD), often called radiation hepatitis, is a syndrome characterized by the development of anicteric ascites approximately 2 weeks to 4 months after hepatic irradiation. There has been a renewed interest in hepatic irradiation because of two significant advances in cancer treatment: three dimensional radiation therapy treatment planning and bone marrow transplantation using total body irradiation. RILD resulting from liver radiation can usually be distinguished clinically from that resulting from the preparative regime associated with bone marrow transplantation. However, both syndromes demonstrate the same pathological lesion: veno-occlusive disease. Recent evidence suggests that elevated transforming growth factor beta levels may play a role in the development of veno-occlusive disease. Three dimensional treatment planning offers the potential to determine the radiation dose and volume dependence of RILD, permitting the safe delivery of high doses of radiation to parts of the liver. The chief therapy for RILD is diuretics, although some advocate steroids for severe cases. The characteristics of RILD permit the development of a grading system modeled after the NCI Acute Common Toxicity Criteria, which incorporates standard criteria of hepatic dysfunction.
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PMID:Hepatic toxicity resulting from cancer treatment. 771 85

High-dose radiation therapy for liver metastases of gastrointestinal malignancies might be improved by combining external-beam irradiation and radioimmunoglobulin therapy. We studied the liver toxicity of the proposed combination in healthy beagle dogs. A total dose of 30 Gy to the whole liver, delivered in 2-Gy fractions over 3 weeks, resulted in mild, temporary veno-occlusive disease (VOD) in three of three dogs. Reversible bone marrow damage was noted after two intravenous injections of 18.5 MBq of yttrium-90-labeled monoclonal antibody ZCE025 per kg body weight in three of three dogs. Administrations of the antibody were separated by 1 week. Three dogs treated by irradiation of the liver with radioimmunoglobulin therapy added during the last 2 weeks of the irradiation showed signs of radiation hepatitis (VOD) starting around 35 days after treatment. One dog had a complete recovery, and two dogs were euthanized in a stage of terminal liver failure around day 90 after treatment. Temporary bone marrow damage was observed after the combined treatment, similar to the bone marrow damage observed after radioimmunoglobulin therapy alone. Earlier studies in the same dog model showed that bone marrow is the dose-limiting organ if radioimmunoglobulin therapy is used alone. The addition of irradiation of the liver to radioimmunoglobulin therapy changes the dose-limiting organ from bone marrow to liver. The radiation hepatitis observed in dogs is very similar to that observed in humans and is reflected in early platelet consumption in the irradiated liver plus late elevations of liver enzymes and VOD in central hepatic veins on histological analysis. Future applications of combined liver irradiation and radioimmunoglobulin therapy in humans should use radioimmunoglobulin therapy agents which show minimal uptake by normal liver.
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PMID:Liver toxicity induced by combined external-beam irradiation and radioimmunoglobulin therapy. 787 Nov 56

Seventy-three BMT procedures (42 allogeneic-BMT, 30 autologous-BMT, 1 syngeneic transplant) were undertaken at the Shariati Hospital in Tehran between March 1991 and November 1993. Allogeneic-BMT was performed for thalassaemia major (n = 23), AML in complete remission (n = 3), severe aplastic anaemia (n = 7), CML (n = 7), dyskeratosis congenita (n = 2) and Fanconi anaemia (n = 1). Conditioning regimens comprised busulphan (BU) plus cyclophosphamide (CY) or CY only. Thirty-two (78%) of the 43 patients remain alive 1-34 months after BMT. Twelve patients died: the causes of death were haemorrhagic cystitis (n = 1), CMV pneumonitis (n = 1), GVHD (n = 3), infection (n = 3), rejection (n = 1), VOD (n = 2) and hepatitis (n = 1). Autologous-BMT was performed for patients with AML in CR (n = 16), ALL in CR (n = 9), lymphoma in relapse (n = 3), Ewing sarcoma (n = 1) and multiple myeloma (n = 1). The median age was 18 years. Conditioning regimens were Ara C plus CY, etoposide plus CY and high-dose melphalan. Sixteen (54%) of the 30 patients survive, 14 in continuous complete remission. The causes of death were relapse (AML (n = 7), ALL (n = 4), lymphoma (n = 1)), VOD (n = 1) and infection (n = 1).
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PMID:Bone marrow transplantation in Iran. 792 Mar 8

A 14-year-old girl with acute lymphoblastic leukemia in second remission received an allogeneic marrow graft from her HLA identical brother. Cyclosporine A and short term methotrexate were given for prophylaxis against graft versus host disease. On day 42 post transplantation elevation of SGOT and SGPT was recognized, rising the next day to 8,560IU and 2,590IU, respectively. Prothrombin activity dropped below 10%. HCV antibody and HBs antigen were both negative. Fulminant hepatitis was diagnosed, therefore plasma exchange was initiated. However, hepatic encephalopathy developed and she died on day 57. The postmortem liver appearance was consistent with early changes of veno-occlusive disease. Such atypical cases of VOD with late onset are difficult to distinguish from fulminant hepatitis but should be kept in mind.
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PMID:[Fulminant hepatitis-like veno-occlusive disease of the liver after allogeneic bone marrow transplantation in acute lymphoblastic leukemia]. 831 37

