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)

This article reviews the primary circulatory liver diseases, which include Budd-Chiari syndrome, obstruction of the hepatic portion of the inferior vena cava, portal vein thrombosis, sinusoidal obstruction syndrome (veno-occlusive disease), nodular regenerative hyperplasia, and peliosis hepatis. In addition, two systemic cardiovascular diseases that impair hepatic circulation, ischemic hepatitis and congestive hepatopathy, are briefly discussed. A characteristic of the primary circulatory liver diseases is that portal hypertension usually precedes liver dysfunction; however, this is not the case with the primary parenchymal liver diseases, in which liver dysfunction always progresses before portal hypertension is manifested. Significant overlap exists among the diseases and risk factors that predispose patients to the primary circulatory liver diseases, though the pathogenesis of individual diseases varies.
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PMID:Vascular liver diseases. 1253 Sep 50

The different types of hepatotoxicity can be induced by drugs. Approximately 2%-5% of patients require hospitalization for jaundice. Drug-induced hepatic lesions are responsible for 10% of hepatitis cases in adults. Most hepatotoxic drug reactions are idiosyncratic and classified either as immunologic (hipersensitivity) or metabolic. In contrast to intrinsic hepatotoxins, these reactions are not dose-dependent nor predictable. The enzyme system responsible for drug biotransformation in liver is cytochrome P450, a large multigene family of enzymes with 300 members. Clinical presentation in patients who develop drug hepatotoxicity can be asymptomatic with mild biochemical abnormalities, resembling acute hepatitis or chronic autoimmune hepatitis, veno-occlusive disease and cirrhosis. Withdrawal of the drug usually leads to reversal of the lesion. A spectrum of drug induced hepatotoxicity, diagnosis and treatment is reviewed.
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PMID:[Clinical aspects and therapy of toxic hepatitis]. 1458 64

Liver disease is a well-known cause of early morbidity and mortality affecting 80% of patients receiving allogeneic bone-marrow transplantation (BMT). Drug toxicity, veno-occlusive disease (VOD), acute graft-versus-host disease (GVHD), and fungal, bacterial, and viral infections are the most frequent hepatic complications during this period. The aim of this retrospective study was to determine the prevalence and etiology of liver disease and its impact on mortality as well as to assess the predictive value of pre BMT hepatic biochemical tests on the subsequent occurrence of acute and/or chronic GVHD and patient mortality. Of a total of 236 patients who underwent allogeneic BMT, 82 were analysed. Liver dysfunction was found in 88%. The causes of liver disease were: acute GVHD, 40.2%; chronic GVHD, 15.9%; unknown, 9.8%; sepsis, 7.3%; hepatotoxicity, 6.1%; VOD, 3.7%; acute hepatitis and disease recurrence, 2.4%. The mortality rate was 37%. We found acute liver failure (ALF) in 10% of the deaths (8 patients). The causes of ALF in these cases were acute GVHD progression in 5, herpetic hepatitis in 1, disease recurrence in 1, and VOD in 1. The correlation coefficients indicating positive predictive values of pre BMT hepatic biochemical tests for the subsequent occurrence of acute GVHD, chronic GVHD, and mortality were 0.27, 0.14, and 0.43, respectively. There was no significant difference between patients with abnormal or normal pre BMT liver function tests in the frequency of acute and chronic GVHD or mortality.
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PMID:[Liver dysfunction in recipients of hematopoietic stem cells. Impact on mortality]. 1607 3

Hepatitis C virus (HCV) is a major cause of liver disease worldwide. After allogeneic Hematopoietic Cell Transplant (HCT), HCV is known to be associated with transient hepatitis in the immediate post-transplant period, and a potential risk factor of veno-occlusive disease (SOS). Very recently, HCV-infected HCT recipients have been shown to be at higher risk of earlier cirrhosis, leading to greater morbidity and mortality. Long-term survivors after HCT are thus at a high risk for HCV-related complications and, as a consequence, the treatment of HCV infection becomes critical. We describe here the potential clinical complications in HCV-infected recipients, in the short, but also the long-term follow-up after HCT. The pathophysiology of liver fibrosis is discussed as well as the present recommended therapy in this particular population.
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PMID:Allogeneic hematopoietic cell transplant in HCV-infected patients. 1843 17

Liver retransplantation carries a significantly higher morbidity and mortality compared with patients after single transplantations. The aim of this study was to review our outcomes in liver retransplantations. From February 1984 to February 2007, 409 liver transplantations were performed on 396 patients, including 13 retransplantations (3.2%) in 12 patients. The mean follow-up was 1.6 +/- 0.4 years (range, 0.1-5.2). The mean duration between the first and the second transplantation was 2.8 +/- 1.0 years (range, 15 days-11.6 years). The indications for the first liver transplantation included biliary atresia (n = 3), hepatitis B virus (HBV)-related cirrhosis with hepatoma (n = 3), fulminant hepatic failure (n = 2), HBV-related end-stage liver disease (n = 1), hepatitis C virus (HCV)-related end-stage liver disease (n = 1), neonatal hepatitis (n = 1), and glycogen storage disease (n = 1). The indications for retransplantations were secondary biliary cirrhosis (n = 3), veno-occlusive disease-related liver failure (n = 2), hepatic arterial occlusion and graft failure (n = 2), chronic rejection with hepatic graft failure (n = 2), recurrent HBV (n = 1) and de novo HBV-related decompensated cirrhosis (n = 1), and idiopathic graft failure (n = 1). There were 4 living donor and 9 deceased donor liver retransplantations. The cumulative survival rate was 71.4 +/- 14.4%, with an estimated mean survival time of 3.9 +/- 0.7 years. Our results showed that minimizing the rate of retransplantation was critical to enhance overall patient survival. Moreover, living donor liver retransplantation is another option within the short, yet critical, waiting period, after failure of the first graft. Provided that a suitable living donor is available, we recommend early retransplantation to minimize the risk of morbidity and mortality.
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PMID:Retransplantation for end-stage liver disease: a single-center Asian experience. 1892 80

We evaluate the outcomes in children with acute leukemia who received allogeneic hematopoietic stem cell transplantation (HCT) using unrelated donor. Fifty-six children in complete remission (CR) received HCT from unrelated donors between 2000 and 2007. Thirty-five had acute myeloid leukemia, and 21 had acute lymphoid leukemia. Stem cell sources included bone marrow in 38, peripheral blood in 4, and cord blood (CB) in 14. Four patients died before engraftment and 52 engrafted. Twenty patients developed grade II-IV acute graft-versus-host disease (GVHD) and 8 developed extensive chronic GVHD. With median follow-up of 39.1 months, event free survival and overall survival were 60.4% and 67.5%, respectively, at 5 yr. Events included relapse in 10 and treatment-related mortality (TRM) in 10. The causes of TRM included sepsis in 4, GVHD in 4 (1 acute GVHD and 3 chronic GVHD), veno-occlusive disease in 1 and fulminant hepatitis in 1. Patients transplanted with CB had event free survival of 57.1%, comparable to 63.2% for those transplanted with other than CB. In conclusion, HCT with unrelated donors is effective treatment modality for children with acute leukemia. In children with acute leukemia candidate for HCT but lack suitable sibling donor, unrelated HCT may be a possible treatment option at the adequate time of their disease.
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PMID:Unrelated hematopoietic stem cell transplantation for children with acute leukemia: experience at a single institution. 1979 91

Thiopurines play a pivotal role in the management of inflammatory bowel disease. Azathioprine and mercaptopurine have been associated with a number of liver abnormalities, including hepatitis, veno-occlusive disease, nodular regenerative hyperplasia, and peliosis hepatitis. Patients treated with azathioprine and mercaptopurine have their liver chemistry tests routinely checked due to this potential for hepatotoxicity. Hepatoportal sclerosis is a cause of non-cirrhotic portal hypertension that is increasingly being recognized; its etiopathogenesis is not well defined. We present the first case report of mercaptopurine-induced hepatoportal sclerosis leading to non-cirrhotic portal hypertension in a patient with Crohn's disease. He had been treated with mercaptopurine for five years, and his liver chemistry tests were always within normal limits. This case underscores the potential serious liver adverse events that may arise silently and go undetected during treatment with mercaptopurine, and should alert clinicians as to the potential need to discontinue mercaptopurine in this setting.
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PMID:Mercaptopurine-induced hepatoportal sclerosis in a patient with Crohn's disease. 2284 Nov 33