Review of liver biopsy or autopsy material from 33 patients with severe combined immunodeficiency or combined immunodeficiency and four patients with DiGeorge syndrome revealed a wide range of hepatic pathology. The most common abnormality was graft-versus-host disease (16 patients), followed by viral infection (4 patients had adenovirus hepatitis, 3 had cytomegalovirus hepatitis). Centrilobular fibrosis with or without veno-occlusive disease was seen in five patients. Three patients had nonspecific hepatitis, four had changes attributed to total parenteral nutrition, and two had lymphoproliferative disorders involving the liver. Both patients with lymphoproliferative disorders had received transplants. Two patients had resolving necrosis probably secondary to non-A, non-B hepatitis. One had atypical mycobacterial infection. Hemosiderosis was a common nonspecific abnormality, seen in nine patients. All patients with hepatic graft-versus-host disease had received transplants or nonirradiated blood products. Hepatic graft-versus-host disease varied in severity from hepatic necrosis with destruction of both large and small bile ducts in a transfusion-associated case to subtle damage to interlobular bile ducts. Even minimal bile duct changes correlated with the clinical impression of graft-versus-host disease in these patients. Late chronic graft-versus-host disease was not seen in any patient, although acute graft-versus-host disease sometimes occurred late after transplant.
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PMID:Pathology of the liver in severe combined immunodeficiency and DiGeorge syndrome. 837 33

The role of hepatitis C virus (HCV) infection in severe liver failure (LF) following bone marrow transplantation is still uncertain. We therefore decided to determine the presence of HCV-RNA in 31 patients who died of severe LF after BMT and in 26 matched BMT controls who did not develop LF. HCV-RNA was identified by polymerase chain reaction and anti-HCV by second generation enzyme-linked immunoassay and by 4-band recombinant immunoblotting assay in serum samples obtained before and after BMT. Biochemical and clinical parameters of liver disease were obtained by reviewing clinical records. LF developed at a median interval of 80 days (20-570) from transplantation and was clinically assessed as VOD (n = 7), liver GVHD (n = 5) or hepatitis (n = 19). HCV-RNA was detected, respectively, in 15/31 (48%) and in 12/26 (46%) of LF patients and controls (P = 0.9). Conversely, the risk of dying of LF was 62% and 53% (P = 0.5) respectively, for HCV-RNA positive and negative patients. Anti-HCV profile did not correlate with viremia, nor with type of liver disease. These findings indicate that, despite a 47% prevalence of HCV infection in our series, HCV-RNA positivity was neither a predictor of VOD nor a marker for life-threatening liver disease.
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PMID:Hepatitis C virus infection and liver failure in patients undergoing allogeneic bone marrow transplantation. 853 14

Patients with systemic lupus erythematosus (SLE) have a 25-50% chance of developing abnormal liver tests in their lifetime. This percentage does not include unconjugated hyperbilirubinaemia due to haemolysis associated with SLE, or elevated aspartate-aminotransferase caused by SLE-associated myositis. The most common cause is drug-induced hepatitis, while mild, predominantly lobular-but sometimes also portal and periportal-hepatitis reflecting SLE activity is another possibility. Other liver disease in SLE can be related to thrombotic events, whether or not associated with the lupus anticoagulant, including Budd-Chiari syndrome and veno-occlusive disease. Other liver abnormalities have been more or less frequently associated with SLE, such as nodular regenerative hyperplasia, perihepatitis, and hepatic or splenic rupture. Also viral hepatitis, obstructive jaundice, autoimmune hepatitis, primary biliary cirrhosis, granulomatous hepatitis, cryptococcus infection of the liver, chronic hepatitis with IgA or IgD deficiency, porphyria or idiopathic portal hypertension co-existing with SLE have been described.
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PMID:The spectrum of liver disease in systemic lupus erythematosus. 871 47

One hundred eighty-one consecutive patients with fulminant hepatic failure (FHF) presenting in a 2-year period were reviewed. In this cohort we examined the impact of pretransplant renal failure on mortality and morbidity following orthotopic liver transplantation (OLTx). Twenty-seven patients (18 female, 9 male) with a median age of 43.5 years (range 19-65 years) underwent OLTx. FHF was due to idiosyncratic drug reaction (n = 4), paracetamol overdose (n = 3), seronegative hepatitis (n = 17), hepatitis B (n = 1), veno-occlusive disease (n = 1), and Wilson's disease (n = 1). Renal failure was present in 14 patients, 7 of whom died (whereas there was 100% survival in patients without renal failure). Pretransplant renal failure was associated with prolonged mechanical ventilation (13 days vs 6 days, P = 0.05), prolonged intensive care stay (17 days vs 8 days, P = 0.01) and prolonged hospital stay (27 vs 21 days, P = NS). Pretransplant renal failure did not predict renal dysfunction at 1 year after OLTx. We conclude that the survival of patients transplanted for FHF is inferior to that of patients transplanted for chronic liver disease (67% vs 88% 1-year survival in Birmingham). For patients with FHF undergoing transplantation, pretransplant renal failure strongly predicts poor outcome with significantly greater consumption of resources.
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PMID:Liver transplantation for fulminant hepatic failure: importance of renal failure. 900 53


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