Abnormal liver biochemical tests are present in up to 30% of patients with inflammatory bowel disease (IBD), and therefore become a diagnostic challenge. Liver and biliary tract diseases are common extraintestinal manifestations for both Crohn's disease and ulcerative colitis (UC), and typically do not correlate with intestinal activity. Primary sclerosing cholangitis (PSC) is the most common hepatobiliary manifestation of IBD, and is more prevalent in UC. Approximately 5% of patients with UC develop PSC, with the prevalence reaching up to 90%. Cholangiocarcinoma and colon cancer risks are increased in these patients. Less common disorders include autoimmune hepatitis/PSC overlap syndrome, IgG4-associated cholangiopathy, primary biliary cirrhosis, hepatic amyloidosis, granulomatous hepatitis, cholelithiasis, portal vein thrombosis, liver abscess, and non-alcoholic fatty liver disease. Hepatitis B reactivation during immunosuppressive therapy is a major concern, with screening and vaccination being recommended in serologically negative cases for patients with IBD. Reactivation prophylaxis with entecavir or tenofovir for 6 to 12 mo after the end of immunosuppressive therapy is mandatory in patients showing as hepatitis B surface antigen (HBsAg) positive, independently from viral load. HBsAg negative and anti-HBc positive patients, with or without anti-HBs, should be closely monitored, measuring alanine aminotransferase and hepatitis B virus DNA within 12 mo after the end of therapy, and should be treated if the viral load increases. On the other hand, immunosuppressive therapy does not seem to promote reactivation of hepatitis C, and hepatitis C antiviral treatment does not influence IBD natural history either. Most of the drugs used for IBD treatment may induce hepatotoxicity, although the incidence of serious adverse events is low. Abnormalities in liver biochemical tests associated with aminosalicylates are uncommon and are usually not clinically relevant. Methotrexate-related hepatotoxicity has been described in 14% of patients with IBD, in a dose-dependent manner. Liver biopsy is not routinely recommended. Biologics-related hepatotoxicity is rare, but has been shown most frequently in patients treated with infliximab. Thiopurines have been associated with veno-occlusive disease, regenerative nodular hyperplasia, and liver peliosis. Routine liver biochemical tests are recommended, especially during the first month of treatment. All these conditions should be considered in IBD patients with clinical or biochemical features suggestive of hepatobiliary involvement. Diagnosis and management of these disorders usually involve hepatologists and gastroenterologists due to its complexity.
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PMID:Hepatobiliary manifestations in inflammatory bowel disease: the gut, the drugs and the liver. 2425 64

Hepatic lesions in nondomestic felids are poorly characterized. The purpose of this study was to evaluate hepatic lesions in 90 captive, nondomestic felids including tigers, cougars, and lions. Hepatic lesions were histologically characterized as vacuolar change (lipidosis or glycogenosis), biliary cysts, biliary hyperplasia, hepatitis, necrosis, neoplasia, fibrosis, veno-occlusive disease, cholestasis, hematoma, congestion, or hemorrhage. Stepwise logistic regression analyses were performed for vacuolar change, benign biliary lesions, hepatitis, lipogranulomas, extramedullary hematopoiesis, and hepatic stellate cell hypertrophy and hyperplasia, with species as the outcome variable. Ninety cats met the inclusion criteria. Seventy livers (78%) contained 1 or more lesions. Hepatocellular vacuolar change (41/90 [46%]) was the most common lesion overall. Extramedullary hematopoiesis, lipogranulomas, and hepatic stellate cell hyperplasia were also common. One snow leopard had veno-occlusive disease. Tigers were more likely than other felids to have no significant hepatic histologic lesions (odds ratio [OR], 12.687; P = .002), and lions were more likely to have biliary cysts (OR, 5.97; P = .021). Six animals (7%) died of hepatic disease: cholangiocellular carcinoma (n = 2) and 1 each of hepatic lipidosis, hepatocellular necrosis, pyogranulomatous hepatitis, and suppurative cholecystitis. Hepatocellular iron and copper accumulations were present in 72 of 90 (80%) and 10 of 90 (11%) sections, respectively. Sinusoidal fibrosis was common (74/90 [82%]) and primarily centrilobular (65/74 [88%]). Hepatocellular iron, copper, and fibrosis were not significantly associated with hepatic lesions. Primary hepatic disease was not a common cause of death in nondomestic felids in this study.
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PMID:Hepatic lesions in 90 captive nondomestic felids presented for autopsy. 2478 21

Veno-occlusive disease/sinusoidal obstruction syndrome (VOD/SOS) of the liver is a serious, early complication of haematopoietic stem cell transplantation (HSCT), severe and very severe forms of which are associated with a high mortality rate. A wide variety of patient, disease and treatment-related risk factors for VOD/SOS have been identified. Several bodies have published recommendations for the diagnosis, prevention and management of VOD/SOS following HSCT. A group of regional experts have developed a consensus statement on the diagnosis, prevention and management of VOD/SOS in the Middle East and North Africa region to help in the management of HSCT patients in the region. Risk factors of particular relevance in the region include iron overload in thalassaemia patients, some hereditary metabolic disorders due to consanguinity and infection with hepatitis virus B or C. Recommendations include diagnosis of VOD/SOS based on established clinical criteria, prophylaxis with defibrotide and/or ursodeoxycholic acid in patients at increased risk of VOD/SOS, and treatment with defibrotide for patients with severe/very severe VOD/SOS (and, if clinically indicated, in those with moderate or rapidly progressing VOD/SOS, as per the new European Society for Blood and Marrow Transplantation classification).
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PMID:Veno-occlusive disease/sinusoidal obstruction syndrome after haematopoietic stem cell transplantation: Middle East/North Africa regional consensus on prevention, diagnosis and management. 2789 44


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